Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 33.819
Filtrar
1.
Ecotoxicol Environ Saf ; 203: 110974, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888622

RESUMO

Ammonia (NH3), an environmental pollutant, poses a serious threat to human and avian health. Although previous studies have showed that NH3 caused kidney injury, the molecular mechanisms of nephrotoxicity induced by NH3 remain unclear. To explore the mechanisms of NH3 nephrotoxicity, a total of 36 broiler chicks at one day of age were exposed to NH3. After 42 days of exposure, blood samples were collected to determine creatinine and uric acid; and kidney samples were weighted and then collected to detect ultrastructural changes, oxidative stress parameters, ATPases, necroptosis- and mitochondrial dynamics-related genes. The results showed that chickens exposed to NH3 showed lower relative kidney weight and an increase concentration in serum creatinine and uric acid. NH3 exposure caused nephrocyte necrosis and increased the expression of necroptosis-related genes (TNF-α, RIPK1, RIPK3, MLKL, and JNK). Besides, the activities of antioxidant systems (SOD, CAT, GSH-Px, and T-AOC) were reduced, whereas the concentrations of H2O2 and MDA were elevated. Lower activities of ATPases were obtained in NH3 treatment groups. Furthermore, the mitochondrial fission-related genes drp1 and mff were activated, and mitochondrial fusion-related genes opa1, mfn1 and mfn2 were suppressed after NH3 exposure. Based on the above results, we conclude that NH3 caused-oxidative stress and mitochondrial dysfunction mediated nephrocyte necroptosis in chickens. This study may provide new insight into NH3 nephrotoxicity.


Assuntos
Amônia/toxicidade , Poluentes Ambientais/toxicidade , Rim/efeitos dos fármacos , Dinâmica Mitocondrial/efeitos dos fármacos , Necroptose/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Animais , Antioxidantes/metabolismo , Galinhas , Expressão Gênica/efeitos dos fármacos , Humanos , Peróxido de Hidrogênio/metabolismo , Rim/ultraestrutura , Testes de Função Renal , Dinâmica Mitocondrial/genética , Tamanho do Órgão/efeitos dos fármacos , Estresse Oxidativo/genética , Proteína Serina-Treonina Quinases de Interação com Receptores/genética
2.
J Environ Pathol Toxicol Oncol ; 39(3): 225-234, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32865914

RESUMO

Asthma is marked by chronic irritation in the airway lumen of the lungs due to the accretion of inflammatory cells that influence the regular inhalation process. An extended buildup of inflammation leads to oxidative pressure and the repression of antioxidant functions. In the current study, a potential compound, boldine, was tested for the containment of provocative markers along the path of antiasthmatic activity in an ovalbumin (OVA)-induced asthmatic mice model. As an effect, the boldine (10 and 20 mg/kg) treatment suppressed inflammatory cells such as eosinophil, macrophage, neutrophil, lymphocyte, and other inflammatory markers in the bronchoalveolar lavage fluid (BALF) of OVA-induced mice. Likewise, immunoglobulin E (IgE) levels were drastically condensed in the serum of boldine-treated animals. Levels of enzymatic and nonenzymatic antioxidants, such as superoxide dismutase (SOD) and glutathione (GSH), were upregulated in the boldine treatment group compared to the asthmatic control group, which displays the antioxidant effects of boldine on asthmatic animals. Interestingly, the reactive oxygen species (ROS) and malonaldehyde (MDA) levels were repressed in the BALF of boldine-treated mice groups. Therefore, the effects of boldine are significant for the management of asthma, reducing the accrual of inflammatory cells, along with other inflammatory markers, while improving antioxidant markers and containing ROS. Hence, boldine may be an option for clinical trials of chronic asthma management.


Assuntos
Antiasmáticos/uso terapêutico , Anti-Inflamatórios/uso terapêutico , Antioxidantes/metabolismo , Aporfinas/uso terapêutico , Asma/tratamento farmacológico , Animais , Antiasmáticos/administração & dosagem , Anti-Inflamatórios/administração & dosagem , Aporfinas/administração & dosagem , Asma/imunologia , Biomarcadores/análise , Líquido da Lavagem Broncoalveolar/química , Líquido da Lavagem Broncoalveolar/citologia , Líquido da Lavagem Broncoalveolar/imunologia , Citocinas/análise , Modelos Animais de Doenças , Eosinófilos/citologia , Imunoglobulina E/sangue , Pulmão/efeitos dos fármacos , Pulmão/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Ovalbumina/imunologia , Espécies Reativas de Oxigênio/metabolismo , Testes de Função Respiratória
3.
Ecotoxicol Environ Saf ; 203: 111054, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888616

