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1.
Wiad Lek ; 74(3 cz 1): 535-538, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-33813464

RESUMEN

OBJECTIVE: The aim: To increase the effectiveness of treatment of sinusitis polyposa patients, develop and introduce a new non-traditional complex method of influencing several links of the pathogenesis of this disease, including laser therapy and laser puncture, used in the postoperative period. PATIENTS AND METHODS: Materials and methods: In 60 rhinosinusitis polyposa patients the indicators of lipid peroxidation and the state of antioxidant protection were studied. Depending on the type of treatment, the patients were divided into two groups: the first included 30 people who underwent traditional surgical intervention, and the second - 30 people who used complex therapy, including in the postoperative period endonasal laser exposure and laser puncture. Methods: clinical data, the functional state of the nasal mucosa, indicators of lipid peroxidation (hydroperoxide, malondialdehyde) and antioxidant activity (glutathione peroxidase, glutathione reductase, reduced glutathione, superoxide cismutase, catalase) of erythrocyte membranes and blood serum were studied. RESULTS: Results: The proposed complex method for treating lipids of erythrocyte membranes and serum, which includes endonasal surgical intervention, endonasal laser therapy and laser puncture leads to the normalization of physiological functions of the nose, activates antioxidant protection and reduces the peroxide activity of lipids in the membranes of erythrocytes and blood serum. CONCLUSION: Conclusions: When examining patients in the long-term (after 1 year) period, a significant improvement in 85.7% of cases, an improvement in 10.7%, and absence of effect in 3.6% was achieved. Thus, the proposed method of therapy can be recommended for widespread use in medical institutions.


Asunto(s)
Sinusitis , Superóxido Dismutasa , Antioxidantes , Catalasa/metabolismo , Glutatión Peroxidasa/metabolismo , Humanos , Peroxidación de Lípido , Sinusitis/terapia , Superóxido Dismutasa/metabolismo
2.
Medicine (Baltimore) ; 100(11): e23666, 2021 Mar 19.
Artículo en Inglés | MEDLINE | ID: mdl-33725925

RESUMEN

ABSTRACT: We aimed to investigate the effect of Kelch-like ECH-associated protein 1/NF-E2 p45-related factor 2 (Keap1/Nrf2) pathway on the biological function of trophoblast cells in oxidative stress model at the cellular level, and analyzed the expression level and clinical significance of Keap1/Nrf2 pathway and related antioxidant factors in placental tissues of Preeclampsia (PE) patients at clinical level. In present study, we found that under hypoxia/reoxygenation conditions, the activity of oxidative stress-related enzymes (CAT, GSH-Px, SOD) in HTR8/SVneo cells was significantly lower than that before treatment (P < .01). The activities of CAT, GSH-Px and SOD in HTR8/SVneo cells in SiRNA+H/R group decreased significantly (P < .01), indicating the important defense effect of Keap1/Nrf2 signaling pathway in oxidative stress. As a control group of Nrf2 SiRNA+H/R group, Si-NC+H/R group had CAT, GSH-Px and SOD activities decreasing, which was similar to that in H/R group. Moreover, the activities of oxidative stress-related active enzymes in patients with PE were further confirmed by detecting and comparing the activities of CAT, GSH-Px and SOD in placental tissues. The results showed that the activity of SOD (P < .001), GSH-Px (P < .01) and CAT (P < .01) in placental tissues of patients with PE were significant different from those of normal placental tissues. The expression level of Keap1 in placenta of patients with PE was slightly lower than that of normal placenta. While the expression of Nrf2 in placenta of patients with PE was significantly higher than that of normal placenta. HO-1 expression in placenta of patients with PE was significantly higher than that of normal placenta. These results implicate the importance of Keap-1/Nrf2 pathway in PE.


Asunto(s)
Hipertensión Inducida en el Embarazo/enzimología , Proteína 1 Asociada A ECH Tipo Kelch/metabolismo , Factor 2 Relacionado con NF-E2/metabolismo , Estrés Oxidativo/fisiología , Preeclampsia/enzimología , Catalasa/metabolismo , China , Femenino , Glutatión Peroxidasa/metabolismo , Humanos , Placenta/citología , Embarazo , Superóxido Dismutasa/metabolismo , Trofoblastos/enzimología
3.
Chem Biol Interact ; 338: 109402, 2021 Apr 01.
Artículo en Inglés | MEDLINE | ID: mdl-33587916

RESUMEN

Cisplatin is an important antineoplastic drug used in multiple chemotherapeutic regimens but unfortunately causes serious toxic effects as ovarian and uterine toxicity. This study aimed to investigate the potential protective effect of resveratrol (RSV) against cisplatin-induced ovarian and uterine toxicity in female rats. Thirty-two female Wistar rats were divided randomly into four groups (n = 8 in each). Control group received oral normal saline for 28 days; RSV group received RSV (10 mg/kg; daily) via oral gavage; CIS group received a single dose of CIS (7 mg/kg; i.p.) on the 21st day; (CIS + RSV) group received both RSV and CIS by the same schedules and doses of RSV and CIS groups, respectively. Results demonstrated a significant decrease in MDA level and a significant increase in both glutathione content and activity of the antioxidant enzymes GPx, SOD, and CAT in the tissues of the ovary and uterus of CIS + RSV group in comparison to that of CIS group (P<0.05), also there are significantly decreased tissue levels of the proinflammatory cytokines and enzymes (NF-κB, IL-1ß, IL-6, TNF-α, COX-2, and iNOS), increased estradiol, progesterone, prolactin and decreased FSH serum levels in CIS + RSV group compared to CIS group (P < 0.05). Moreover, there is downregulation of tissues Cleaved Caspase-3, NF-κB and Cox-2 proteins as shown in Western blot analysis, also apoptosis was significantly inhibited, evidenced by downregulation of Bax and upregulation of Bcl-2 proteins, and the ovarian and uterine histological architecture and integrity were maintained in CIS + RSV group compared to CIS group. In conclusion, these findings indicate that RSV has beneficial effects in ameliorating cisplatin-induced oxidative stress, inflammation, and apoptosis in the ovarian and uterine tissues of female rats.


