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1.
Ecotoxicol Environ Saf ; 208: 111683, 2021 Jan 15.
Artículo en Inglés | MEDLINE | ID: mdl-33396015

RESUMEN

The possibility of detecting the damaging effect of cadmium salts on red blood cells (RBC) membrane by atomic force microscopy and light microscopy was studied. White wistar rats RBC were incubated with cadmium chloride in concentrations of 1 µg/l, 10 µg/l, 100 µg/l, and 1000 µg/l for the research. A comparison of sample preparation methods proposed by other authors in previous studies is made. The optimal method that does not significantly affect the change in the morphological features of the cell is selected. The quantitative assessment of damaged and destroyed RBC depending on the concentration of cadmium was performed by optical microscopy. The study showed that CdCl2 has a damaging effect on the RBC membrane, which leads to the formation of non-specific cell forms. A comparative assessment was made between the methods of optical microscopy and atomic force microscopy for the suitability of studying the morphological characteristics of abnormal forms of the RBC. It is shown that the method of atomic force microscopy allows registering morphological changes in the RBC that cannot be registered by optical microscopy. It is pointed that CdCl2 has effect on destruction of the RBC and the formation of specific bulges on the RBC membrane. Influence of CdCl2 on the RBC mechanical properties was studied using atomic force microscopy. The possibility of using atomic force microscopy in studies of morphology and mechanical properties of the RBC under toxicity effect of cadmium is shown.


Asunto(s)
Cloruro de Cadmio/toxicidad , Contaminantes Ambientales/toxicidad , Membrana Eritrocítica/efectos de los fármacos , Eritrocitos/efectos de los fármacos , Microscopía de Fuerza Atómica/métodos , Animales , Relación Dosis-Respuesta a Droga , Membrana Eritrocítica/patología , Eritrocitos/citología , Eritrocitos/metabolismo , Humanos , Metalotioneína/metabolismo , Ratas , Ratas Wistar , Especies Reactivas de Oxígeno/metabolismo
2.
Chem Biol Interact ; 337: 109379, 2021 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-33453195

RESUMEN

Cadmium (Cd) is a toxic metal, which seems to be crucial during the prepubertal period. Cd can destroy the structural integrity of the blood-brain barrier (BBB) and enters into the brain. Although the brain is susceptible to neurotoxicity induced by Cd, the effects of Cd on the brain, particularly hypothalamic transcriptome, are still relatively poorly understood. Therefore, we investigated the molecular effects of Cd exposure on the hypothalamus by profiling the transcriptomic response of the hypothalamus to high dose of Cd (25 mg/kg bw/day cadmium chloride (CdCl2)) during the prepubertal period in Sprague-Dawley female rats. After sequencing and annotation, differential expression analysis revealed 1656 genes that were differentially expressed that 108 of them were classified into 37 transcription factor (TF) families. According to gene ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, these differentially expressed genes (DEGs) were involved in different biological processes and neurological disorders including Alzheimer's disease (AD), Huntington's disease (HD), and Parkinson's disease (PD), prolactin signaling pathway, PI3K/Akt signaling, and dopaminergic synapse. Five transcripts were selected for further analyses with Real-time quantitative PCR (RT-qPCR). The RT-qPCR results were mostly consistent with those from the high throughput RNA sequencing (RNA-seq). Cresyl violet staining clearly showed an increased neuronal degeneration in the dorsomedial hypothalamus (DMH) and arcuate (Arc) nuclei of the CdCl2 group. Overall, this study demonstrates that prepubertal exposure to high doses of Cd induces hypothalamic injury through transcriptome profiling alteration in female rats, which reveals the new mechanisms of pathogenesis of Cd in the hypothalamus.


Asunto(s)
Cloruro de Cadmio/toxicidad , Hipotálamo/efectos de los fármacos , Transcriptoma/efectos de los fármacos , Animales , Núcleo Arqueado del Hipotálamo/efectos de los fármacos , Núcleo Arqueado del Hipotálamo/metabolismo , Núcleo Arqueado del Hipotálamo/patología , Glucemia/análisis , Regulación hacia Abajo/efectos de los fármacos , Femenino , Ontología de Genes , Redes Reguladoras de Genes/efectos de los fármacos , Hipotálamo/metabolismo , Hipotálamo/patología , Sistema Inmunológico/efectos de los fármacos , Sistema Inmunológico/metabolismo , Neuropéptidos/genética , Neuropéptidos/metabolismo , Prolactina/sangre , Ratas , Ratas Sprague-Dawley , Factores de Transcripción/genética , Factores de Transcripción/metabolismo , Regulación hacia Arriba/efectos de los fármacos
3.
Ecotoxicol Environ Saf ; 209: 111817, 2021 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-33383339

RESUMEN

Plants as sessile organisms have developed some unique strategies to withstand environmental stress and adaptive response (AR) is one of them. In the present study Cadmium (Cd)-induced AR was evaluated to ameliorate the genotoxicity of a known chemical mutagen ethyl methanesulphonate (EMS) based on cytotoxicity, genotoxicity and oxidative stress in two model plant systems Allium cepa L. and Vicia faba L. Priming the plants with cadmium chloride (CdCl2, 25 and 50 µM) reduced the genotoxicity of EMS (0.25 mM). Cd-induced AR was evident by the magnitude of adaptive response (MAR) values calculated for cytotoxicity, genotoxicity and biochemical parameters. In addition the involvement of some major metabolic pathways and epigenetic modifications in AR was investigated. Metabolic blockers of protein kinase cascades, DNA repair, oxidative stress and de novo translation interfered with the adaptive response implying their role in AR whereas, inhibitors involved in post-replication repair and autophagy were ineffective implicating that they probably have no role in the AR studied. Moreover to find the role of DNA methylation in AR, methylation-sensitive comet assay was carried out. Simultaneously 5-methyl- 2'-deoxycytidine (5mdC) levels were quantified by HPLC (high performance liquid chromatography). AR was eliminated in cells treated with a demethylating agent, 5-aza- 2'deoxycytidine (AZA). Results implied a contribution of DNA hypermethylation. To the best of our knowledge this is a first report correlating DNA methylation to Cd-induced adaptive response in plants undergoing genotoxic stress.


