Assement on CNSL Toxicity in liver injury.pptx

Assement on CNSL Toxicity in liver injury

1. CNSL Toxicity Assessment of Oxidative Liver Injury by CNSL

2. Introduction This study evaluates the toxic effects of Cashew Nut Shell Liquid (CNSL) applied topically on male Wistar rats for 45 days, examining biochemical, molecular, and histological changes in the liver and kidney.

3. Oxidative Liver Injury by CNSL 01

4. Background and Toxicity of CNSL CNSL , derived from cashew nut shells, contains cardanol and cardol which pose health risks such as dermatitis and metabolic injury. It alters skin and internal organ functions due to its toxic, mutagenic nature.

5. Experimental Design with Wistar Rats Male Wistar rats were divided into control, CNSL-treated, and sunflower oil groups. CNSL and sunflower oil were topically applied daily on shaved dorsal skin for 45 days to evaluate systemic effects. Samples were collected on day 46 for analysis.

6. Biochemical and Antioxidant Changes CNSL treatment significantly increased liver enzymes SGPT and SGOT , indicating liver dysfunction. Antioxidant enzymes SOD and catalase activities decreased, while serum LDH increased, reflecting oxidative stress and possible hepatocytic necrosis. Elevated inflammatory markers IL-6 and TNF-α were observed, suggesting acute tissue inflammation.

7. Bcl2 Interaction Study 02

8. Expression of Apoptotic and Inflammatory Genes CNSL exposure upregulated pro-apoptotic p53 and Akt genes, while downregulating anti-apoptotic Bcl-2 gene in liver tissue. This shift promotes apoptosis and contributes to oxidative stress-induced liver injury.

9. Histopathological Findings in Liver and Kidney CNSL-treated rats showed liver tissue inflammation with central vein dilation and blood cell infiltration. Kidney showed disrupted Bowmans capsule and tubular degeneration, indicating tissue damage not present in controls or sunflower oil groups.

10. In-silico Molecular Docking of CNSL Components with Bcl2 Molecular docking revealed cardanol binds to BH1 domain and cardol to BH4 domain of human Bcl2 protein. Binding energies were −5.62 and −3.59 kcal/mol respectively, potentially inhibiting Bcl2 anti-apoptotic function.

11. Conclusions Topical CNSL exposure causes oxidative liver injury and kidney damage via inflammatory, necrotic, and apoptotic pathways. Interaction of CNSL components with Bcl2 gene contributes to apoptosis. Protective measures are essential for workers exposed to CNSL to prevent serious metabolic and skin damages.

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