RESUMO

Quinclorac (3,7-dichloroquinoline-8-carboxylic acid, QNC) is a highly selective auxin herbicide that is typically applied to paddy rice fields. Its residue is a serious problem in crop rotations. In this study, Oryza sativa L. seedlings was used as a model plant to explore its biochemical response to abiotic stress caused by QNC and nZVI coexposure, as well as the interactions between QNC and nZVI treatments. Exposure to 5 and 10 mg/L QNC reduced the fresh biomass by 26.6% and 33.9%, respectively, compared to the control. The presence of 50 and 250 mg/L nZVI alleviated the QNC toxicity, but the nZVI toxicity was aggravated by the coexist of QNC. Root length was enhanced upon exposure to low or medium doses of both QNC and nZVI, whereas root length was inhibited under high-dose coexposure. Both nZVI and QNC, either alone or in combination, significantly inhibited the biosynthesis of chlorophyll, and the inhibition rate increased with elevated nZVI and QNC concentration. It was indicated that nZVI or QNC can affect the plant photosynthesis, and there was a significant interaction between the two treatments. Effects of QNC on the antioxidant response of Oryza sativa L. differed in the shoots and roots; generally, the introduction of 50 and 250 mg/L nZVI alleviated the oxidative stress (POD in shoots, SOD and MDA in roots) induced by QNC. However, 750 mg/kg nZVI seriously damaged Oryza sativa L. seedlings, which likely resulted from active iron deficiency. QNC could be removed from the culture solution by nZVI; as a result, nZVI suppressed QNC uptake by 20%-30%.


Assuntos
Antioxidantes/metabolismo , Ferro/toxicidade , Nanopartículas/toxicidade , Oryza/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Quinolinas/toxicidade , Poluentes do Solo/toxicidade , Transporte Biológico , Biomassa , Clorofila/metabolismo , Relação Dose-Resposta a Droga , Interações Medicamentosas , Oryza/crescimento & desenvolvimento , Oryza/metabolismo , Raízes de Plantas/efeitos dos fármacos , Raízes de Plantas/crescimento & desenvolvimento , Raízes de Plantas/metabolismo , Plântula/efeitos dos fármacos , Plântula/crescimento & desenvolvimento , Plântula/metabolismo
4.
Anticancer Res ; 40(10): 5701-5706, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32988895

RESUMO

BACKGROUND/AIM: The simultaneous increase of antioxidant CAT (catalase) enzyme and plasma MDA (malonidialdehyde) concentrations versus the numeric rating scale (NRS) pain score following surgery is unknown. Patients and Methods: The study included 114 patients with gallstone disease and 29 patients in the cancer group. RESULTS: Following surgery, the plasma CAT concentrations increased and plasma MDA concentrations decreased in all patients and especially in cancer patients. The linear mixed model time-effect was statistically significant in CAT and MDA (p<0.001 and p=0.02, respectively). In addition, a significant correlation between NRS pain score values and plasma MDA median concentrations in cancer patients was identified (r=0.430, p<0.001). CONCLUSION: The plasma MDA concentrations decreased and CAT concentrations increased significantly in all patients and especially in cancer patients following surgery. The simultaneous increase of antioxidant CAT enzyme with the decrease of plasma MDA may be an important ROS inhibiting mechanism to help patients return to normal antioxidant-oxidant status.


Assuntos
Catalase/sangue , Cálculos Biliares/sangue , Malondialdeído/sangue , Neoplasias/sangue , Dor/sangue , Antioxidantes/metabolismo , Feminino , Cálculos Biliares/patologia , Cálculos Biliares/cirurgia , Glutationa Peroxidase/sangue , Humanos , Masculino , Pessoa de Meia-Idade , Neoplasias/patologia , Neoplasias/cirurgia , Estresse Oxidativo/genética , Dor/patologia , Dor/cirurgia , Medição da Dor , Espécies Reativas de Oxigênio/metabolismo , Superóxido Dismutase/sangue
5.
Chemosphere ; 258: 127411, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32947668

RESUMO

Non-steroidal anti-inflammatory drugs as an important group of emerging environmental contaminants in irrigation water and soils can influence biochemical and physiological processes essential for growth and development in plants as non-target organisms. Plants are able to take up, transport, transform, and accumulate drugs in the roots. Root biomass in ten-days old pea plants was lowered by 6% already under 0.1 mg/L naproxen (NPX) due to a lowered number of lateral roots, although 0.5 mg/L NPX stimulated the total root length by 30% as against control. Higher section area (by 40%) in root tip, area of xylem (by 150%) or stele-to-section ratio (by 10%) in zone of maturation, and lower section area in zone of lateral roots (by 18%) prove the changes in primary root anatomy and its earlier differentiation at 10 mg/L NPX. Accumulated NPX (up to 10 µg/g DW at 10 mg/L) and products of its metabolization in roots increased the amounts of hydrogen peroxide (by 33%), and superoxide (by 62%), which was reflected in elevated lipid peroxidation (by 32%), disruption of membrane integrity (by 89%) and lowering both oxidoreductase and dehydrogenase activities (by up to 40%). Elevated antioxidant capacity (SOD, APX, and other molecules) under low treatments decreased at 10 mg/L NPX (both by approx. 30%). Naproxen was proved to cause changes at both cellular and tissue levels in roots, which was also reflected in their anatomy and morphology. Higher environmental loading through drugs thus can influence even the root function.