Asunto(s)
Cadmio/toxicidad , Daño del ADN/fisiología , Contaminantes del Suelo/toxicidad , Cloruro de Cadmio/toxicidad , Ensayo Cometa , Metilación de ADN , Reparación del ADN , Metanosulfonato de Etilo/toxicidad , Mutágenos/toxicidad , Cebollas/efectos de los fármacos , Cebollas/fisiología , Estrés Oxidativo , Raíces de Plantas/efectos de los fármacos , Vicia faba/efectos de los fármacos , Vicia faba/fisiología
4.
Toxicol Lett ; 340: 101-113, 2021 Apr 01.
Artículo en Inglés | MEDLINE | ID: mdl-33338565

RESUMEN

Toxicity caused by the heavy metal Cadmium leads to liver diseases; this finding has generated interest among researchers. We detected DNA methylation using Whole Genome Bisulfite Sequencing (WGBS) to study the relationship between Cadmium exposure and liver damage. Forty-eight Sprague-Dawley rats were randomly divided into six groups, and given normal saline or 2.5, 5, 10, 20, and 40 mg/kg body weight per day CdCl2 by gavage. Twelve weeks later, their liver tissues were collected for pathological examination and DNA extraction. Increased exposure to Cadmium led to a reduction in the amount of weight gain as well as pathological degeneration and necrosis of liver cells of the rats. Using WGBS, we found that DNA methylation changes in the high-dose exposure group were more remarkable, and most of the changes occurred in the gene promoter region. GO enrichment analysis showed that the genes were enriched in the biological process of "response to stimulus." KEGG analysis revealed that metabolic pathways, like MAPK, PI3K-Akt and cAMP, had the largest number of enriched genes. Using Integrative Genomics Viewer (IGV), the demethylation of F2rl3 after Cadmium poisoning was established. This finding may explain why there are changes in liver metabolism after Cadmium poisoning.


Asunto(s)
Cloruro de Cadmio/toxicidad , Metilación de ADN/efectos de los fármacos , Animales , Regulación de la Expresión Génica/efectos de los fármacos , Hígado/efectos de los fármacos , Hígado/metabolismo , Distribución Aleatoria , Ratas , Ratas Sprague-Dawley , Secuenciación Completa del Genoma
5.
Toxicol Lett ; 333: 80-89, 2020 Oct 15.
Artículo en Inglés | MEDLINE | ID: mdl-32738273

RESUMEN

Exposure to high concentrations of cadmium (Cd), widely used in many industries and found in air, food and contaminated water, is not uncommon. Cd damages the cardiovascular system, but the vascular mechanisms involved are not fully understood. This study investigated the mechanisms involved in cardiovascular damage after exposure to high Cd concentrations. Three-month-old male Wistar rats were treated intraperitoneally for 14 days with distilled water (Untreated group) or 1 mg/kg cadmium chloride (Cd group). We investigated the systolic blood pressure (SBP) and vascular reactivity of mesenteric resistance arteries (MRA) and the aorta by analysing contractile and relaxation responses in the absence and presence of the endothelium; we also evaluated pathways involved in vascular tone regulation. Superoxide anion production, COX-2 protein expression and in situ detection of COX-2, AT-1, and NOX-1 were evaluated. Oxidative status, creatinine level and angiotensin-converting enzyme (ACE) activity in plasma were also evaluated. Fourteen-day exposure to a high Cd concentration induced hypertension associated with vascular dysfunction in MRA and the aorta. In both vessels, there was increased participation of cyclooxygenase 2 (COX2), angiotensin II type 1 (AT1) receptor and NOX1. MRA also presented endothelial dysfunction, denoted by impaired acetylcholine-mediated relaxation. All vascular changes were accompanied by increased reactive oxygen species production and COX2, NOX1 and AT1 receptor expression in vascular tissue. Overall, high Cd concentrations induced cardiovascular damage: hypertension, endothelial dysfunction and vascular damage in conductance and resistance arteries, NADPH oxidase, renin-angiotensin system and COX2 pathway activation.