Asunto(s)
Apoptosis/efectos de los fármacos , Cisplatino/efectos adversos , Inflamación/patología , Ovario/patología , Estrés Oxidativo/efectos de los fármacos , Sustancias Protectoras/farmacología , Resveratrol/farmacología , Útero/patología , Animales , Antioxidantes/metabolismo , Biomarcadores/metabolismo , Catalasa/metabolismo , Ciclooxigenasa 2/metabolismo , Citocinas/metabolismo , Estradiol/sangre , Femenino , Hormona Folículo Estimulante/sangre , Glutatión/metabolismo , Glutatión Peroxidasa/metabolismo , Malondialdehído/metabolismo , Modelos Biológicos , FN-kappa B/metabolismo , Óxido Nítrico Sintasa de Tipo II/metabolismo , Ovario/efectos de los fármacos , Progesterona/sangre , Prolactina/sangre , Carbonilación Proteica/efectos de los fármacos , Ratas Wistar , Superóxido Dismutasa/metabolismo , Proteína X Asociada a bcl-2/metabolismo
4.
Artículo en Chino | MEDLINE | ID: mdl-33535330

RESUMEN

Objective: To investigate the neurotoxicity of crotonaldehyde exposure in male rats and its possible mechanism of action. Methods: From July to October 2019, 24 specific pathogen-free male Wistar rats were randomly divided into control group and 2.5, 4.5, and 8.5 mg/kg exposure groups, with 6 rats in each group, and the rats in these groups were given oral administration of crotonaldehyde solution at doses of 0.0, 2.5, 4.5, and 8.5 mg/kg, respectively, 5 times a week for 90 consecutive days. Body weight was measured after exposure, and brain tissue and liver tissue were collected. The activity of acetylcholinesterase (AChE) in brain tissue and the level of acetylcholine (ACh) in liver tissue were measured; The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the levels of malondialdehyde (MDA) and reduced glutathione (GSH) in brain tissue were measured; ELISA was used to measure the levels of interleukin-6 (IL-6) , interleukin-1ß (IL-1ß) , and tumor necrosis factor-α (TNF-α) in brain tissue. Results: Compared with the control group, the 2.5, 4.5, and 8.5 mg/kg exposure groups had a significant reduction in the activity of AChE in brain tissue, and the 8.5 mg/kg exposure group had a significant increase in the level of ACh in liver tissue (P<0.05) . Compared with the control group, the 4.5 and 8.5 mg/kg exposure groups had a significant increase in the level of MDA and significant reductions in the level of GSH and the activities of SOD and GSH-Px in brain tissue (P<0.05) . Compared with the control group, the 2.5, 4.5, and 8.5 mg/kg exposure groups had significant increases in the levels of TNF-α and IL-6 in brain tissue, and the 4.5 and 8.5 mg/kg exposure groups had a significant increase in the level of IL-1ß (P<0.05) . Conclusion: Crotonaldehyde exposure can induce nervous system injury in rats, possibly by altering oxidative balance and upregulating the expression of inflammatory factors in brain tissue.


Asunto(s)
Aldehídos , Estrés Oxidativo , Animales , Glutatión Peroxidasa/metabolismo , Masculino , Malondialdehído , Ratas , Ratas Wistar , Superóxido Dismutasa/metabolismo
5.
Chem Biol Interact ; 337: 109337, 2021 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-33548266

RESUMEN

This study aimed to evaluate the in vitro effects of syringic acid on human colorectal cancer cells (SW-480) and the effect of orally administered syringic acid on in vivo models of colorectal cancer induced in rats by administration of 1,2-dimethylhydrazine (DMH). In vitro effects of syringic acid treatment on human colorectal cancer SW-480 cell lines were assessed by performing cell proliferation assay (MTT and Trypan Blue staining), apoptosis assays (TUNEL assay, Annexin-V/PI flowcytometry and lactate dehydrogenase release assay), measuring reactive oxygen species (ROS), antioxidant enzymes and DNA damage, and evaluating protein levels of proliferative genes, and autophagy markers. In vitro anti-cancer roles of syringic acid were studied in rats with DMH-induced colorectal cancer cells. The effect of orally administered syringic acid (50 mg/kg) on tumor growth and incidence was studied in four groups (n = 6) of animals injected with DMH and treated for 15 weeks. Syringic acid treatment resulted in a significant dose-dependent inhibition of cellular proliferation, induction of apoptosis through increasing cellular ROS and DNA damage levels, as well as downregulating major proliferative genes. In vivo, treatment of rats with syringic acid demonstrated a statistically significant tumor volume and incidence reduction when compared to the control. This is the first study demonstrating an in vivo growth inhibitory effect of orally administered syringic acid on colorectal tumors in rats.


Asunto(s)
Antineoplásicos/farmacología , Apoptosis/efectos de los fármacos , Ácido Gálico/análogos & derivados , Animales , Antineoplásicos/uso terapéutico , Autofagia/efectos de los fármacos , Catalasa/metabolismo , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Neoplasias Colorrectales/tratamiento farmacológico , Neoplasias Colorrectales/patología , Daño del ADN/efectos de los fármacos , Ácido Gálico/farmacología , Ácido Gálico/uso terapéutico , Glutatión Peroxidasa/metabolismo , Humanos , Proteínas Proto-Oncogénicas c-akt/metabolismo , Ratas , Especies Reactivas de Oxígeno/metabolismo , Trasplante Heterólogo , Proteína p53 Supresora de Tumor/metabolismo
6.
Ecotoxicol Environ Saf ; 213: 111987, 2021 Apr 15.
Artículo en Inglés | MEDLINE | ID: mdl-33582408