Assuntos
Anti-Inflamatórios não Esteroides/toxicidade , Naproxeno/toxicidade , Ervilhas/fisiologia , Antioxidantes/metabolismo , Peróxido de Hidrogênio/metabolismo , Peroxidação de Lipídeos , Estresse Oxidativo/efeitos dos fármacos , Ervilhas/efeitos dos fármacos , Raízes de Plantas
6.
Chemosphere ; 258: 127337, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32947656

RESUMO

The experiment was designed to evaluate the roles of Rhizophagus irregularis on chlorophyll fluorescence and chromium bioaccumulation in a grass species (Brachiaria mutica) by supplementing Cr+6 at different concentrations. Arbuscular Mycorrhizal Fungi (AMF) association facilitated lessening of chromium level in contaminated soil and enhanced chromium bioavailability in Brachiaria mutica. The mycorrhizal inoculated increased the chlorophyll (0.925 mg/g), carotenoid (0.127 mg/g), protein (2.883 mg/g), proline (0.889 mg/g) contents and activities of antioxidant enzymes like catalase, ascorbate peroxidase and glutathione peroxidase. The mycorrhizal inoculated plants also showed enhanced overall photosynthetic performance (PIϕ = 2.473) and enhanced PS-II to PS-I electron transport as evident from yield parameter (0.712) and TR0/RC (2.419) for 60 mg/kg Cr+6 treatment. The observations suggest that AMF association could defend the plants from chromium stress by elevating the number of antioxidants in plants. Rhizophagus irregularis was found to maintain a successful symbiotic relationship with Brachiaria mutica in chromium contaminated soil. The observations recommended that Rhizophagus irregularis in association with Brachiaria mutica would be an innovative approach for decontamination of Cr+6.


Assuntos
Biodegradação Ambiental , Brachiaria/metabolismo , Cromo/metabolismo , Poluentes do Solo/metabolismo , Antioxidantes/metabolismo , Bioacumulação , Clorofila/metabolismo , Cromo/análise , Glomeromycota/metabolismo , Micorrizas/metabolismo , Fotossíntese , Plantas/metabolismo , Poaceae/metabolismo , Solo , Poluentes do Solo/análise , Simbiose
7.
Chemosphere ; 258: 127385, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32947675

RESUMO

2,2,4,4-tetrabromodiphenyl ether (BDE-47) has received considerable attention because of its high detection level in biological samples and potential developmental toxicity. Here, using zebrafish (Danio rerio) as the experimental animal, we investigated developmental effects of BDE-47 and explored the potential mechanism. Zebrafish embryos at 4 h post-fertilization (hpf) were exposed to 0.312, 0.625 and 1.25 mg/L BDE-47 to 74-120 hpf. We found that BDE-47 instigated a dose-related developmental toxicity, evidenced by reduced embryonic survival and hatching rate, shortened body length and increased aberration rate. Meanwhile, higher doses of BDE-47 reduced mitochondrial membrane potential and ATP production but increased apoptosis in zebrafish embryos. Expression of genes involved in mitochondrial oxidative phosphorylation (OXPHOS) (ndufb8, sdha, uqcrc1, cox5ab and atp5fal) were negatively related to BDE-47 doses in zebrafish embryos. Moreover, exposure to BDE-47 at 0.625 or 1.25 mg/L impaired mitochondrial biogenesis and mitochondrial dynamics. Our data further showed that BDE- 47 exposure induced excessive reactive oxygen species (ROS) and oxidative stress, which was accompanied by the activation of c-Jun N-terminal Kinase (JNK). Antioxidant NAC and JNK inhibition could mitigate apoptosis in embryos and improve embryonic development in BDE-47-treated zebrafish, suggesting the involvement of ROS/JNK pathway in embryonic developmental changes induced by BDE-47. Altogether, our data suggest here that developmental toxicity of BDE-47 may be associated with mitochondrial ROS-mediated JNK signaling in zebrafish embryo.


Assuntos
Éteres Difenil Halogenados/toxicidade , Poluentes Químicos da Água/toxicidade , Animais , Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Embrião não Mamífero/efeitos dos fármacos , Desenvolvimento Embrionário/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases , Mitocôndrias/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , Peixe-Zebra/metabolismo
8.
Ecotoxicol Environ Saf ; 203: 111016, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888590

RESUMO

Selenium (Se) is considered a beneficial element to higher plants based on its regulation of antioxidative system under abiotic or biotic stresses. However, the limit of beneficial and toxic physiological effects of Se is very narrow. In the present study, the antioxidant performance, nutritional composition, long-distance transport of Se, photosynthetic pigments, and growth of Coffea arabica genotypes in response to Se concentration in solution were evaluated. Five Coffea arabica genotypes (Obatã, IPR99, IAC125, IPR100 and Catucaí) were used, which were grown in the absence and presence of Se (0 and 1.0 mmol L-1) in nutrient solution. The application of 1 mmol L-1 Se promoted root browning in all genotypes. There were no visual symptoms of leaf toxicity, but there was a reduction in the concentration of phosphorus and sulfur in the shoots of plants exposed to high Se concentration. Except for genotype Obatã, the coffee seedlings presented strategies for regulating Se uptake by reducing long-distance transport of Se from roots to shoots. The concentrations of total chlorophyll, total pheophytin, and carotenoids were negatively affected in genotypes Obatã, IPR99, and IAC125 upon exposure to Se at 1 mmol L-1. H2O2 production was reduced in genotypes IPR99, IPR100, and IAC125 upon exposure to Se, resulting in lower activity of superoxide dismutase (SOD), and catalase (CAT). These results suggest that antioxidant metabolism was effective in regulating oxidative stress in plants treated with Se. The increase in sucrose, and decrease in SOD, CAT and ascorbate peroxidase (APX) activities, as well as Se compartmentalization in the roots, were the main biochemical and physiological modulatory effects of coffee seedlings under stress conditions due to excess of Se.