Asunto(s)
Cloruro de Cadmio/toxicidad , Ciclooxigenasa 2/metabolismo , Endotelio Vascular/efectos de los fármacos , Contaminantes Ambientales/toxicidad , Hipertensión/inducido químicamente , NADPH Oxidasas/metabolismo , Sistema Renina-Angiotensina/efectos de los fármacos , Animales , Aorta/efectos de los fármacos , Aorta/enzimología , Presión Sanguínea/efectos de los fármacos , Cloruro de Cadmio/sangre , Relación Dosis-Respuesta a Droga , Endotelio Vascular/enzimología , Endotelio Vascular/patología , Endotelio Vascular/fisiopatología , Contaminantes Ambientales/sangre , Hipertensión/enzimología , Hipertensión/patología , Hipertensión/fisiopatología , Inyecciones Intraperitoneales , Masculino , Arterias Mesentéricas/efectos de los fármacos , Arterias Mesentéricas/enzimología , Estrés Oxidativo/efectos de los fármacos , Ratas Wistar , Transducción de Señal , Vasoconstricción/efectos de los fármacos
6.
Toxicol Lett ; 332: 130-139, 2020 Oct 10.
Artículo en Inglés | MEDLINE | ID: mdl-32645461

RESUMEN

Cadmium (Cd) is an environmental contaminant that triggers toxic effects in various tissues such as the kidney, liver, and lung. Cd can also cause abnormal iron metabolism, leading to anemia. Iron homeostasis is regulated by intestinal absorption. However, whether Cd affects the iron absorption pathway is unclear. We aimed to elucidate the relationship between the intestinal iron transporter system and Cd-induced iron deficiency anemia. C57BL/6J female and male mice, 129/Sv female mice, and DBA/2 female mice were given a single oral dose of CdCl2 by gavage. After 3 or 24 h, Cd decreased serum iron concentrations and inhibited the expression of iron transport-related genes in the duodenum. In particular, Cd decreased the levels of divalent metal transporter 1 and ferroportin 1 in the duodenum. In addition, human colon carcinoma Caco-2 cells were treated with CdCl2. After 72 h, Cd decreased the expression of iron transport-related factors in Caco-2 cells with a pattern similar to that seen in the murine duodenum. These findings suggest that Cd inhibits iron absorption through direct suppression of iron transport in duodenal enterocytes and contributes to abnormal iron metabolism.


Asunto(s)
Anemia Ferropénica/inducido químicamente , Cadmio/toxicidad , Duodeno/efectos de los fármacos , Duodeno/metabolismo , Hierro/metabolismo , Animales , Transporte Biológico Activo/efectos de los fármacos , Células CACO-2 , Cadmio/farmacocinética , Cloruro de Cadmio/toxicidad , Proteínas de Transporte de Catión/metabolismo , Femenino , Humanos , Hígado/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Endogámicos DBA
7.
Environ Sci Pollut Res Int ; 27(32): 40749-40756, 2020 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-32671713

RESUMEN

Retrotransposons, as vital regulator of male fertility, are essential for spermatogenesis. Cadmium (Cd) is an environmental toxicant and endocrine disruptor, targeting the reproductive system. Growing evidence shows that Cd exposure can induce male infertility in mammals. In this study, we generated a male C57BL/6 J mice model with consecutive 35 days cadmium chloride (CdCl2) in different concentrations of 0, 0.25, 0.5, 1.0, and 2.0 mg/kg. The results indicated that 1.0 and 2.0 mg/kg CdCl2 significantly affected the body weight. Meanwhile, the highest dose group with 2.0 mg/kg CdCl2 presented low fertility. Furthermore, the expression of retrotransposon mRNA was markedly increased in the higher doses group. We examined methylcytosine (mC) levels of the three active LINE-1 subfamilies TfI, A, and GfII in testis. Conclusively, Cd exposure probably undermines the male mice fertility by disrupting DNA methylation to regulate the retrotransposons. Further studies are required for identifying whether retrotransposon activation has any significant impacts on genome structure, stability, and expression in Cd-induced testicular injury, laying foundation for the treatment for male infertility.


Asunto(s)
Cadmio , Enfermedades Testiculares , Animales , Cadmio/toxicidad , Cloruro de Cadmio/toxicidad , Metilación de ADN , Humanos , Masculino , Ratones , Ratones Endogámicos C57BL , Retroelementos/genética , Testículo
8.
An Acad Bras Cienc ; 92(1): e20191121, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32428092

RESUMEN

Cadmium, present in the environment, accumulates in different organs of animals and humans, and has deleterious effects on the kidney. In this study, we investigated the protective effects of the methanolic extract of Pleurotus ostreatus in comparison with silymarin on renal function in cadmium-intoxicated rats for five days. Rats intraperitoneally injected with cadmium chloride (1 mg/kg). These rats were treated with either P. ostreatus extract (200 mg/kg) or silymarin to investigate the protective effects of the extract. Cadmium treatment induced significant histopathological impairments and increased cadmium levels, DNA fragmentation, and renal oxidative stress. However, treatment with P. ostreatus extract or silymarin improved the pathology, reduced the level of cadmium in renal tissue, and restored DNA fragmentation. In addition, a significant reduction in lipid peroxidation and reactive oxygen species levels, and a significant increase in the levels of glutathione and catalase activity were observed. Thus, protective effects of P. ostreatus extract to its components. Chromatographic analysis of the P. ostreatus confirmed the presence of five phenolics (gallic acid, chlorogenic acid, catechin, propyl gallate, and cinnamic acid) that exhibit strong antioxidant properties as free radical scavengers. Therefore, our findings demonstrate that treatment with P. ostreatus extract protects against cadmium-induced nephrotoxicity in female rats.


