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From the Research
Nephrotoxicity of Lambda-Cyhalothrin
- Lambda-Cyhalothrin, a synthetic pyrethroid insecticide, has been shown to cause nephrotoxicity in various studies 1, 2, 3, 4.
- The mechanism of nephrotoxicity is believed to be related to oxidative stress, which leads to damage to the kidney cells and tissues 1, 2, 4.
- Studies have shown that exposure to Lambda-Cyhalothrin can cause an increase in serum urea nitrogen, creatinine, and urea levels, indicating kidney damage 1, 2, 3.
- Histological examination of the kidney has also revealed marked histopathological changes, including vacuolations, cell infiltration, and widened tubular lumen 1, 2.
Oxidative Stress and Antioxidant Mechanisms
- Oxidative stress is thought to play a key role in the nephrotoxicity of Lambda-Cyhalothrin, with studies showing an increase in lipid peroxidation, superoxide anion generation, and nitrite levels 1, 2, 4.
- The activities of antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione-S-transferase, have been shown to be depleted in the kidney following exposure to Lambda-Cyhalothrin 1, 2.
- The use of antioxidants, such as ascorbic acid, has been shown to ameliorate the nephrotoxic effects of Lambda-Cyhalothrin 2.
Biomarkers of Exposure
- The metabolites of Lambda-Cyhalothrin, such as cis-3-(2-chloro-3-trifluoroprop-1-en-1-yl)-2-dimethylcyclopropanecarboxylic acid (CFMP) and 3-phenoxybenzoic acid (3-PBA), have been identified as useful biomarkers of exposure in humans 5.
- These metabolites have been shown to have short half-lives, with a mean half-life of approximately 5-6 hours, and are excreted in urine at a rate of approximately 21-30% of the dose 5.