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Background <p>Pentachlorophenol (PCP) and its derivatives generate ROS to cause toxicity. In our previous study, rats treated with PCP showed oxidative damage to the blood, liver, kidney, and intestine. We hypothesized that pretreatment with curcumin (CUR) and gallic acid (GA) would abrogate PCP-mediated hemotoxicity in rats.</p> Results <p>PCP alone causes oxidation of proteins, lipids, and thiols in rat blood. Elevated XO activity and H<sub>2</sub>O<sub>2</sub> levels indicate an oxidative stress condition in the blood. The activities of AO, glycolytic, and membrane-bound enzymes were also inhibited. PCP increased plasma creatinine, BUN, ALT, and AST levels in treated rats, suggesting kidney and liver damage. Histology of the liver shows dead and shrunken hepatocytes, dilatation of the sinusoidal spaces, hemorrhage, and dissolution of the hepatic cords in the PCP-alone group. Pretreatment with CUR effectively alleviated PCP-mediated oxidative changes, whereas GA provided partial protection.</p> Conclusion <p>These findings show that CUR and GA reverse PCP-induced oxidative damage in rat blood and can be potent therapeutics against chlorophenol-induced hemotoxicity.</p>

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Mitigating effect of curcumin and gallic acid against pentachlorophenol-induced oxidative damage in rat blood under in vivo conditions

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月22日

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  • Nikhil Maheshwari

摘要

Background

Pentachlorophenol (PCP) and its derivatives generate ROS to cause toxicity. In our previous study, rats treated with PCP showed oxidative damage to the blood, liver, kidney, and intestine. We hypothesized that pretreatment with curcumin (CUR) and gallic acid (GA) would abrogate PCP-mediated hemotoxicity in rats.

Results

PCP alone causes oxidation of proteins, lipids, and thiols in rat blood. Elevated XO activity and H2O2 levels indicate an oxidative stress condition in the blood. The activities of AO, glycolytic, and membrane-bound enzymes were also inhibited. PCP increased plasma creatinine, BUN, ALT, and AST levels in treated rats, suggesting kidney and liver damage. Histology of the liver shows dead and shrunken hepatocytes, dilatation of the sinusoidal spaces, hemorrhage, and dissolution of the hepatic cords in the PCP-alone group. Pretreatment with CUR effectively alleviated PCP-mediated oxidative changes, whereas GA provided partial protection.

Conclusion

These findings show that CUR and GA reverse PCP-induced oxidative damage in rat blood and can be potent therapeutics against chlorophenol-induced hemotoxicity.