Asunto(s)
Antioxidantes/farmacología , Cloruro de Cadmio/toxicidad , Riñón/efectos de los fármacos , Extractos Vegetales/farmacología , Pleurotus/química , Silimarina/farmacología , Animales , Apoptosis/efectos de los fármacos , Cloruro de Cadmio/análisis , Femenino , Riñón/patología , Estrés Oxidativo/efectos de los fármacos , Sustancias Protectoras/farmacología , Ratas
9.
Life Sci ; 254: 117770, 2020 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-32407846

RESUMEN

AIMS: Cadmium chloride has various industrial applications and considered an industrial and environmental pollutant. The aim of this study was to evaluate the effect of atorvastatin on Cadmium chloride-induced hepatotoxicity in male rats. MATERIALS AND METHODS: Fifty-six adult male rats, randomly were divided into 8 groups. Groups 1-3 were received atorvastatin (20 mg/kg) intragastrically for 15 days during which Cadmium chloride (1, 2, and 3 mg/kg) were given intraperitoneally from days 8 to 15. Groups 4-6 were as first three groups but animals were received vehicle of atorvastatin. Group 7 was received vehicle of atorvastatin and vehicle of Cadmium chloride and Group 8 was received atorvastatin and vehicle of Cadmium chloride according to timeline of other groups. On day 16, under full anesthesia, blood sampling was prepared from heart, and livers were dissected out to analyses the biochemical and histopathology studies. KEY FINDINGS: Cadmium chloride significantly increased aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP) in the serum. Malondialdehyde (MDA) significantly increased and superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione (GSH) significantly decreased the in the liver following Cadmium chloride administration. Atorvastatin significantly improved the levels of MDA, SOD, GPx, GSH, but not ALT, AST, and ALP in Cadmium chloride-treated rats. In histopathological studies, atorvastatin could not improve injured liver tissues induced by Cadmium chloride. SIGNIFICANCE: Atorvastatin has beneficial effects in improving Cadmium chloride-induced antioxidative enzymes disturbance which may be contribute to improving liver function in male rats.


Asunto(s)
Atorvastatina/farmacología , Alanina Transaminasa/sangre , Fosfatasa Alcalina/metabolismo , Animales , Antioxidantes/farmacología , Aspartato Aminotransferasas/sangre , Atorvastatina/metabolismo , Cadmio/toxicidad , Cloruro de Cadmio/efectos adversos , Cloruro de Cadmio/farmacología , Cloruro de Cadmio/toxicidad , Enfermedad Hepática Inducida por Sustancias y Drogas/metabolismo , Glutatión/metabolismo , Glutatión Peroxidasa/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Hígado/metabolismo , Masculino , Malondialdehído/metabolismo , Estrés Oxidativo/efectos de los fármacos , Ratas , Ratas Wistar , Superóxido Dismutasa/metabolismo
10.
Ecotoxicol Environ Saf ; 191: 110241, 2020 Mar 15.
Artículo en Inglés | MEDLINE | ID: mdl-32007925

RESUMEN

One of the major mechanisms of heavy metal toxicity is the induction of oxidative stress. Redox-active heavy metals, like chromium, can induce it directly, whereas redox-inactive metals, like cadmium, play an indirect role in the generation of reactive oxygen species (ROS). Living organisms defend themselves against oxidative stress taking advantage of low-molecular-weight antioxidants and ROS-detoxifying enzymes. Tocopherols and plastoquinol are important plastid prenyllipid antioxidants, playing a role during acclimation of Chlamydomonas reinhardtii to heavy metal-induced stress. However, partial inhibition of synthesis of these prenyllipids by pyrazolate did not decrease the tolerance of C. reinhardtii to Cr- and Cd-induced stress, suggesting redundancy between antioxidant mechanisms. To verify this hypothesis we have performed comparative analyses of growth, photosynthetic pigments, low-molecular-weight antioxidants (tocopherols, plastoquinol, plastochromanol, ascorbate, soluble thiols, proline), activities of the ascorbate peroxidase (APX), catalase and superoxide dismutase (SOD) and cumulative superoxide production in C. reinhardtii exposed to Cd2+ and Cr2O72- ions in the presence or absence of pyrazolate. The decreased α-tocopherol and plastoquinol content resulted in the increase in superoxide generation and APX activity in pyrazolate-treated algae. The application of heavy metal ions and pyrazolate had a pronounced impact on Asc and total thiol content, as well as SOD and APX activities (the latter only in Cd-exposed cultures), when compared with algae grown in the presence of heavy metal ions or pyrazolate alone. The superoxide production in cultures exposed to heavy metal ions and pyrazolate decreased when compared to the cultures exposed to either heavy metal ions or an inhibitor alone.


Asunto(s)
Antioxidantes/metabolismo , Cloruro de Cadmio/toxicidad , Cromatos/toxicidad , Plastoquinona/análogos & derivados , Compuestos de Potasio/toxicidad , Tocoferoles/metabolismo , Chlamydomonas reinhardtii/metabolismo , Relación Dosis-Respuesta a Droga , Iones , Estrés Oxidativo/efectos de los fármacos , Fotosíntesis/efectos de los fármacos , Plastoquinona/metabolismo , Especies Reactivas de Oxígeno/metabolismo
11.
Ecotoxicol Environ Saf ; 193: 110322, 2020 Apr 15.
Artículo en Inglés | MEDLINE | ID: mdl-32109582