RESUMEN

Protective effects of estrogen (E2) on traumatic brain injury (TBI) have been determined. In this study, the hepatoprotective effects of E2 after TBI through its receptors and oxidative stress regulation have been evaluated. Diffuse TBI induced by the Marmarou method in male rats. G15, PHTPP, MPP, and ICI182-780 as selective antagonists of E2 were injected before TBI. The results indicated that TBI induces a significant increase in liver enzymes [Alkaline phosphatase (ALP), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Glutamyl transferase (GGT)], and oxidants levels [Malondialdehyde (MDA), Nitric oxide (NO)] and decreases in antioxidant biomarkers [Glutathione peroxidase (GPx) and Superoxide dismutase (SOD)] in the brain and liver, and plasma. We also found that E2 significantly preserved levels of these biomarkers and enzymatic activity. All antagonists inhibited the effects of E2 on increasing SOD and GPx. Also, the effects of E2 on brain MDA levels were inhibited by all antagonists, but in the liver, only ICI + G15 + E2 + TBI group was affected. The impacts of E2 on brain and liver and plasma NO levels were inhibited by all antagonists. The current findings demonstrated that E2 probably improved liver injury after TBI by modulating oxidative stress. Also, both classic (ERß, ERα) and non-classic [G protein-coupled estrogen receptor (GPER)] receptors are affected in the protective effects of E2.


Asunto(s)
Estradiol/farmacología , Sustancias Protectoras/farmacología , Alanina Transaminasa/metabolismo , Animales , Antioxidantes/metabolismo , Aspartato Aminotransferasas/metabolismo , Lesiones Traumáticas del Encéfalo/metabolismo , Estradiol/metabolismo , Receptor alfa de Estrógeno/metabolismo , Receptor beta de Estrógeno/metabolismo , Estrógenos/metabolismo , Glutatión Peroxidasa/metabolismo , Hígado/efectos de los fármacos , Masculino , Malondialdehído/metabolismo , Estrés Oxidativo/efectos de los fármacos , Ratas , Receptores Estrogénicos/metabolismo , Superóxido Dismutasa/metabolismo
7.
Int J Mol Sci ; 22(2)2021 Jan 15.
Artículo en Inglés | MEDLINE | ID: mdl-33467410

RESUMEN

Ethanol abuse is a common issue in individuals with sedentary lifestyles, unbalanced diets, and metabolic syndrome. Both ethanol abuse and metabolic syndrome have negative impacts on the central nervous system, with effects including cognitive impairment and brain oxidative status deterioration. The combined effects of ethanol abuse and metabolic syndrome at a central level have not yet been elucidated in detail. Thus, this work aims to determine the effects of ethanol intake on a mouse model of metabolic syndrome at the behavioral and biochemical levels. Seven-week-old male control (B6.V-Lep ob/+JRj) and leptin-deficient (metabolic syndrome) (B6.V-Lep ob/obJRj) mice were used in the study. Animals were divided into four groups: control, ethanol, obese, and obese-ethanol. Ethanol consumption was monitored for 6 weeks. Basal glycemia, insulin, and glucose overload tests were performed. To assess short- and long-term memory, an object recognition test was used. In order to assess oxidative status in mouse brain samples, antioxidant enzyme activity was analyzed with regard to glutathione peroxidase, glutathione reductase, glutathione, glutathione disulfide, lipid peroxidation products, and malondialdehyde. Ethanol intake modulated the insulin response and impaired the oxidative status in the ob mouse brain.


Asunto(s)
Modelos Animales de Enfermedad , Etanol/farmacología , Síndrome Metabólico/metabolismo , Receptores de Leptina/deficiencia , Animales , Antioxidantes/metabolismo , Glucemia/metabolismo , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Depresores del Sistema Nervioso Central/administración & dosificación , Depresores del Sistema Nervioso Central/farmacología , Etanol/administración & dosificación , Glutatión/metabolismo , Glutatión Peroxidasa/metabolismo , Glutatión Reductasa/metabolismo , Humanos , Insulina/sangre , Insulina/metabolismo , Masculino , Malondialdehído/metabolismo , Síndrome Metabólico/sangre , Síndrome Metabólico/genética , Ratones Endogámicos C57BL , Ratones Noqueados , Obesidad/sangre , Obesidad/genética , Obesidad/metabolismo , Receptores de Leptina/genética
8.
Int J Mol Sci ; 22(1)2021 Jan 02.
Artículo en Inglés | MEDLINE | ID: mdl-33401717

RESUMEN

Risperidone, a second-generation antipsychotic drug used for schizophrenia treatment with less-severe side effects, has recently been applied in major depressive disorder treatment. The mechanism underlying risperidone-associated metabolic disturbances and liver and renal adverse effects warrants further exploration. This research explores how risperidone influences weight, glucose homeostasis, fatty liver scores, liver damage, and renal impairment in high-fat diet (HFD)-administered C57BL6/J mice. Compared with HFD control mice, risperidone-treated obese mice exhibited increases in body, liver, kidney, and retroperitoneal and epididymal fat pad weights, daily food efficiency, serum triglyceride, blood urea nitrogen, creatinine, hepatic triglyceride, and aspartate aminotransferase, and alanine aminotransferase levels, and hepatic fatty acid regulation marker expression. They also exhibited increased insulin resistance and glucose intolerance but decreased serum insulin levels, Akt phosphorylation, and glucose transporter 4 expression. Moreover, their fatty liver score and liver damage demonstrated considerable increases, corresponding to increases in sterol regulatory element-binding protein 1 mRNA, fatty acid-binding protein 4 mRNA, and patatin-like phospholipid domain containing protein 3 expression. Finally, these mice demonstrated renal impairment, associated with decreases in glutathione peroxidase, superoxide dismutase, and catalase levels. In conclusion, long-term administration of risperidone may exacerbate diabetes syndrome, nonalcoholic fatty liver disease, and kidney injury.


