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1.
Biomedical and Environmental Sciences ; (12): 760-770, 2020.
Article in English | WPRIM | ID: wpr-878294

ABSTRACT

Objective@#This research was performed to evaluate the effect of tebuconazole (TBZ) on reproductive organs of male rats and to assess the protective role of combined essential trace elements in alleviating the detrimental effect of TBZ on male reproductive function.@*Methods@#For this purpose, 48 rats were exposed to 100 mg/kg TBZ, TBZ supplemented with zinc (Zn), selenium (Se), copper (Cu), and iron (Fe), TBZ + (Se + Zn); TBZ + Cu; or TBZ + Fe. The experiment was conducted for 30 consecutive days.@*Results@#TBZ caused a significant perturbation in mineral levels and reduction in reproductive organs weights, plasma testosterone level, and testicular antioxidant enzyme activities. The TBZ-treated group also showed a significant increase in sperm abnormalities (count, motility, and viability percent), plasma follicle-stimulating hormone and luteinizing hormone concentrations, lipid peroxidation, protein oxidation, and severe DNA degradation in comparison with the controls. Histopathologically, TBZ caused testis impairments. Conversely, treatment with trace elements, in combination or alone, improved the reproductive organ weights, sperm characteristics, TBZ-induced toxicity, and histopathological modifications in testis.@*Conclusion@#TBZ exerts significant harmful effects on male reproductive system. The concurrent administration of trace elements reduces testis dysfunction, fertility, and toxicity induced by TBZ.


Subject(s)
Animals , Male , Rats , Animal Feed/analysis , Antioxidants/metabolism , Diet , Dietary Supplements/analysis , Fungicides, Industrial/adverse effects , Minerals/metabolism , Mutagenicity Tests , Rats, Wistar , Spermatozoa/physiology , Testis/physiology , Trace Elements/metabolism , Triazoles/adverse effects
2.
Biomedical and Environmental Sciences ; (12): 115-125, 2018.
Article in English | WPRIM | ID: wpr-776073

ABSTRACT

OBJECTIVE@#The current study aimed to elucidate the effect of vanillin on behavioral changes, oxidative stress, and histopathological changes induced by potassium bromate (KBrO3), an environmental pollutant, in the cerebellum of adult mice.@*METHODS@#The animals were divided into four groups: group 1 served as a control, group 2 received KBrO3, group 3 received KBrO3 and vanillin, and group 4 received only vanillin. We then measured behavioral changes, oxidative stress, and molecular and histological changes in the cerebellum.@*RESULTS@#We observed significant behavioral changes in KBrO3-exposed mice. When investigating redox homeostasis in the cerebellum, we found that mice treated with KBrO3 had increased lipid peroxidation and protein oxidation in the cerebellum. These effects were accompanied by decreased Na+-K+ and Mg2+ ATPase activity and antioxidant enzyme gene expression when compared to the control group. Additionally, there was a significant increase in cytokine gene expression in KBrO3-treated mice. Microscopy revealed that KBrO3 intoxication resulted in numerous degenerative changes in the cerebellum that were substantially ameliorated by vanillin supplementation. Co-administration of vanillin blocked the biochemical and molecular anomalies induced by KBrO3.@*CONCLUSION@#Our results demonstrate that vanillin is a potential therapeutic agent for oxidative stress associated with neurodegenerative diseases.


Subject(s)
Animals , Mice , Antioxidants , Metabolism , Behavior, Animal , Benzaldehydes , Pharmacology , Bromates , Toxicity , Cerebellum , Metabolism , Pathology , Cytokines , Genetics , Metabolism , Environmental Pollutants , Toxicity , Gene Expression , Lipid Peroxidation , Oxidative Stress , Rotarod Performance Test
3.
Biomedical and Environmental Sciences ; (12): 340-351, 2012.
Article in English | WPRIM | ID: wpr-235549

ABSTRACT

<p><b>OBJECTIVE</b>To determine the efficiency of selenium and/or vitamin E to alleviate lung oxidative damage induced by dimethoate, an organophosphorus compound.</p><p><b>METHODS</b>Adult Wistar rats were exposed during 30 days either to dimethoate (0.2 g/L of drinking water), dimethoate+selenium (0.5 mg/kg of diet), dimethoate+vitamin E (100 mg/kg of diet), or dimethoate+selenium+vitamin E.</p><p><b>RESULTS</b>Exposure to dimethoate caused oxidative stress in lung evidenced by an increase of malondialdehyde, protein carbonyl groups and advanced oxidation protein products. An increase in glutathione peroxidase, superoxide dismutase, catalase and a decrease in acetylcholinesterase and butyrylcholinesterase activities, glutathione, non-protein thiols and vitamins C levels were observed. Histopathological changes in lung tissue were noted as emphysema, hemorrhages and hemosiderin deposits. Co-administration of selenium or vitamin E to the diet of dimethoate treated rats ameliorated the biochemical parameters as well as histological impairments. The joint effect of these elements was more powerful in antagonizing dimethoate-induced lung oxidative damage.</p><p><b>CONCLUSION</b>We concluded that selenium and vitamin E ameliorated the toxic effects of this pesticide in lung tissue suggesting their role as potential antioxidants.</p>


Subject(s)
Animals , Rats , Acetylcholinesterase , Metabolism , Antioxidants , Pharmacology , Ascorbic Acid , Metabolism , Biomarkers , Butyrylcholinesterase , Metabolism , Dimethoate , Glutathione , Metabolism , Lipid Peroxidation , Lung Diseases , Diagnosis , Oxidative Stress , Rats, Wistar , Selenium , Pharmacology , Vitamin E , Pharmacology
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