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首页> 外文期刊>Life sciences >Cytoprotective and antioxidant role of diallyl tetrasulfide on cadmium induced renal injury: an in vivo and in vitro study.
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Cytoprotective and antioxidant role of diallyl tetrasulfide on cadmium induced renal injury: an in vivo and in vitro study.

机译：二烯丙基四硫化物对镉诱导的肾损伤的细胞保护和抗氧化作用：体内和体外研究。

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摘要

Cadmium (Cd) is an environmental and industrial pollutant that affects various organs in humans and animals. A body of evidence has accumulated implicating the free radical generation with subsequent oxidative stress in the biochemical and molecular mechanisms of Cd toxicity. Since kidney is the critical target of Cd toxicity, we carried out this study to investigate the effects of diallyl tetrasulfide (DTS), an organosulfur compound derived from garlic on Cd induced toxicity in the kidney of rats and also in the kidney cell line (vero cells). In experimental rats, subcutaneous administration of Cd (3 mg/kg bw/day) for 3 weeks induced renal damage, which was evident from significantly increased levels of serum urea and creatinine with significant decrease in creatinine clearance. A markedly increased levels of lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydroperoxides) and protein carbonyl contents with significant decrease in nonenzymic antioxidants (total sulphydryl groups, reduced glutathione, vitamin C and vitamin E) and enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase) as well as glutathione metabolizing enzymes (glutathione reductase, and glucose-6-phosphate dehydrogenase) were also observed in Cd intoxicated rats. Coadministration of DTS (40 mg/kg bw/day) and Cd resulted in the reversal of the kidney function accompanied by a significant decrease in lipid peroxidation and increase in the antioxidant defense system. In vitro studies with vero cells showed that incubation of DTS (5-50 microg/ml) with Cd (10 microM) significantly reduced the cell death induced by Cd. DTS at 40 microg/ml effectively blocked the cell death and lipid peroxidation induced by Cd (10 microM) indicating its cytoprotective property. Further, the flow cytometric assessment on the level of intracellular reactive oxygen species using a fluorescent probe 2', 7'-dichlorofluorescein diacetate (DCF-DA) confirmed the Cd induced intracellular oxidative stress in vero cells, which was significantly suppressed by DTS (40 microg/ml). The histopathological studies in the kidney of rats also showed that DTS (40 mg/kg bw/day) markedly reduced the toxicity of Cd and preserved the architecture of renal tissue. The present study suggests that the cytoprotective potential of DTS in Cd toxicity might be due to its antioxidant and metal chelating properties, which could be useful for achieving optimum effects in Cd induced renal damage.
机译：镉（Cd）是一种环境和工业污染物，会影响人类和动物的各个器官。大量证据表明，在Cd毒性的生物化学和分子机制中，自由基的产生与随后的氧化应激有关。由于肾脏是Cd毒性的关键目标，因此我们进行了这项研究，以研究二烯丙基四硫化物（DTS）（一种大蒜衍生的有机硫化合物）对Cd诱导的大鼠肾脏以及肾脏细胞系毒性的影响（vero细胞）。在实验大鼠中，皮下注射Cd（3 mg / kg bw /天）持续3周可引起肾脏损害，这从血清尿素和肌酐水平的显着升高和肌酐清除率的显着降低中可以明显看出。脂质过氧化标记（硫代巴比妥酸反应性物质和脂质氢过氧化物）和蛋白质羰基含量显着增加，非酶类抗氧化剂（总硫代基团，谷胱甘肽，维生素C和维生素E减少）和酶类抗氧化剂（超氧化物歧化酶，过氧化氢酶，在镉中毒的大鼠中还观察到了谷胱甘肽过氧化物酶和谷胱甘肽-S-转移酶以及谷胱甘肽代谢酶（谷胱甘肽还原酶和葡萄糖-6-磷酸脱氢酶）。 DTS（40 mg / kg bw /天）和Cd的共同给药导致肾功能逆转，同时脂质过氧化作用显着降低，抗氧化防御系统增强。 Vero细胞的体外研究表明，将DTS（5-50 microg / ml）与Cd（10 microM）一起孵育可显着降低Cd诱导的细胞死亡。 40 µg / ml的DTS有效阻断了Cd（10 microM）诱导的细胞死亡和脂质过氧化反应，表明其具有细胞保护作用。此外，使用荧光探针2'，7'-二氯荧光素二乙酸酯（DCF-DA）对细胞内活性氧种类的水平进行流式细胞术评估，证实了Cd诱导了Vero细胞的细胞内氧化应激，DTS可以显着抑制该氧化应激（40微克/毫升）。在大鼠肾脏中的组织病理学研究还表明，DTS（40 mg / kg bw /天）显着降低了Cd的毒性并保留了肾脏组织的结构。本研究表明，DTS在Cd毒性中的细胞保护潜力可能是由于其抗氧化剂和金属螯合特性，对于在Cd诱导的肾损伤中获得最佳效果可能有用。

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