RESUMEN

The γ-aminobutyric acid (GABA) shunt is closely associated with plant tolerance; however, little is known about its mechanism. This study aimed to decipher the responses of the GABA shunt and related carbon-nitrogen metabolism in poplar seedlings (Populus alba × Populus glandulosa) treated with different NaCl and CdCl2 concentrations for 30 h. The results showed that the activities of glutamate decarboxylase (GAD) and GABA-transaminase (GABA-T) were activated, as well as α-ketoglutarate dehydrogenase (α-KGDH) and succinate dehydrogenase (SDH) activities were enhanced by NaCl and CdCl2 stresses, except for SDH under CdCl2 stress. Meanwhile, the expression levels of GADs, GABA-Ts SDHs, succinyl-CoA ligases (SCSs), and succinic acid aldehyde dehydrogenases (SSADHs) were also increased. Notably, significant increases in the key components of GABA shunt, Glu and GABA, were observed under both stresses. Soluble sugars and free amino acids were enhanced, whereas citrate, malate and succinate were almost inhibited by both NaCl and CdCl2 stresses except that citrate was not changed or just increased by 50-mM NaCl stress. Thus, these results suggested that the carbon-nitrogen balance could be altered by activating the GABA shunt when main TCA-cycle intermediates were inhibited under NaCl and CdCl2 stresses. This study can enhance the understanding about the functions of the GABA shunt in woody plants under abiotic stresses and may be applied to the genetic improvement of trees for phytoremediation.


Asunto(s)
Cloruro de Cadmio/toxicidad , Carbono/metabolismo , Nitrógeno/metabolismo , Populus/efectos de los fármacos , Cloruro de Sodio/toxicidad , Estrés Fisiológico/efectos de los fármacos , Ácido gamma-Aminobutírico/metabolismo , Aminoácidos/metabolismo , Cloruro de Cadmio/metabolismo , Ciclo del Ácido Cítrico/efectos de los fármacos , Glutamato Descarboxilasa/metabolismo , Populus/crecimiento & desarrollo , Populus/metabolismo , Plantones/efectos de los fármacos , Plantones/crecimiento & desarrollo , Plantones/metabolismo , Cloruro de Sodio/metabolismo
12.
Life Sci ; 242: 117250, 2020 Feb 01.
Artículo en Inglés | MEDLINE | ID: mdl-31899225

RESUMEN

BACKGROUND: Endocrine disruptor such as cadmium has been widely reported to cause testicular toxicity, which contributes to recent decline in male fertility worldwide. Glutamine, the most abundant amino acid in the body has been demonstrated to exert protective effects in cellular toxicity. However, its role in testicular toxicity is unknown. The present study is therefore aimed at investigating the effects of glutamine supplementation on cadmium-induced testicular toxicity, and the possible involvement of glucose-6-phosphate dehydrogenase (G6PD) activity. MATERIALS AND METHOD: Male Wistar rats weighing 160-190 g were allotted into 4 groups (n = 5/group): The groups received vehicle (distilled water; p.o.), glutamine (1gkg-1; p.o.), cadmium chloride (5mgkg-1p.o.) and Cadmium chloride plus glutamine respectively, daily for 30 days. Biochemical and histological analyses were performed with appropriate method. RESULTS: Administration of cadmium significantly decreased body weight, sperm count, motility and viability, as well as altered sperm morphology and progressivity. Cadmium also caused atrophy of the seminiferous tubule in addition to disrupted testicular architecture, lumen, Sertoli cells and spermatogonia. Similarly, serum and testicular aspartate transaminase, and malondialdehyde significantly increased, and G6PD, glutathione, nicotinamide adenine dinucleotide phosphate and nitric oxide significantly decreased with corresponding decrease in follicle stimulating hormone, luteinizing hormone and testosterone in cadmium-treated animals compared with control groups. However, supplementation with glutamine attenuated these alterations. CONCLUSION: The present study demonstrates that cadmium induces testicular dysfunction that is attributable to defective G6PD and accompanied by increased lipid peroxidation and impaired NO-dependent endothelial function. Interestingly, glutamine supplementation ameliorates cadmium-induced testicular dysfunction through enhancement of G6PD activity.


Asunto(s)
Cloruro de Cadmio/toxicidad , Glucosafosfato Deshidrogenasa/metabolismo , Glutamina/farmacología , Testículo/efectos de los fármacos , Animales , Glucosafosfato Deshidrogenasa/efectos de los fármacos , Peroxidación de Lípido/efectos de los fármacos , Masculino , Estrés Oxidativo/efectos de los fármacos , Ratas , Ratas Wistar , Recuento de Espermatozoides , Motilidad Espermática/efectos de los fármacos , Espermatozoides/efectos de los fármacos , Espermatozoides/ultraestructura , Testículo/enzimología
13.
J Anim Sci ; 98(2)2020 Feb 01.
Artículo en Inglés | MEDLINE | ID: mdl-31974567