Assuntos
Antioxidantes/metabolismo , Coffea/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Selênio/farmacologia , Coffea/genética , Coffea/metabolismo , Coffea/fisiologia , Genótipo , Oxirredução , Fotossíntese/efeitos dos fármacos , Raízes de Plantas/efeitos dos fármacos , Raízes de Plantas/genética , Raízes de Plantas/metabolismo , Plântula/efeitos dos fármacos , Plântula/genética , Plântula/metabolismo , Plântula/fisiologia , Selênio/análise , Selênio/metabolismo , Especificidade da Espécie
9.
J Environ Pathol Toxicol Oncol ; 39(2): 113-123, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32749121

RESUMO

Liver cancer or hepatocellular carcinoma is considered to be the third leading cause of death among all other cancers. The rate of liver cancer occurrence is high, and the rate of recovery is low. In this study, we investigated the therapeutic efficacy of vicenin-2 against the diethylnitrosamine-induced liver carcinoma in experimental rats. Diethylnitrosamine was widely employed as a carcinogenic agent to stimulate the cancer in animal models. Our results indicated that vicenin-2 administration effectively attenuates the diethylnitrosamine-induced physiological and pharmacological alterations in the experimental rats. Vicenin-2 treatment significantly enhanced the pathological lesions and decreased the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and α-fetoprotein (AFP) in serum. We also observed that vicenin-2 reduced the production of reactive oxygen species, decreased the liver weight, upregulated expression of apoptotic proteins, and decreased the histological changes in the liver, which are induced by the diethylnitrosamine in rats. Moreover, vicenin-2 downregulates antiapoptotic Bcl-2 and Bcl-xL, and upregulates the proapoptotic Bax and caspase. Hence, our results suggested that vicenin-2 had a highly therapeutic effect in reversing diethylnitrosamine-induced liver carcinoma in rats, which might be related to the apoptosis induced by vicenin-2. Therefore vicenin-2 could be a good candidate for future therapeutic use to inhibit chemically induced liver cancer.


Assuntos
Apigenina/farmacologia , Carcinoma Hepatocelular/tratamento farmacológico , Glucosídeos/farmacologia , Neoplasias Hepáticas Experimentais/tratamento farmacológico , 8-Hidroxi-2'-Desoxiguanosina/metabolismo , Animais , Antineoplásicos Fitogênicos/farmacologia , Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Apoptose/fisiologia , Biomarcadores Tumorais/sangue , Proteínas Sanguíneas/análise , Peso Corporal/efeitos dos fármacos , Carcinoma Hepatocelular/induzido quimicamente , Carcinoma Hepatocelular/patologia , Dietilnitrosamina/toxicidade , Enzimas/sangue , Neoplasias Hepáticas Experimentais/induzido quimicamente , Neoplasias Hepáticas Experimentais/patologia , Masculino , Estresse Oxidativo/efeitos dos fármacos , Ratos Wistar , Soroglobulinas/análise
10.
J Environ Pathol Toxicol Oncol ; 39(2): 137-147, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32749123

RESUMO

Lung carcinogenesis is one of the main sources of cancer-related mortality globally and it is estimated that nearly 1 million people die from it every year. The 5-year survival rate of lung carcinogenesis is reported at just 15%. The aim of the current research was to investigate the immunomodulatory effect of eriocitrin against benzo(a)pyrene [B(a) P]-induced lung tumorigenesis in Swiss albino mice. The lung sarcoma was provoked through oral gavage of B(a)P (50 mg/kg body weight) two times/week for four weeks. CEA, lung weight, lipid peroxidation (LPO), body weight, immuno-globulin (IgG, IgA, and IgM), tumor incidence, serum marker enzymes (LDH, AHH, λ-GT, and 5'-NTs), hematological counts (leucocytes, lymphocytes, neutrophils, absolute numbers of lymphocytes and neutrophils), antioxidants (SOD and CAT), inflammatory modulators (IL-1ß, IL-6, and TNF-α), immune complexes (avidity index, phagocyte index, NBT reduction, and SIC) and histopathological changes were analyzed. Moreover, the status of apoptosis proteins (Bax, caspase-9, and caspase-3) and cell proliferative protein (cyclin D1 and cyclin A) expression was determined by Western blot and PCNA by immunohistochemical analysis. B(a)P-challenged cancer-bearing mice exhibited augmented levels of lipid peroxidation, tumor incidence, lung weight, CEA, serum marker enzymes, IgA, SIC, cell proliferative markers, and inflammatory cytokines with concurrent decrease in body weight, antioxidant levels, hematological counts, immunoglobulins, immune complexes, and apoptotic protein expression. The eriocitrin treatments caused significant reversion of all these marker to previous levels. Overall, the results propose the immunomodulatory prospective of eriocitrin against B(a) P-induced lung carcinogenesis on Swiss albino mice.


