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Hepatotoxic effects elicited by n-hexane or n-heptane
S K Goel1, G S Rao, K P Pandya
1Industrial Toxicology Research Centre, Lucknow, India.
Journal of Applied Toxicology : JAT
|April 1, 1988
Summary
Hepatotoxic effects of n-hexane and n-heptane were studied in rats. Both solvents decreased hepatic protein and sulfhydryl content, increasing lipid peroxidation and reducing drug metabolism.
Area of Science:
- Toxicology
- Biochemistry
- Pharmacology
Background:
- n-Hexane and n-heptane are common industrial solvents.
- Exposure to solvents can lead to adverse health effects, particularly on the liver.
- Understanding the specific hepatotoxic mechanisms is crucial for risk assessment.
Purpose of the Study:
- To investigate the hepatotoxic effects of n-hexane and n-heptane in albino rats.
- To evaluate biochemical and functional changes in the liver following solvent exposure.
- To determine the time-dependent toxicity of these solvents.
Main Methods:
- Albino rats were administered n-hexane or n-heptane intraperitoneally (1 ml/kg body weight).
- Liver samples were analyzed for protein content, total sulfhydryl content, and lipid peroxidation at 1, 2, 7, and 45 days.
- Drug metabolizing activity and pentobarbitone sleeping time were assessed.
- Hepatic glucose-6-phosphatase activity was measured as a microsomal marker.
Main Results:
- Both n-hexane and n-heptane significantly decreased hepatic protein and total sulfhydryl content.
- A significant increase in lipid peroxidation was observed within 24-48 hours of exposure.
- Drug metabolizing activity was markedly reduced, leading to increased pentobarbitone sleeping time.
- Hepatic glucose-6-phosphatase activity, a key microsomal enzyme, showed a significant decrease.
Conclusions:
- n-Hexane and n-heptane induce significant hepatotoxicity in rats.
- These solvents disrupt hepatic biochemical pathways, indicated by reduced protein, sulfhydryl content, and enzyme activity.
- Increased lipid peroxidation and impaired drug metabolism highlight the oxidative stress and functional deficits caused by exposure.