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Subchronic exposure to arsenic trioxide-induced oxidative DNA damage in kidney tissue of mice
Zongyuan Li1, Fengyuan Piao, Shuang Liu
1Department of Occupational and Environmental Health, Dalian Medical University, No. 9 Western Section of Lushun South Road, Dalian, LiaoNing 116044, PR China.
Abstract:
To evaluate the oxidative DNA damage in kidney tissue of mice exposed to arsenic trioxide (As) subchronically, expression of 8-hydroxy-2-deoxyguanosine (8-OHdG) and pathologic changes were observed. Forty mice were randomly divided into 4 groups of 10 each (5 mice of each sex). Group 1 received drinking water alone (control). Groups 2, 3 and 4 received 1, 2 and 4 mg/L arsenic trioxide, respectively. Arsenic trioxide was given through drinking water for 60 days. The expression of 8-OHdG in the kidney tissue of mice was analyzed observed in these 4 groups. The groups treated with As showed pathologic changes in the kidney tissue and significant increase in the level of 8-OHdG expression (P<0.01). Moreover, the dose-dependent increase between As exposure and renal damages were observed. Especially, its immunoactivity was strong in the proximal convoluted tubule and Bowman's capsule. These results suggest that chronic exposure to As induces damages to kidney tissue, and especially the epithelial cells of proximal convoluted tubule and the podocytes of the Bowman's capsule may be more sensitive to As-induced nephrotoxicity.
Insights
Subchronic exposure to arsenic trioxide (As) causes significant oxidative DNA damage in mouse kidney tissue, indicated by increased 8-hydroxy-2-deoxyguanosine (8-OHdG) levels and observable pathologic changes, particularly in the proximal convoluted tubule and Bowman's capsule.
Area of Science:
- Toxicology
- Nephrology
- Molecular Biology
Background:
- Arsenic trioxide (As) is a toxic metalloid with known adverse health effects.
- Oxidative stress is a key mechanism in arsenic-induced toxicity.
- Kidney damage is a significant concern following arsenic exposure.
Purpose of the Study:
- To investigate the subchronic effects of arsenic trioxide on kidney tissue in mice.
- To evaluate the induction of oxidative DNA damage, specifically 8-hydroxy-2-deoxyguanosine (8-OHdG) expression.
- To correlate arsenic exposure levels with observed renal histopathology.
Main Methods:
- Subchronic exposure of mice to varying doses of arsenic trioxide (1, 2, and 4 mg/L) in drinking water for 60 days.
- Assessment of pathological changes in kidney tissue.
- Quantification of 8-hydroxy-2-deoxyguanosine (8-OHdG) expression in kidney tissue via immunohistochemistry.
Main Results:
- Arsenic trioxide exposure led to significant pathological alterations in kidney tissue.
- A statistically significant increase (P<0.01) in 8-OHdG expression was observed in arsenic-treated groups.
- A dose-dependent relationship was found between arsenic exposure and the severity of renal damage.
- Elevated 8-OHdG immunoactivity was prominent in the proximal convoluted tubule and Bowman's capsule.
Conclusions:
- Subchronic exposure to arsenic trioxide induces oxidative DNA damage in mouse kidneys.
- The proximal convoluted tubule epithelial cells and Bowman's capsule podocytes are particularly susceptible to arsenic-induced nephrotoxicity.
- These findings highlight the potential for arsenic trioxide to cause significant kidney damage with prolonged exposure.
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