Asunto(s)
Intolerancia a la Glucosa/metabolismo , Insulina/sangre , Enfermedad del Hígado Graso no Alcohólico/enzimología , Enfermedad del Hígado Graso no Alcohólico/metabolismo , Risperidona/farmacología , Adipocitos/citología , Adipocitos/efectos de los fármacos , Adiponectina/metabolismo , Alanina Transaminasa/sangre , Animales , Aspartato Aminotransferasas/sangre , Peso Corporal/efectos de los fármacos , Catalasa/metabolismo , Proteínas de Unión al ADN/metabolismo , Ácido Graso Sintasas/sangre , Proteínas de Unión a Ácidos Grasos/genética , Proteínas de Unión a Ácidos Grasos/metabolismo , Glutatión Peroxidasa/metabolismo , Resistencia a la Insulina , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Obesos , Fosfolipasas A2 Calcio-Independiente/metabolismo , Fosforilación , Proteínas Proto-Oncogénicas c-akt/metabolismo , Proteína 1 de Unión a los Elementos Reguladores de Esteroles/genética , Proteína 1 de Unión a los Elementos Reguladores de Esteroles/metabolismo , Superóxido Dismutasa-1/metabolismo , Factores de Transcripción/metabolismo , Triglicéridos/sangre
9.
Ecotoxicol Environ Saf ; 211: 111930, 2021 Mar 15.
Artículo en Inglés | MEDLINE | ID: mdl-33472113

RESUMEN

Emerging research in mammalian cells suggests that ionic (AgNO3) and nano silver (AgNP) can disrupt the metabolism of selenium which plays a vital role in oxidative stress control. However, the effect of silver (Ag) on selenoprotein function in fish is poorly understood. Here we evaluate the effects of AgNO3 and citrate coated AgNP (cit-AgNP) on selenoprotein function and oxidative stress using a fish cell line derived from the rainbow trout (Oncorhynchus mykiss) intestine (RTgutGC). Cell viability was evaluated using a cytotoxicity assay which measures simultaneously metabolic activity, membrane integrity and lysosome integrity. Cells exposed to equimolar amounts of AgNO3 and cit-AgNP accumulated the same amount of silver intracellularly, however AgNO3 was more toxic than cit-AgNP. Selenoenzymes glutathione peroxidase (GPx) and thioredoxin reductase (TrxR) mRNA levels and enzyme activity were measured. While mRNA levels remained unaffected by AgNO3 or cit-AgNP, the enzyme activity of GPx was inhibited by AgNO3 (1 µM) and cit-AgNP (5 µM) and TrxR activity was inhibited by AgNO3 (0.4 µM) and cit-AgNP (1, 5 µM). Moreover, cells exposed to 1 µM of AgNO3 and cit-AgNP showed an increase in metallothionein b (MTb) mRNA levels at 24 h of exposure, confirming the uptake of silver, but returned to control levels at 72 h suggesting silver scavenging by MTb. Oxidative stress was not observed at any of the doses of AgNO3 or cit-AgNP tested. Overall, this study shows that AgNO3 or cit-AgNP can inhibit the activity of selenoenzymes but do not induce oxidative stress in RTgutGC cells.


Asunto(s)
Nanopartículas del Metal/toxicidad , Selenoproteínas/metabolismo , Plata/toxicidad , Animales , Línea Celular , Supervivencia Celular/efectos de los fármacos , Citratos , Ácido Cítrico , Glutatión Peroxidasa/metabolismo , Intestinos , Iones/metabolismo , Metalotioneína/metabolismo , Oncorhynchus mykiss/metabolismo , Estrés Oxidativo/efectos de los fármacos , Selenio , Nitrato de Plata/toxicidad
10.
Ecotoxicol Environ Saf ; 211: 111920, 2021 Mar 15.
Artículo en Inglés | MEDLINE | ID: mdl-33497861

RESUMEN

Azoxystrobin is a broad-spectrum strobilurin fungicide for use on a wide range of crops available to end-users as formulated products. Due to its extensive application, it has been detected in aquatic ecosystems, raising concerns about its environmental impact, which is still poorly explored. The objective of this work was to study the effects of a commercial formulation of azoxystrobin in the zebrafish embryo model. Sublethal and lethal effects were monitored during the exposure period from 2 h post fertilisation (hpf) to 96 hpf after exposure to azoxystrobin concentrations (1, 10 and 100 µg L-1). The responses of antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR)) as well as detoxifying enzymes (glutathione-s-transferase (GST) and carboxylesterase (CarE)) were evaluated at 96 hpf. Similarly, glutathione levels (reduced (GSH) and oxidised (GSSG) glutathione), neurotransmission (acetylcholinesterase (AChE)) and anaerobic respiration (lactate dehydrogenase (LDH)) -related enzymes were assayed. At 120 hpf, larvae from each group were used for behaviour analysis. Results from this study showed concentration-dependent teratogenic effects, particularly by increasing the number of malformations (yolk and eye), with a higher prevalence at the highest concentration. However, it was found that the lowest concentration induced a high generation of reactive oxygen species (ROS) and increased activity of SOD, GST, and CarE. In addition, GR and GSSG levels were decreased by the lowest concentration, suggesting an adaptive response to oxidative stress, which is also supported by the increased AChE activity and absence of behavioural changes. These findings advance the knowledge of the azoxystrobin developmental and environmental impacts, which may impose ecotoxicological risks to non-target species.


Asunto(s)
Embrión no Mamífero/efectos de los fármacos , Fungicidas Industriales/toxicidad , Pirimidinas/toxicidad , Estrobilurinas/toxicidad , Contaminantes Químicos del Agua/toxicidad , Pez Cebra/embriología , Animales , Antioxidantes/farmacología , Catalasa/metabolismo , Ecosistema , Embrión no Mamífero/fisiología , Glutatión Peroxidasa/metabolismo , Glutatión Reductasa/metabolismo , Glutatión Transferasa/metabolismo , Estrés Oxidativo/efectos de los fármacos , Especies Reactivas de Oxígeno , Estrobilurinas/farmacología , Superóxido Dismutasa/metabolismo , Pez Cebra/metabolismo
11.
Aquat Toxicol ; 231: 105737, 2021 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-33422861