RESUMEN

In this study, we identified cadmium (Cd) as a potential endocrine disruptor that impairs laying performance, egg quality, and eggshell deposition and induces oxidative stress and inflammation in the eggshell glands of laying hens. A total of 480 38-wk-old laying hens were randomly assigned into 5 groups that were fed a basal diet (control) or a basal diet supplemented with Cd (provided as CdCl2·2.5 H2O) at 7.5, 15, 30, and 60 mg Cd per kg feed for 9 wk. The results showed that, when compared with the control group, a low dose of dietary Cd (7.5 mg/kg) had positive effects on egg quality by improving albumen height, Haugh unit, yolk color, and shell thickness at the third or ninth week. However, with the increase in the dose and duration of Cd exposure, the laying performance, egg quality, and activities of eggshell gland antioxidant enzymes (catalase [CAT], glutathione peroxide [GSH-Px]), and ATPase (Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase) deteriorated, and the activity of total nitric oxide synthase (T-NOS) and the level of malondialdehyde (MDA) increased significantly (P < 0.05). The histopathology and real-time quantitative PCR results showed that Cd induced endometrial epithelial cell proliferation accompanied by upregulation of the mRNA levels of progesterone receptor (PgR) and epidermal growth factor receptor (EGFR), downregulation of the mRNA levels of estrogen receptor α (ERα) and interleukin 6 (IL6), and inflammation of the eggshell gland accompanied by significantly increased expression of complement C3 and pro-inflammatory cytokine tumor necrosis factor α (TNFα) (P < 0.05). In addition, the ultrastructure of the eggshell showed that dietary supplementation with 7.5 mg/kg Cd increased the palisade layer and total thickness of the shell, but with the increase in dietary Cd supplementation (30 and 60 mg/kg) the thickness of the palisade layer and mammillary layer decreased significantly (P < 0.05), and the outer surface of the eggshell became rougher. Correspondingly, the expression of calbindin 1 (CALB1), ovocalyxin-32 (OCX-32), ovocalyxin-36 (OCX-36), osteopontin (SPP1), and ovocledidin-17 (OC-17) decreased significantly (P < 0.05) with increasing dietary Cd supplementation. Conclusively, the present study demonstrates that dietary supplementation with Cd negatively affects laying performance, egg quality, and eggshell deposition by disturbing the metabolism of eggshell glands in laying hens but has a positive effect on egg quality at low doses.


Asunto(s)
Cloruro de Cadmio/toxicidad , Calcificación Fisiológica/efectos de los fármacos , Pollos , Cáscara de Huevo/metabolismo , Alimentación Animal/análisis , Animales , Antioxidantes/farmacología , Cloruro de Cadmio/administración & dosificación , Dieta/veterinaria , Cáscara de Huevo/química , Femenino
14.
Chemosphere ; 246: 125776, 2020 May.
Artículo en Inglés | MEDLINE | ID: mdl-31918093

RESUMEN

The impairments of gestational cadmium (Cd) exposure on testicular development and male fertility in offspring have been reported. Here, we investigated the effect of paternal low-concentration cadmium exposure on testicular development and spermatogenesis in offspring. Five-week-old male mice were exposed to cadmium chloride (100 mg/L) in drinking water for 20 weeks. Results presented that Cd did not affect the testicular histology and sperm count in mice. After mating with untreated females, pregnant mice and pups were then evaluated. No significant difference in the rate for successful pregnancy and the body weight of pups was observed in Cd-exposed mice compared to the controls. Male offspring were given with a chow and high-fat diet from postnatal day (PND) 35 to PND70. Our data indicated that high-fat diet obviously decreased No. of sperm in epididymides of adult offspring due to paternal Cd exposure. Testicular histology revealed that the percentage of seminiferous tubules in stages IX-XII and the atypical residual bodies positive tubules in CdH (paternal cadmium exposure and pubertal high-fat diet) group were higher than these in CdC (paternal cadmium exposure and pubertal chow diet) group. Further analysis demonstrated that high-fat diet markedly accelerated testicular apoptosis, as determined by TUNEL assay and immunostaining for cleaved caspase-3, in male offspring due to paternal Cd exposure. Collectively, high-fat diet exacerbates the damage of testicular development and spermatogenesis in offspring due to paternal cadmium exposure.


Asunto(s)
Cadmio/toxicidad , Exposición Dietética , Contaminantes Ambientales/toxicidad , Espermatogénesis/efectos de los fármacos , Testículo/efectos de los fármacos , Animales , Apoptosis/efectos de los fármacos , Peso Corporal/efectos de los fármacos , Cloruro de Cadmio/toxicidad , Dieta , Femenino , Masculino , Ratones , Tamaño de los Órganos/efectos de los fármacos , Embarazo , Túbulos Seminíferos , Espermatozoides/efectos de los fármacos
15.
Mar Environ Res ; 154: 104844, 2020 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-31784109

RESUMEN

A wide range of contaminants, industrial by-products, plastics, and pharmaceutics belonging to various categories, have been found in sea water. Although these compounds are detected at concentrations that might be considered as sub-lethal, under certain conditions they could act synergistically producing unexpected effects in term of toxicity or perturbation of biochemical markers leading to standard pathway. In this study, the Sparus aurata fibroblast cell line SAF-1, was exposed to increasing concentrations of carbamazepine (CBZ), polybrominated diphenyl ether 47 (BDE-47) and cadmium chloride (CdCl2) until 72 h, to evaluate the cytotoxicity and the expression of genes related to antioxidant defense, cell cycle and energetic balance. In general, both vitality and gene expression were affected by the exposure to the different toxicants, in terms of antioxidant defense and cell cycle control, showing the most significant effects in cells exposed to the mixture of the three compounds, respect to the single compounds separately. The synergic effect of the compounds on the analyzed biomarkers, underlie the potential negative impact of the contaminants on health of marine organisms.