Assuntos
Flavanonas/farmacologia , Fatores Imunológicos/farmacologia , Neoplasias Pulmonares/prevenção & controle , Animais , Anticarcinógenos/farmacologia , Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Benzo(a)pireno/toxicidade , Peso Corporal/efeitos dos fármacos , Citocinas/metabolismo , Imunoglobulinas/sangue , Peroxidação de Lipídeos/efeitos dos fármacos , Pulmão/efeitos dos fármacos , Pulmão/patologia , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/imunologia , Neoplasias Pulmonares/patologia , Camundongos , Camundongos Endogâmicos C57BL , Tamanho do Órgão/efeitos dos fármacos , Fagócitos/efeitos dos fármacos
11.
Ecotoxicol Environ Saf ; 202: 110916, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32800251

RESUMO

Selenium (Se) at low concentration is considered benefit element to plants. The range between optimal and toxic concentration of Se is narrow and varies among plant species. This study aimed to evaluate the phenotypic, physiological and biochemical responses of four rice genotypes (BRS Esmeralda, BRSMG Relâmpago, BRS Bonança and Bico Ganga) grown hydroponically treated with sodium selenate (1.5 mM L-1). Selenium treated plants showed a dramatically decrease of soluble proteins, chlorophylls, and carotenoids concentration, resulting in the visual symptoms of toxicity characterized as leaf chlorosis and necrosis. Selenium toxicity caused a decrease on shoot and root dry weight of rice plants. Excess Se increased the oxidative stress monitored by the levels of hydrogen peroxide and lipid peroxidation. The enzymatic antioxidant system (catalase, superoxide dismutase, and ascorbate peroxidase) increased in response to Se supply. Interestingly, primary metabolism compounds such as sucrose, total sugars, nitrate, ammonia and amino acids increased in Se-treated plants. The increase in these metabolites may indicate a defense mechanism for the osmotic readjustment of rice plants to mitigate the toxicity caused by Se. However, these metabolites were not effective to minimize the damages on phenotypic traits such as leaf chlorosis and reduced shoot and root dry weight in response to excess Se. Increased sugars profile combined with antioxidant enzymes activities can be an effective biomarkers to indicate stress induced by Se in rice plants. This study shows the physiological attributes that must be taken into account for success in the sustainable cultivation of rice in environments containing excess Se.


Assuntos
Oryza/fisiologia , Selênio/toxicidade , Poluentes do Solo/toxicidade , Antioxidantes/metabolismo , Ascorbato Peroxidases/metabolismo , Catalase/metabolismo , Clorofila/metabolismo , Peróxido de Hidrogênio/metabolismo , Hidroponia , Peroxidação de Lipídeos , Oryza/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Folhas de Planta/metabolismo , Ácido Selênico/metabolismo , Superóxido Dismutase/metabolismo
12.
Int J Nanomedicine ; 15: 5005-5016, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32764932

RESUMO

Background and Aim: With the wide applications of chitosan and gold nanoparticles in drug delivery and many consumer products, there is limited available information about their effects on drug-metabolizing enzymes (DMEs). Changes in DMEs could result in serious drug interactions. Therefore, this study aimed to investigate the effects of exposure to chitosan or gold nanoparticles on hepatic Phase I and II DMEs, liver function and integrity, oxidative damage and liver architecture in male rats. Methods: Animals were divided into three equal groups: a control group, a group treated with chitosan nanoparticles (200 mg/kg, 50±5 nm) and a group treated with gold nanoparticles (4 mg/kg, 15±5 nm). Rats were orally administered their respective doses daily for 10 days. Results: Both chitosan and gold nanoparticles decreased the body weights by more than 10%. Gold nanoparticles reduced the activities of antioxidants (superoxide dismutase and catalase), and reduced glutathione level and elevated the malondialdehyde level in the liver. Gold nanoparticles caused significant reductions in CYP1A1, CYP2E1, quinone oxidoreductase1, and glutathione S-transferase and elevated CYP2D6 and N-acetyl transferase2. Chitosan elevated CYP2E1 and CYP2D6 and reduced UDP-glucuronosyltransferase 1A1. Both nanoparticles disturbed the architecture of the liver, but the deleterious effects after gold nanoparticles treatment were more prominent. Conclusion: Taken together, gold nanoparticles severely perturbed the DMEs and would result in serious interactions with many drugs, herbs, and foods.


Assuntos
Antioxidantes/metabolismo , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Inativação Metabólica/efeitos dos fármacos , Fígado/efeitos dos fármacos , Nanopartículas Metálicas/efeitos adversos , Animais , Catalase/genética , Catalase/metabolismo , Quitosana/química , Citocromo P-450 CYP1A1/metabolismo , Citocromo P-450 CYP2E1/genética , Citocromo P-450 CYP2E1/metabolismo , Interações Medicamentosas , Glucuronosiltransferase/genética , Glucuronosiltransferase/metabolismo , Glutationa/metabolismo , Glutationa Transferase/genética , Glutationa Transferase/metabolismo , Ouro/química , Ouro/farmacocinética , Fígado/metabolismo , Fígado/patologia , Masculino , Malondialdeído/metabolismo , Nanopartículas Metálicas/química , Ratos Wistar , Superóxido Dismutase/genética , Superóxido Dismutase/metabolismo
13.
Ecotoxicol Environ Saf ; 204: 111104, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32791360