RESUMEN

Increasing global research has identified microplastics (MPs) to be impacting marine organisms. The present work aimed at investigating the physiological and behavioral effects of thirty-six juvenile Sparus aurata exposed to control, virgin and weathered MPs enriched diets during a 21-day period under controlled conditions. Physiological effects were assessed in liver and brain using the following biomarkers: activities of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GRd), the detoxifying enzyme glutathione S-transferase (GST) and malondialdehyde (MDA) as indicative of lipid peroxidation. Individuals were recorded for behavior analysis (i.e. social interactions and feeding behavior). Results revealed an increase in cellular stress from control to weathered fish groups, with the virgin group showing intermediate levels in all quantified biomarkers. Significant differences were found in the liver for all biomarkers except for MDA, suggesting that exposure time to MPs in this experiment is long enough to trigger the activation of antioxidant enzymes but not to produce cell damage by lipid peroxidation. In brain tissue samples, fish from the weathered group presented significantly higher values for CAT and SOD, highlighting its function as primary antioxidants. Regarding behavioral effects, results showed that the two MPs enriched groups were significantly bolder during social interactions and, although no significantly, tended to be more active during feeding. In conclusion, MPs which have been weathered in marine environmental conditions produces a higher physiological response than virgin MPs but also, a physiological response is variable depending on the tissue analyzed. In addition, a short period to MP exposure seems to affect overall social and feeding behavior but, further research is needed to assess long-term effects of MP ingestion and its potential consequences on fish populations.


Asunto(s)
Conducta Animal , Ingestión de Alimentos , Microplásticos/toxicidad , Dorada/fisiología , Animales , Antioxidantes/metabolismo , Biomarcadores/metabolismo , Catalasa/metabolismo , Glutatión Peroxidasa/metabolismo , Glutatión Reductasa/metabolismo , Glutatión Transferasa/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Hígado/efectos de los fármacos , Hígado/metabolismo , Malondialdehído/metabolismo , Estrés Oxidativo/efectos de los fármacos , Análisis de Componente Principal , Superóxido Dismutasa/metabolismo , Contaminantes Químicos del Agua/toxicidad
12.
Ecotoxicol Environ Saf ; 211: 111896, 2021 Mar 15.
Artículo en Inglés | MEDLINE | ID: mdl-33440267

RESUMEN

Maduramicin, an extensively used anticoccidial drug, has been introduced into environment due to poorly absorbed in the intestine of broiler chicken. To understand the potential ecological toxicity of maduramicin on aquatic organisms, acute and subacute toxicity, hemolymph biochemistry, histopathology and the expressions of drug metabolism and stress response genes of crayfish (Procambius clarkii) were investigated in this study. For the first time, the 96 h median lethal concentration (LC50) of maduramicin on crayfish was 67.03 mgL-1 with a 95% confidence interval (54.06-81.32 mgL-1). Then, the crayfish were exposed to 0.7 mgL-1 (1/100 LC50), 3.5 mgL-1 (1/20 LC50) and 7.0 mgL-1 (1/10 LC50) maduramicin for 28 days. Maduramicin significantly altered biochemical parameters including AST, ALT, CK, LDH and ALP of hemolymph in crayfish at several time points. The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) of crayfish gills, hepatopancreas and abdominal muscle were significantly decreased or elevated by different concentrations of maduramicin treatment at varying time points. Furthermore, histopathological damage of crayfish gills, hepatopancreas and abdominal muscle were observed in a concentration-dependent manner. The expressions of metabolic and stress response genes (CYP450, GST, COX1, COX2, HSP70 and MT) in hepatopancreas of crayfish were significantly up-regulated by maduramicin (7.0 mgL-1) treatment for 8 h to 7 d, and returned to normal levels after the removal of maduramicin for 3-7 days. In conclusion, our findings demonstrated that environmental exposure of maduramicin threaten to the health of crayfish living in the areas nearby livestock farms or pharmaceutical factory. Crayfish exhibited resistance to the stress of maduramicin via activating drug metabolite and detoxification pathways.


Asunto(s)
Antibacterianos/toxicidad , Astacoidea/fisiología , Lactonas/toxicidad , Contaminantes Químicos del Agua/toxicidad , Animales , Organismos Acuáticos/metabolismo , Astacoidea/efectos de los fármacos , Catalasa/metabolismo , Branquias/efectos de los fármacos , Glutatión Peroxidasa/metabolismo , Hemolinfa/metabolismo , Hepatopáncreas/efectos de los fármacos , Inactivación Metabólica , Estrés Oxidativo/efectos de los fármacos , Alimentos Marinos , Superóxido Dismutasa/metabolismo
13.
Ecotoxicol Environ Saf ; 212: 111966, 2021 Apr 01.
Artículo en Inglés | MEDLINE | ID: mdl-33513483

RESUMEN

Triphenyltin (TPT) is a widely used pesticide that is highly toxic to a variety of organisms, including humans, and is a potential contributor to environmental pollution. The present study was conducted to evaluate the oxidative stress and immunotoxicity induced by TPT in goldfish (Carassius auratus) and the protective effects of fructooligosaccharide (FOS). Goldfish (mean weight of 13.3 ± 0.2 g) were randomly divided into six groups with three replicates: (G1) the control group, (G2) the 10 ng/L TPT group, (G3) the 0.4% FOS group, (G4) the 10 ng/L TPT + 0.4% FOS group, (G5) the 0.8% FOS group, and (G6) the 10 ng/L TPT + 0.8% FOS group. The results showed that 10 ng/L TPT induced oxidative stress and significantly decreased the activities of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), in the liver and the gene expression of SOD, GPx, metallothionein (MT), and peroxiredoxin-4 (Prdx-4). The concentration of malondialdehyde (MDA) and the gene expression of cytochrome P450 (CYP) and glutathione S-transferase (GST) in the liver were significantly increased in the TPT-treated group. Exposure to 10 ng/L TPT in water induced immune suppression and significantly decreased the activities of immune enzymes, such as lysozyme, myeloperoxidase (MPO), alternative complement (ACH50), acid phosphatase (ACP) and alkaline phosphatase (AKP), in the serum. TPT could stimulate the fish to generate large amounts of proinflammatory cytokines, including increased tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1ß (IL-1ß), and nitric oxide (NO) levels and TNF-α, IL-6, IL-1ß, and NF-κB mRNA expression. However, TPT-induced toxicity was significantly ameliorated in the groups treated with FOS, and FOS partly prevented alterations in the activities of antioxidant enzymes and the expression of antioxidant- and ROS scavenger-related genes. In addition, TPT-induced immune toxicity was significantly ameliorated in the groups treated with FOS. FOS markedly suppressed TNF-α, IL-6, IL-1ß, and NO production and TNF-α, IL-6, and IL-1ß mRNA expression in the TPT-treated groups. The study indicated that TPT-induced oxidative stress may play a critical role in inhibiting immunity. However, FOS administration attenuates TPT-induced oxidative stress and immune suppression in goldfish.