Asunto(s)
Ciclo Celular , Metabolismo Energético , Regulación de la Expresión Génica , Oxidorreductasas , Contaminantes Químicos del Agua , Animales , Biomarcadores/metabolismo , Cloruro de Cadmio/toxicidad , Carbamazepina/toxicidad , Ciclo Celular/efectos de los fármacos , Ciclo Celular/genética , Línea Celular , Metabolismo Energético/efectos de los fármacos , Metabolismo Energético/genética , Activación Enzimática/efectos de los fármacos , Regulación de la Expresión Génica/efectos de los fármacos , Éteres Difenilos Halogenados/toxicidad , Estrés Oxidativo/efectos de los fármacos , Oxidorreductasas/genética , Contaminantes Químicos del Agua/toxicidad
16.
Hum Exp Toxicol ; 39(5): 653-661, 2020 May.
Artículo en Inglés | MEDLINE | ID: mdl-31876186

RESUMEN

BACKGROUND: Cadmium is an environmental pollutant which can induce the overproduction of free radicals while suppressing the antioxidant defense system. Curcumin is considered a free-radical scavenger and a potent antioxidant. This study was conducted to investigate the effect of curcumin on serum antioxidant enzymes and histopathological changes in mice treated with cadmium. METHODS: In this experimental study, adult mice were divided into four groups, namely, control, cadmium chloride (5 mg kg-1), curcumin (100 mg kg-1), and curcumin+cadmium chloride. The animals received curcumin 24 h prior to cadmium chloride injection. After 24 h, blood samples were collected and used to assess the levels of malondialdehyde (MDA), antioxidant enzymes activity (catalase, superoxide dismutase, and glutathione peroxidase), total glutathione, total thiol, and hydrogen peroxide. Histopathological evaluation was also performed for testicular tissue. RESULTS: Mice treated with cadmium showed a significant (p < 0.001) decrease in the activity of antioxidant enzymes, serum amounts of total glutathione and total thiol, and the diameter of seminiferous tubules compared to the control group. This pollutant also significantly (p < 0.001) increased serum levels of MDA and hydrogen peroxide and the lumen diameter of seminiferous tubules compared to the control group. In the curcumin+cadmium group, curcumin significantly (p < 0.001) reversed the adverse effects of cadmium, compared to the cadmium group. In addition, curcumin alone significantly (p < 0.001) increased serum glutathione peroxidase activity and thiol content compared to the control group. CONCLUSION: Curcumin, as a potent antioxidant, could compensate the adverse effects of cadmium on lipid and protein peroxidation, potentiated serum antioxidant defense system, and ameliorated some morphometrical parameters in the testis of cadmium-treated mice.


Asunto(s)
Cloruro de Cadmio/toxicidad , Curcumina/farmacología , Estrés Oxidativo/efectos de los fármacos , Sustancias Protectoras/farmacología , Testículo/efectos de los fármacos , Animales , Catalasa/metabolismo , Glutatión/sangre , Glutatión Peroxidasa/metabolismo , Peróxido de Hidrógeno/sangre , Masculino , Malondialdehído/sangre , Ratones , Superóxido Dismutasa/metabolismo , Testículo/patología
17.
Food Chem Toxicol ; 136: 110971, 2020 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-31751644

RESUMEN

Outbred male rats were repeatedly injected intraperitoneally two-level sub-lethal doses of lead acetate and/or cadmium chloride solutions 3 times a week during 6 weeks. The animals developed explicit, even if moderate, subchronic intoxication characterized by a large number of indices, both common to both metals (including increased DNA fragmentation coefficient) and lead-specific. Special attention was paid to hemodynamic and electrocardiographic effects. The combined action of lead and cadmium was modeled with the help of the Response Surface Methodology to obtain additional support for the previously substantiated postulates of combined toxicity's typological ambiguity. This is dependent on which particular effect comes under consideration, on its level, and on the acting dose ratio. For one and the same toxic combination, the type of combined toxic action can vary from synergistic to contra-directional. In particular, the actions of lead and cadmium on blood pressure were found to be opposite in direction. Furthermore, it is shown once again that the systemic toxic effects of a metal combination, its in vivo genotoxicity included, can be more or less attenuated by background administration of a theoretically justified composition of biologically active agents.


Asunto(s)
Cadmio/toxicidad , Plomo/toxicidad , Animales , Animales no Consanguíneos , Cadmio/sangre , Cloruro de Cadmio/administración & dosificación , Cloruro de Cadmio/toxicidad , Fragmentación del ADN/efectos de los fármacos , Sinergismo Farmacológico , Ecocardiografía/efectos de los fármacos , Corazón/efectos de los fármacos , Hemodinámica/efectos de los fármacos , Inyecciones Intraperitoneales , Riñón/efectos de los fármacos , Riñón/patología , Plomo/sangre , Masculino , Mutágenos/toxicidad , Miocardio/patología , Compuestos Organometálicos/administración & dosificación , Compuestos Organometálicos/toxicidad , Ratas , Pruebas de Toxicidad Subcrónica
18.
Environ Sci Pollut Res Int ; 27(6): 5981-5992, 2020 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-31863371

