Objectives: Arsenic is a ubiquitous element that is widely distributed in the environment to which man and animals are exposed. Cardiovascular disease is one of the aftermaths of chronic arsenic exposure-related morbidity and mortality. This study sought to investigate the possibility of reversal from arsenic-induced cardio-renal toxicity following exposure and subsequent withdrawal. The study also seeks to understand the mechanism of action of this reversal.

Methods: Rats were orally exposed to sodium arsenite at 10, 20 and 40 mg/kg daily for 4 weeks followed by 4 weeks of withdrawal.

Results: Exposure to arsenic caused a significant increase in malondialdehyde, H₂O₂ generation but decrease total thiol and reduced glutathione levels in both cardiac and renal tissues. Furthermore, increases in superoxide dismutase, glutathione-S-transferase and catalase with significant increases in glutathione peroxidase activities were observed in the cardiac tissues. On the contrary, a significant reduction in the renal antioxidant enzyme activity was recorded following exposure. Also, antioxidant defense system did not return to apparent values after arsenic withdrawal. Immunohistochemistry revealed a reduction in the expression of the pro-survival protein–protein kinase B (Akt/PKB) following exposure to arsenic and this was not reversed by withdrawal

Discussion: Exposure to arsenic caused cardio-renal toxicity via induction of oxidative stress and down-regulation of Akt/PKB expressions.

目标：砷是一种普遍存在的元素，广泛分布在人和动物所接触的环境中。心血管疾病是慢性砷暴露相关发病率和死亡率的后果之一。本研究旨在调查在暴露和随后撤药后逆转砷诱导的心肾毒性的可能性。该研究还试图了解这种逆转的作用机制。

方法：大鼠口服亚砷酸钠，剂量分别为每天 10、20 和 40 mg/kg，持续 4 周，然后停药 4 周。

结果：暴露于砷导致丙二醛、H ₂ O ₂生成显着增加，但降低了心脏和肾脏组织中的总硫醇和谷胱甘肽水平。此外，在心脏组织中观察到超氧化物歧化酶、谷胱甘肽-S-转移酶和过氧化氢酶的增加以及谷胱甘肽过氧化物酶活性的显着增加。相反，暴露后肾抗氧化酶活性显着降低。此外，在砷戒断后，抗氧化防御系统没有恢复到表观值。免疫组织化学显示暴露于砷后促存活蛋白激酶 B (Akt/PKB) 的表达降低，并且这并未因戒断而逆转

讨论：暴露于砷通过诱导氧化应激和下调 Akt/PKB 表达而导致心肾毒性。