Publication: Potentiation of carbon tetrachloride induced hepatotoxicity by thinner inhalation
Issued Date
1990-01-01
Resource Type
ISSN
03881350
Other identifier(s)
2-s2.0-0025369704
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Journal of Toxicological Sciences. Vol.15, No.2 (1990), 75-86
Suggested Citation
C. Toskulkao, J. Nhongsaeng, T. Glinsukon Potentiation of carbon tetrachloride induced hepatotoxicity by thinner inhalation. Journal of Toxicological Sciences. Vol.15, No.2 (1990), 75-86. doi:10.2131/jts.15.75 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/16171
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Potentiation of carbon tetrachloride induced hepatotoxicity by thinner inhalation
Author(s)
Other Contributor(s)
Abstract
The interaction of thinner and carbon tetrachloride (CCl 4 ) induced hepatotoxicity was studied in the rats using the activity of plasma GOT and GPT, liver triglyceride and histopathologic changes of liver necrosis as indices. The animals were housed in a chamber with the continuous flow of thinner vapour (1.11 g/litre/hr) for 2 hrs prior to i.p. administration of CCl 4 (0.1 ml/kg BW) at 18 hrs after thinner inhalation. Thinner inhalation potentiated CCl 4 induced hepatotoxicity in a dose-dependent manner. The maximal enhanced effect was observed at 24 hrs after CCl 4 administration by which the activities of PGOT and PGPT were significantly increased (3-folds). Thinner itself caused an additive effect on CCl 4 induced liver triglyceride accumulation. At 18 hrs after thinner inhalation, the activity of NADPH cytochrome C reductase was markedly increased (2.2 folds) but no change in the activity of aminopyrine N-demethylase which was able to increase the 14 ·CCl 3 free radicals and binding to both the hepatic microsomal proteins (1.8 folds) and lipids (1.4 folds). In addition, thinner pretreatment somehow increased hepatic lipid peroxidation by 1.4 folds. These results suggest that thinner pretreatment causes an increase in mixed function oxidases to activate the formation of ·CCl 3 free radicals and binding to the microsomal proteins and lipids, which in turn stimulate hepatic damage via lipid peroxidation in the membrane.