Asunto(s)
Carpa Dorada/fisiología , Sistema Inmunológico/efectos de los fármacos , Oligosacáridos/toxicidad , Compuestos Orgánicos de Estaño/toxicidad , Animales , Antioxidantes/metabolismo , Catalasa/metabolismo , Citocinas/metabolismo , Glutatión Peroxidasa/metabolismo , Carpa Dorada/metabolismo , Hígado/efectos de los fármacos , FN-kappa B/metabolismo , Estrés Oxidativo/fisiología , Superóxido Dismutasa/metabolismo
14.
Chem Biol Interact ; 337: 109392, 2021 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-33497687

RESUMEN

Arsenic is a toxic metalloid abundantly found in nature and used in many industries. Consumption of contaminated water mainly results in human exposure to arsenic. Toxicity (arsenicosis) resulting from arsenic exposure causes cerebral neurodegeneration. Protocatechuic acid (PCA), a phenol derived from edible plants, has antioxidant properties. The present study investigated the neuroprotective potential of PCA against arsenic-induced neurotoxicity in mice. Male Swiss albino mice were divided into four groups: (i) orally administered physiological saline, (ii) orally administered 100 mg/kg PCA, (iii) orally administered 5 mg/kg NaAsO2, and (iv) orally administered 100 mg/kg PCA 120 min prior to oral administration of 5 mg/kg NaAsO2. Each group received its respective treatment for 1 week, after which cortical tissues from each group were analyzed for various parameters of oxidative stress, proinflammatory cytokines, apoptosis-related proteins, and changes in histopathology. NaAsO2-treatment resulted in a significant increase in lipid peroxidation (LPO), inducible nitric oxide synthetase (iNOs), and NO levels, with a decrease in the levels of both enzymatic (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) and non-enzymatic (glutathione) antioxidant markers. Arsenic increased proinflammatory cytokine (tumor necrosis factor-α and interleukin-1ß) levels, enhanced caspase-3 and Bax expression, and reduced Bcl-2 expression. Furthermore, arsenic-exposure in mice decreased significantly acetylcholinesterase activity and brain-derived neurotrophic factor level in the cerebral cortex. Histopathological examination revealed changes in nerve cell cyto-architecture and distribution in arsenic-exposed brain tissue sections. PCA treatment before arsenic administration resulted in a positive shift in the oxidative stress and cytokine levels with decreased levels of LPO, iNOS, and NO. PCA pre-treatment considerably attenuated arsenic-associated histopathological changes in murine brain tissue. This study suggested that the presence of PCA may be responsible for the prevention of arsenic-induced neurotoxicity.


Asunto(s)
Apoptosis/efectos de los fármacos , Arseniatos/toxicidad , Hidroxibenzoatos/farmacología , Fármacos Neuroprotectores/farmacología , Estrés Oxidativo/efectos de los fármacos , Acetilcolinesterasa/metabolismo , Animales , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Encéfalo/patología , Factor Neurotrófico Derivado del Encéfalo/metabolismo , Catalasa/genética , Catalasa/metabolismo , Citocinas/genética , Citocinas/metabolismo , Glutatión Peroxidasa/metabolismo , Masculino , Ratones , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Superóxido Dismutasa/metabolismo
15.
Ecotoxicol Environ Saf ; 209: 111784, 2021 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-33316727

RESUMEN

Cysteine (Cys) is incorporated into several compounds which are involved in detoxification of heavy metals. It is evident from recent studies that Cys is effective in alleviating the toxicity of heavy metals. Nevertheless, little is known about the Cys-mediated alleviation of chromium (Cr) toxicity. In our study, the impacts of exogenous Cys on Cr-stressed maize (Zea mays L.) were examined by using physiological and proteomic analyses. The results showed that Cr (100 µM) increased the accumulation of hydrogen peroxide, decreased cell viability, enhanced lipid peroxidation and consequently inhibited plant growth. The application of Cys (500 µM) attenuated the adverse effects of Cr on seedling growth. Cys supplementation to Cr treated plants decreased Cr accumulation in the shoots and increased Cr accumulation in roots. Cys treatment also modulated the activities of antioxidant enzymes and increased endogenous Cys content. Sixty proteins in root tissue were significantly affected by exogenous Cys under Cr stress using two-dimensional electrophoresis. Forty-six differentially expressed proteins were successfully identified by MALDI-TOF/TOF mass spectrometry. These differentially expressed proteins were involved in various biological pathways such as stress response (41.3%), energy and carbohydrate metabolism (21.7%), protein metabolism (6.5%), amino acid metabolism (6.5%), and others of unknown functions. The defense response-related proteins including glutathione peroxidase, glutathione S-transferases, pathogenesis-related proteins, glyoxalases and superoxide dismutase were differently regulated by Cys suggesting their roles in the Cys-mediated Cr tolerance.