RESUMO

Since development of antioxidant defence system is high energy demanding event, innate defence system and stress tolerance of plant is strictly governed by plant age. This study is aimed towards evaluating variation of tolerance in germinating seeds and seedlings of Oryza sativa L. cv. Swarna against nano-scale zero valent iron (nZVI). A comparative study of several physiological and biochemical parameters have been carried out among 2 distinct plant groups, Group I treated with variable concentrations of nZVI (50, 100, 150 and 200 mg L-1) during germination and Group II treated with similar nZVI doses on 7th day after germination. Upon treatment with higher nZVI concentrations, Group I seedlings showed susceptibility towards oxidative stress while Group II seedlings showed tolerance against these higher doses of nZVI. Significant growth enhancement was observed upon treatment with 50-150 mg L-1 nZVI, since up-regulation of plant's endogenous antioxidant system protected relatively aged Group II seedlings from oxidative damages. Hierarchical clustering based on overall physiological, biochemical and stress parameters confirmed that in Group I seedlings 100-200 mg L-1 nZVI treatments were toxic where as in Group II seedlings 50-150 mg L-1 nZVI treatments showed growth promoting effects. This differential response is due to developmental stage related resistance in plants.


Assuntos
Germinação/efeitos dos fármacos , Nanopartículas Metálicas/toxicidade , Oryza/crescimento & desenvolvimento , Antioxidantes/metabolismo , Ferro/metabolismo , Oryza/efeitos dos fármacos , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Plântula/efeitos dos fármacos , Sementes/metabolismo
14.
Ecotoxicol Environ Saf ; 204: 111098, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32798749

RESUMO

Cadmium (Cd) is a detrimental element that can be toxic to plants. The physiological and biochemical responses of plants to Cd stress have been extensively studied, but the molecular mechanisms remain unclear. The present study showed that Cd severely inhibited the growth of roots and shoots and reduced plant biomass of mung bean seedlings. To further investigate the gene profiles and molecular processes in response Cd stress, transcriptome analyses of mung bean roots exposed to 100 µM Cd for 1, 5, and 9 days were performed. Cd treatment significantly decreased global gene expression levels at 5 and 9 d compared with the control. A total of 6737, 10279, and 9672 differentially expressed genes (DEGs) were identified in the 1-, 5-, and 9-day Cd-treated root tissues compared with the controls, respectively. Based on the analysis of DEG function annotation and enrichment, a pattern of mung bean roots response to Cd stress was proposed. The processes detoxification and antioxidative defense were involved in the early response of mung bean roots to Cd. Cd stress downregulated the expressions of a series of genes involved in cell wall biosynthesis, cell division, DNA replication and repair, and photosynthesis, while genes involved in signal transduction and regulation, transporters, secondary metabolisms, defense systems, and mitochondrial processes were upregulated in response to Cd, which might be contributed to the improvement of plant tolerance. Our results provide some novel insights into the molecular processes for growth and adaption of mung bean roots in response to Cd and many candidate genes for further biotechnological manipulations to improve plant tolerance to heavy metals.


Assuntos
Cádmio/toxicidade , Poluentes do Solo/toxicidade , Aclimatação , Adaptação Fisiológica , Antioxidantes/metabolismo , Cádmio/metabolismo , Poluição Ambiental , Fabaceae/metabolismo , Perfilação da Expressão Gênica , Regulação da Expressão Gênica de Plantas , Metais Pesados/metabolismo , Raízes de Plantas/metabolismo , Plântula/metabolismo , Poluentes do Solo/metabolismo , Transcriptoma , Vigna/metabolismo
15.
Ecotoxicol Environ Saf ; 204: 111148, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32818843

RESUMO

To disclose how phosphorus deficiency influence phytoremediation of Cd contamination using poplars, root architecture, Cd absorption, Cd translocation and antioxidant defense in poplar roots were investigated using a clone of Populus × euramericana. Root growth was unaltered by Cd exposure regardless of P conditions, while the degree of root proliferation upon P deficiency was changed by high level of Cd exposure. The concentration and content of Cd accumulation in roots were increased by P deficiency. This can be partially explained by the increased expression of genes encoding PM H + -ATPase under the combined conditions of P deficiency and high Cd exposure, which enhanced Cd2+-H+ exchanges and led to an increment of Cd uptake under P deficiency. Despite of the increasing Cd accumulation in roots, the translocation of Cd from roots to aerial tissues sharply decreased upon P deficiency. The relative expression of genes responsible for Cd translocation (HMA4) decreased upon P deficiency and thus inhibited Cd translocation via xylem. GR activity was decreased by P deficiency, which can inhibit the form of GSH and GSH-Cd complexes and decrease Cd translocation via GSH-Cd complexes. The transportation of PC-Cd complexes into vacuole decreased under P deficiency as a result of the low expression of PCS and ABCC1, and thus suppressed Cd tolerance and Cd detoxification in roots. Moreover, P deficiency decreased the levels of antioxidase (GR and CAT) and phytohormones including JA, ABA and GA3, which synchronously reduced antioxidant capacity in roots.


