To evaluate the involvement of mineralocorticoid receptor (MR) in the redox imbalance during early stages of cardiac and renal toxicity induced by ethanol.
Approach:
Key Findings:
MR blockade prevented increases in lipoperoxidation and superoxide levels in the left ventricle and renal cortex of ethanol-treated rats.
Hydrogen peroxide levels increased in the renal cortex of ethanol-treated rats, but this response was prevented by MR blockade.
Ethanol treatment increased cardiac thromboxane B2 and renal prostaglandin E2 levels, which were abrogated by MR blockade.
Interpretation:
The MR pathway mediates pro-oxidative effects in the early stages of ethanol-induced cardiorenal dysfunction.
Limitations:
Study conducted only in male Wistar Hannover rats, limiting generalizability to other populations.
Long-term effects of MR blockade beyond the five-week treatment period were not assessed.
Conclusion:
The findings suggest that MR activation plays a significant role in the early cardiorenal injury associated with ethanol exposure.