Asunto(s)
Antioxidantes/farmacología , Cromo/toxicidad , Cisteína/farmacología , Contaminantes del Suelo/toxicidad , Zea mays/fisiología , Antioxidantes/metabolismo , Cromo/metabolismo , Cisteína/metabolismo , Glutatión Peroxidasa/metabolismo , Peróxido de Hidrógeno/metabolismo , Lactoilglutatión Liasa/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Proteoma/efectos de los fármacos , Proteómica , Plantones/efectos de los fármacos , Superóxido Dismutasa/metabolismo , Zea mays/metabolismo
16.
Ecotoxicol Environ Saf ; 209: 111671, 2021 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-33360290

RESUMEN

Lead (Pb) is a toxic heavy metal pollutants and can damage male reproductive function. Selenium (Se) possesses an ability of antagonizing Pb toxicity. However, biological events in the process of Pb toxicity and mitigative effect of Se are not well understood. The aim of present research was to investigate potential mechanism of Se against Pb toxicity from the perspective of oxidative stress, heat shock response and autophagy in the spermatogonia and Leydig cell of chicken. The cells from one-day-old male Hyline chickens were treated with Se (0.5 µmol/L) and/or Pb (20 µmol/L) for 24 h, respectively. Cell viability, cell ultrastucture, Pb and Se concentrations, testosterone level, oxidative stress indicators and relative expression of heat shock proteins (HSPs) and autophagy-related genes were measured. The results showed that spermatogonia was more tolerant to Pb than Leydig cell; cell injury was confirmed via histological assessment, cell viability and testosterone level; oxidative stress was further indicated by the decrease of catalase, glutathione peroxidase, glutathione-s-transferase and superoxide dismutase activities and the increase of malondialdehyde and reactive oxygen species contents. Pb increased expression of HSPs (27, 40, 60, 70 and 90). Meanwhile Pb induced autophagy through up-regulation of autophagy-related proteins 5, Beclin 1, Dynein, light chain 3 (LC3)-I and LC3-II and down-regulation of mammalian target of rapamycin in two type cells of chicken. However, Se intervention mitigated the aforementioned alterations caused by Pb. In conclusion, Pb led to oxidative stress, which triggered heat shock response and autophagy; Se administration mitigated reproductive toxicity of Pb through strengthening antioxidant defense in the spermatogonia and Leydig cell of chicken.


Asunto(s)
Antioxidantes/farmacología , Plomo/toxicidad , Células Intersticiales del Testículo/efectos de los fármacos , Selenio/farmacología , Espermatogonias/fisiología , Animales , Antioxidantes/metabolismo , Autofagia/efectos de los fármacos , Catalasa/metabolismo , Pollos/metabolismo , Contaminantes Ambientales/metabolismo , Glutatión Peroxidasa/metabolismo , Proteínas de Choque Térmico/metabolismo , Plomo/metabolismo , Células Intersticiales del Testículo/metabolismo , Masculino , Malondialdehído/metabolismo , Estrés Oxidativo/efectos de los fármacos , Especies Reactivas de Oxígeno/metabolismo , Espermatogonias/metabolismo
17.
Ecotoxicol Environ Saf ; 209: 111801, 2021 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-33383342

RESUMEN

Hydrogen sulfide (H2S), a common air pollutant and toxic gas, is detrimental to organisms and the environment. Exposure to highly concentrated H2S can induce oxidative stress and autophagy. However, the mechanism underlying the liver damage caused by H2S has not been identified. Lipopolysaccharide (LPS), the key component of endotoxin, can induce oxidative stress and autophagy. For this experiment, we used one-day-old chickens as model organisms to evaluate the effects of H2S combined with LPS on oxidative stress and autophagy. The four groups (control group, LPS group, H2S group and H2S-LPS group) were observed by electron microscopy, detected by oxidative stress kit, analyzed by quantitative real-time quantitative PCR, and analyzed by Western blot. We found that the activities of antioxidant enzymes (superoxide dismutase, antioxidant glutathione, catalase, and glutathione peroxidase) decreased in the H2S group compared to those in the control group; however, malondialdehyde levels in the H2S group increased. Molecular-level studies showed that the expression of genes associated with the PI3K/ AKT/ TOR pathways in the H2S group decreased, whereas the expression of other autophagy-related genes (Beclin1, ATG5 and the ratio of LC3-II/ LC3-I) increased compared to that in the control group. These findings suggest that H2S caused oxidative stress and induced autophagy through the PI3K/ AKT/ TOR pathway in chicken liver cells. Additionally, exposure to H2S aggravated LPS-induced oxidative stress and autophagy injury. Capsule: Aerial exposure to H2S can cause oxidative stress in chicken livers and induce autophagy through the PI3K/AKT/TOR pathway, and can aggravate LPS-induced oxidative stress and autophagy.


Asunto(s)
Sulfuro de Hidrógeno/toxicidad , Lipopolisacáridos/metabolismo , Estrés Oxidativo/fisiología , Animales , Antioxidantes/metabolismo , Autofagia/efectos de los fármacos , Catalasa/metabolismo , Pollos/metabolismo , Glutatión Peroxidasa/metabolismo , Hepatocitos/metabolismo , Sulfuro de Hidrógeno/metabolismo , Hepatopatías , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Superóxido Dismutasa/metabolismo
18.
Life Sci ; 267: 118965, 2021 Feb 15.
Artículo en Inglés | MEDLINE | ID: mdl-33383050

RESUMEN

Arsenic as a one of the most important toxic metals could induce hepatotoxicity. Previous reports revealed the significance of oxidative stress in promoting of arsenic-induced liver toxicity. The aim of the present investigation is to evaluate the effect of chrysin (CHR), a natural flavonoid with potent antioxidant activity, against sodium arsenite (SA)-induced hepatotoxicity. Thirty male Wistar rats were divided into four groups: Group 1: received normal saline (2 ml/kg/day, orally for 21 days), Group 2: received SA (10 mg/kg/day, orally for 14 days), Group 3, 4 and 5: received CHR (25, 50 and 100 mg/kg/day, respectively, orally for 21 days) and SA (10 mg/kg/day, orally for 14 days) from the 7th day. Serum levels of alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase were evaluated. Moreover, liver glutathione peroxidase and myeloperoxidase activity as well as levels of protein carbonylation, malondialdehyde, glutathione, catalase, nitric oxide, superoxide dismutase, tumor necrosis factor-α and interleukin-1ß were evaluated. Moreover, histological evaluation was done. Our results revealed that treatment with CHR (more potentially at the dose of 100 mg/kg/day) before and alongside with SA significantly mitigated the SA-induced hepatotoxicity. Also, the hepatoprotective effect of CHR was verified by the histological evaluation of the liver. The results of current study demonstrated that CHR (100 mg/kg/day) could mitigate the oxidative stress and inflammation induced by SA in liver tissue.