Assuntos
Cádmio/metabolismo , Fósforo/metabolismo , Populus/fisiologia , Adaptação Fisiológica , Antioxidantes/metabolismo , Biodegradação Ambiental , Transporte Biológico , Cádmio/toxicidade , Proliferação de Células , Reguladores de Crescimento de Planta/metabolismo , Raízes de Plantas/metabolismo , Populus/metabolismo , Xilema/metabolismo
16.
Aquat Toxicol ; 227: 105607, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32861022

RESUMO

The ubiquitous contamination of environmental lead (Pb) remains a worldwide threat. Improper Pb mine waste disposal from an abandoned lead-zinc mine has recently unearthed widespread Pb poisoning in children in Kabwe Zambia. Although the adverse effects of Pb on human health have begun to receive attention, the ecotoxicological effects on aquatic vertebrates still need further investigation. In addition, there is paucity in the knowledge on the behavioural and molecular subcellular responses in larval zebrafish exposed to Pb within the range of environmental relevant concentration (average 3 µg/L with maximum of 94 µg/L) on aquatic organisms such as zebrafish. The adverse effects of environmentally relevant levels of Pb on larval zebrafish was evaluated by measuring swimming behaviour under alternating dark and light conditions. Larval zebrafish acutely exposed to environmentally relevant Pb exhibited neuro-behavioural alteration including enhanced hyperactivity under light conditions evidenced by increased distanced covered and speed compared to the control. The alteration of entire behavioral profiles was further associated with the disturbed expression patterns of mRNA level of key genes associated with antioxidant (HO-1, Ucp-2 and CoxI), proapoptotic gene (TP53), and antiapoptotic gene (Bcl-2). To our knowledge, this is the first report on the effects of environmentally relevant Pb levels from Kabwe, Zambia and their adverse neurobehavioural effects and subcellular molecular oxidative responses in larval zebrafish acutely exposed within a 30 min period. The current results would be beneficial in our understanding of the effects of low Pb levels acutely discharged into an aquatic environment and the life of aquatic organisms.


Assuntos
Chumbo/toxicidade , Poluentes Químicos da Água/toxicidade , Peixe-Zebra/fisiologia , Animais , Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Humanos , Larva/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Testes de Toxicidade Aguda
17.
Chem Biol Interact ; 330: 109230, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32828744

RESUMO

Although physiological levels of iron are essential for numerous biological processes, excess iron causes critical tissue injury. Under iron overload conditions, non-chelated iron generates reactive oxygen species that mediate iron-induced tissue injury with subsequent induction of apoptosis, necrosis, and inflammatory responses. Because liver is a central player in iron metabolism and storage, it is vulnerable to iron-induced tissue injury. Taxifolin is naturally occurring compound that has shown potent antioxidant and potential iron chelation competency. The aim of the current study was to investigate the potential protective effects of taxifolin against iron-induced hepatocellular injury and to elucidate the underlining mechanisms using rats as a mammalian model. The results of the current work indicated that taxifolin inhibited iron-induced apoptosis and enhanced hepatocellular survival as demonstrated by decreased activity of caspase-3 and activation of the pro-survival signaling PI3K/AKT, respectively. Western blotting analysis revealed that taxifolin enhanced liver regeneration as indicated by increased PCNA protein abundance. Taxifolin mitigated the iron-induced histopathological aberration and reduced serum activity of liver enzymes (ALT and AST), highlighting enhanced liver cell integrity. Mechanistically, taxifolin modulated the redox-sensitive MAPK signaling (p38/c-Fos) and improved redox status of the liver tissues as indicated by decreased lipid peroxidation and protein oxidation along with enhanced total antioxidant capacity. Interestingly, it decreased liver iron content and down-regulated the pro-inflammatory cytokines TNF-α, IL-6, and IL-1ß. Collectively, these data highlight, for the first time, the ameliorating effects of taxifolin against iron overload-induced hepatocellular injury that is potentially mediated through anti-inflammatory, antioxidant, and potential iron chelation activities.


Assuntos
Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Sobrecarga de Ferro/complicações , Regeneração Hepática/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Quercetina/análogos & derivados , Animais , Anti-Inflamatórios não Esteroides/farmacologia , Anti-Inflamatórios não Esteroides/uso terapêutico , Antioxidantes/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Doença Hepática Induzida por Substâncias e Drogas/patologia , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Ferro/metabolismo , Quelantes de Ferro/farmacologia , Quelantes de Ferro/uso terapêutico , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Quercetina/farmacologia , Quercetina/uso terapêutico , Ratos
18.
Chem Biol Interact ; 330: 109232, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32860822

RESUMO

Currently, whether nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation contributes to neuropathy induced by 2,5-Hexanedione (HD), the toxic metabolite of n-hexane, remains unknown. In this study, we found that HD intoxication elevated NLRP3 expression, caspase-1 activation and interleukin-1ß production in sciatic nerve of rats, indicating activation of NLRP3 inflammasome. The increased cleavage of gasdermin D (GSDMD) protein, an important mediator of pyroptosis, and axon degeneration were also observed in sciatic nerves of HD-intoxicated rats. Interestingly, glybenclamide, a widely used inhibitor of NLRP3 inflammasome, significantly reduced NLRP3 inflammasome activation, which was associated with decreased GSDMD cleavage and axon degeneration as well as improved motor performance of HD-intoxicated rats. Subsequently, we found that inhibition of NLRP3 inflammasome by glybenclamide attenuated macrophage infiltration, activation and M1 polarization in sciatic nerves of HD-intoxicated rats. Furthermore, decreased malondialdehyde (MDA) contents and increased glutathione (GSH) level and total anti-oxidative capacity were also observed in sciatic nerves of rats treated with combined glybenclamide and HD compared with HD alone group. Altogether, our findings suggest that NLRP3 inflammasome activation contributes to HD-induced neurotoxicity by enhancing macrophage infiltration and activation as well as oxidative stress, providing a novel mechanism of neuropathy induced by this neurotoxicant.