RESUMEN

Senna alexandrina is traditionally used for its antioxidant and anti-inflammatory properties, but little information is available concerning its potential protective effects against cadmium, which is a widespread environmental toxicant that causes hepatotoxicity. Here, we explored the effects of S. alexandrina extract (SAE) on cadmium chloride (CdCl2)-induced liver toxicity over 4 weeks in rats. Rats were allocated into four groups: control, SAE (100 mg/kg), CdCl2 (0.6 mg/kg), and SAE + CdCl2, respectively. Cadmium level in hepatic tissue, blood transaminases, and total bilirubin as indicators of liver function were assessed. Oxidative stress indices [malondialdehyde (MDA), nitrate/nitrite (NO), and glutathione (GSH)], antioxidant molecules [superoxide dismutase (SOD, catalase (CAT), glutathione-derived enzymes, and nuclear factor erythroid 2-related factor 2 (Nrf2)], pro-inflammatory mediators [interleukin-1 beta (IL-1ß) and tumor necrosis factor-alpha (TNF-α)], apoptosis proteins (Bcl-2, Bax, and caspase-3), and histological alterations to the liver were examined. SAE administration before CdCl2 exposure decreased cadmium deposition in liver tissue and the blood liver function indicators. SAE pre-treatment prevented oxidative, inflammatory, and apoptotic reactions and decreased histological alterations to the liver caused by CdCl2 exposure. SAE can be used as a promising protective agent against CdCl2-induced hepatotoxicity by increasing Nrf2 expression. Graphical abstract.


Asunto(s)
Cloruro de Cadmio/toxicidad , Sustancias Peligrosas/toxicidad , Sustancias Protectoras/farmacología , Extracto de Senna/farmacología , Senna (Planta) , Animales , Antioxidantes , Apoptosis , Cadmio , Suplementos Dietéticos , Hígado , Estrés Oxidativo , Ratas , Senósidos , Superóxido Dismutasa
19.
Drug Chem Toxicol ; 43(3): 225-233, 2020 May.
Artículo en Inglés | MEDLINE | ID: mdl-29927664

RESUMEN

The current study aimed to investigate the protective role of polydatin (PD) and grape seed extracts (GSEs) against the effects of cadmium chlorine (CD) application in the rats. Forty-nine adult Wistar albino male rats were used in the study. Rats were assigned into control (saline), CD (5 mg/kg CdCI2), PD (120 mg/kg PD), GSE (120 mg/kg GSE), CD + PD (5 mg/kg CdCI2 + 120 mg/kg PD), CD + GSE (5 mg/kg CdCI2 + 120 mg GSE), and CD + PD + GSE (5 mg/kg CdCI2+120 mg/kg PD +120 mg/kg GSE) treatments (n = 7 per group). The treatments were administered orally for four weeks. CD accumulation was observed in all tissues studied except for the brain tissue. PD and GSE inhibited CD accumulation in erythrocytes and tissues at varying levels. The liver, kidney, brain, and testes showed extensive degenerative histopathological changes in CD group. Liver total oxidant status (TOS) in the CD group increased significantly compared to the control. TOS of kidney, brain, and testis suggested that PD and GSE did not show a strong antioxidant effect in these tissues. Malondialdehyde (MDA) levels in blood and liver raised significantly in CD-treated rats compared to controls. PD, GSE, and their combinations increased antioxidant potential in all tissues and decreased MDA levels in blood plasma and liver. Overall, the protective effects of PD were more effective than GSE. Results suggested that although the initiation of histopathological changes was present in all tissues, the initiating factor was not the oxidative stress in the tissues studied except for the liver and blood.


Asunto(s)
Cloruro de Cadmio/toxicidad , Glucósidos/farmacología , Extracto de Semillas de Uva/farmacología , Estrés Oxidativo/efectos de los fármacos , Estilbenos/farmacología , Animales , Antioxidantes/administración & dosificación , Antioxidantes/farmacología , Glucósidos/administración & dosificación , Extracto de Semillas de Uva/administración & dosificación , Masculino , Malondialdehído/metabolismo , Ratas , Ratas Wistar , Estilbenos/administración & dosificación
20.
Arch Physiol Biochem ; 126(1): 82-88, 2020 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-30269601

RESUMEN

The natural flavonoid (catechin) has been shown to possess a multitude of pharmacological activities. However, oral administrated catechin (CT) failed to fulfil its therapeutic potential due to poor absorption and low bioavailability. Thus, is a pressing need to develop a new approach from to increase its intestinal absorption and improved bioavailability. In this work, we intended the increase the bioavailability of CT by preparing catechin-phospholipid complex (CT-PH) and evaluate the protective effect of CT-PH complex against cadmium caused liver injuries in rats. Oral bioavailability of CT and CT-PH complex was evaluated in rats and the plasma CT was estimated by HPLC analysis. The greater absorption of CT-PH complex rats indicated that improved bioavailability. Liver function markers, lipid peroxidation, protein oxidation, antioxidant status and histopathological changes were determined in normal and treated rats. Moreover, biochemical analysis and histopathological examinations indicated that CT-PH provided better protection to rat liver than free CT.


Asunto(s)
Antioxidantes/farmacología , Catequina/farmacología , Enfermedad Hepática Inducida por Sustancias y Drogas/prevención & control , Hígado/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Fosfatidilcolinas/farmacocinética , Administración Oral , Animales , Antioxidantes/química , Antioxidantes/farmacocinética , Disponibilidad Biológica , Cloruro de Cadmio/toxicidad , Catalasa/metabolismo , Catequina/química , Catequina/farmacocinética , Enfermedad Hepática Inducida por Sustancias y Drogas/metabolismo , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Esquema de Medicación , Portadores de Fármacos , Expresión Génica/efectos de los fármacos , Glutatión/metabolismo , Glutatión Peroxidasa/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Hígado/metabolismo , Hígado/patología , Pruebas de Función Hepática , Masculino , Malondialdehído/metabolismo , Fosfatidilcolinas/química , Ratas , Ratas Wistar , Superóxido Dismutasa/metabolismo
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