Asunto(s)
Enfermedad Hepática Inducida por Sustancias y Drogas/tratamiento farmacológico , Flavonoides/farmacología , Hígado/metabolismo , Alanina Transaminasa/metabolismo , Fosfatasa Alcalina/metabolismo , Animales , Antioxidantes/farmacología , Arsenitos/toxicidad , Aspartato Aminotransferasas/metabolismo , Flavonoides/metabolismo , Glutatión/metabolismo , Glutatión Peroxidasa/metabolismo , Hígado/patología , Masculino , Malondialdehído/metabolismo , Oxidación-Reducción , Estrés Oxidativo/efectos de los fármacos , Ratas , Ratas Wistar , Compuestos de Sodio/toxicidad , Superóxido Dismutasa/metabolismo
19.
Mol Med Rep ; 23(1): 1, 2021 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-33215218

RESUMEN

S100a8 serves an important role in cell differentiation and is abnormally expressed in common tumors, but there are few studies on the association between S100a8 and brain I/R injury. The present study aimed to investigate the role of S100a8 in oxygen­glucose deprivation and reoxygenation (OGD/R)­induced BV2 microglia cell injury, and to elucidate the potential underlying molecular mechanisms. BV2 cells were exposed to OGD/R to mimic ischemia/reperfusion (I/R) injury in vitro. S100a8 expression was detected via reverse transcription­quantitative PCR and western blot analyses. Following transfection with short hairpin RNAs targeting S100a8, the levels of inflammatory cytokines and oxidative stress­related factors were determined using commercial kits. Apoptosis was assessed using flow cytometric analysis and the expression levels of apoptosis­related proteins were determined using western blot analysis. Subsequently, the mRNA and protein levels of Grb2­associated binder 1 (GAB1) were assessed following S100a8 silencing. Immunoprecipitation (IP) was performed to verify the association between S100a8 and GAB1. The levels of inflammation, oxidative stress and apoptosis were assessed following GAB1 silencing, along with S100a8 silencing in BV2 cells subjected to OGD/R. The results indicated that exposure to OGD/R markedly upregulated S100a8 expression in BV2 cells. S100a8 silencing inhibited inflammation, oxidative stress and apoptosis, accompanied by changes in the expression of related proteins. The IP assay revealed a strong interaction between GAB1 and S100a8. In addition, GAB1 silencing reversed the inhibitory effects of S100a8 silencing on inflammation, oxidative stress and apoptosis in OGD/R­stimulated BV2 cells. Taken together, the results of the present study demonstrated that S100a8 silencing alleviated inflammation, oxidative stress and the apoptosis of BV2 cells induced by OGD/R, partly by upregulating the expression of GAB1. Thus, these findings may potentially provide a novel direction to develop therapeutic strategies for cerebral I/R injury.


Asunto(s)
Proteínas Adaptadoras Transductoras de Señales/metabolismo , Calgranulina A/metabolismo , Inflamación/metabolismo , Estrés Oxidativo , Daño por Reperfusión/metabolismo , Proteínas Adaptadoras Transductoras de Señales/genética , Animales , Apoptosis/genética , Calgranulina A/genética , Línea Celular , Silenciador del Gen , Glucosa/metabolismo , Glutatión Peroxidasa/metabolismo , Inflamación/genética , Interleucina-1beta/metabolismo , Interleucina-6/metabolismo , Malondialdehído/metabolismo , Ratones , Microglía/metabolismo , Estrés Oxidativo/genética , Oxígeno/metabolismo , Daño por Reperfusión/etiología , Superóxido Dismutasa/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo , Regulación hacia Arriba
20.
Ecotoxicol Environ Saf ; 207: 111231, 2021 Jan 01.
Artículo en Inglés | MEDLINE | ID: mdl-32916527

RESUMEN

Lead, a common metallic contaminant, is widespread in the living environment, and has deleterious effects on the reproductive systems of humans and animals. Although numerous toxic effects of lead have been reported, the effects and underlying mechanisms of the impacts of lead exposure on the female reproductive system, especially oocyte maturation and fertility, remain unknown. In this study, mice were treated by gavage for seven days to evaluate the reproductive damage and role of Nrf2-mediated defense responses during lead exposure. Lead exposure significantly reduced the maturation and fertilization of oocytes in vivo. Additionally, lead exposure triggered oxidative stress with a decreased glutathione level, increased amount of reactive oxygen species, and abnormal mitochondrial distribution. Moreover, lead exposure caused histopathological and ultrastructural changes in oocytes and ovaries, along with decreases in the activities of catalase, glutathione peroxidase, total superoxide dismutase, and glutathione-S transferase, and increases in the levels of malonaldehyde in mouse ovaries. Further experiments demonstrated that lead exposure activated the Nrf2 signaling pathway to protect oocytes against oxidative stress by enhancing the transcription levels of antioxidant enzymes. In conclusion, our study demonstrates that lead activates the Nrf2/Keap1 pathway and impairs oocyte maturation and fertilization by inducing oxidative stress, leading to a decrease in the fertility of female mice.


Asunto(s)
Sustancias Peligrosas/toxicidad , Plomo/toxicidad , Animales , Antioxidantes/metabolismo , Catalasa/metabolismo , Femenino , Glutatión Peroxidasa/metabolismo , Humanos , Proteína 1 Asociada A ECH Tipo Kelch/metabolismo , Plomo/metabolismo , Malondialdehído/metabolismo , Ratones , Factor 2 Relacionado con NF-E2/metabolismo , Oocitos/efectos de los fármacos , Oogénesis/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Especies Reactivas de Oxígeno/metabolismo , Transducción de Señal/efectos de los fármacos , Superóxido Dismutasa/metabolismo
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