Assuntos
Hexanonas/toxicidade , Macrófagos/patologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/farmacologia , Síndromes Neurotóxicas/etiologia , Animais , Antioxidantes/metabolismo , Movimento Celular/efeitos dos fármacos , Glutationa/metabolismo , Glibureto/farmacologia , Inflamassomos/metabolismo , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Macrófagos/imunologia , Macrófagos/metabolismo , Masculino , Proteína 3 que Contém Domínio de Pirina da Família NLR/antagonistas & inibidores , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Síndromes Neurotóxicas/tratamento farmacológico , Estresse Oxidativo , Proteínas de Ligação a Fosfato/metabolismo , Piroptose , Ratos , Nervo Isquiático/metabolismo , Nervo Isquiático/patologia
19.
Life Sci ; 258: 118227, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32781074

RESUMO

AIM: eEF1A2 is highly expressed in postmitotic cells and has been reported to interact with the antioxidant enzyme peroxiredoxin 1 (PRDX1). PRDX1 is involved in motor neuron differentiation. Here, we studied the relationship between eEF1A2 and PRDX1 during dopaminergic neuron differentiation, and examined their possible association in an oxidative stress model of Parkinson's disease (PD). MAIN METHODS: Expression of eEF1A2 and PRDX1 in SH-SY5Y cells at various durations of retinoic acid (RA) induction was detected using qRT-PCR, Western blotting and immunofluorescence. Neurons of 10-day differentiation were treated with the PRDX1 inhibitor H7, MPP+ and H7 plus MPP+. The cell viability, the amounts of apoptotic nuclei, DHE signals, and the expression of p53, p-Akt and p-mTOR were determined. The colocalization of eEF1A2 and PRDX1 was visualized using confocal microscopy. KEY FINDINGS: eEF1A2 gradually increased after RA-induced differentiation of SH-SY5Y cells, while PRDX1 protein gradually decreased. MPP+ treatment increased eEF1A2 in both undifferentiated and differentiated neurons; however, PRDX1 appeared to elevate only in mature neurons. The inhibition of the PRDX1 activity with H7 promoted MPP+-induced cell death, as evidenced by decreased cell viability, increased apoptotic nuclei, increased the DHE signal, and increased p53. However, H7 induced the activation of the prosurvival Akt and mTOR in MPP+-treated cells. Besides, a colocalization of eEF1A2 and PRDX1 was evidenced in MPP+-treated neurons. This colocalization was possibly prevented by inhibiting the PRDX1 activity, resulting in aggravated neuronal death. SIGNIFICANCE: Our results suggest that the possible association between eEF1A2 and PRDX1 may be a promising target for modifying neuronal death in PD.


Assuntos
1-Metil-4-fenilpiridínio/toxicidade , Diferenciação Celular/fisiologia , Fator 1 de Elongação de Peptídeos/metabolismo , Peroxirredoxinas/antagonistas & inibidores , Peroxirredoxinas/metabolismo , Antioxidantes/metabolismo , Morte Celular/efeitos dos fármacos , Morte Celular/fisiologia , Diferenciação Celular/efeitos dos fármacos , Linhagem Celular Tumoral , Herbicidas/toxicidade , Humanos , Fator 1 de Elongação de Peptídeos/análise , Peroxirredoxinas/análise
20.
Bull Environ Contam Toxicol ; 105(3): 358-365, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32740748

RESUMO

Sulfamethoxazole (SMZ) is a kind of sulfonamides antibiotic, which is widely used in human life. This study investigated the effects of SMZ on physiological and biochemical indexes of Chlorella vulgaris (C. vulgaris) and Microcystis aeruginosa (M. aeruginosa) for 35-day. The results showed that SMZ inhibited the growth and Chl-a content of C. vulgaris and M. aeruginosa, and growth inhibition rate was 8.06%-95.86%, Chl-a content decreased 2.44%-98.04%. SMZ resulting in increased SOD and CAT activity and destroyed the dynamic balance of antioxidant system. In addition, SMZ increased the content of malondialdehyde (MDA) in algae, destroyed the cell membrane to a certain extent, which was 1.8-7.3 folds higher than the control group. High concentration of SMZ can make algae cells exceed the limit of cell antioxidant capacity. Coupled with the serious damage of cell membrane, algae cells begin to appear a large number of death phenomenon.


Assuntos
Antibacterianos/toxicidade , Chlorella vulgaris/fisiologia , Microcystis/fisiologia , Sulfametoxazol/toxicidade , Antioxidantes/metabolismo , Chlorella vulgaris/efeitos dos fármacos , Malondialdeído/metabolismo , Microcystis/efeitos dos fármacos , Sulfametoxazol/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA