M. Ghazi- Khansari
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
M. Karami
Department of Toxicology, School of Pharmacy, Sari University of Medical Sciences, Sari: Iran
M. Rezayat
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
M. Abdollahi
Department of Toxicology, School of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
B. Minaie
Department of Toxicology, School of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
O. Sabzevari
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
ABSTRACT
The purpose of this study was to evaluate protective effects of vitamin E, selenium and propranolol on TCDD induced changes of biochemical parameters using the rat liver perfusion system. Various concentrations of TCDD (0.3, 3, 20, 30 μg L-1) were added to the perfusion fluid and biochemical changes in perfusion fluid of isolated rat liver were examined within 2 h. The results showed that TCDD significantly increases the aminotransferase activities in a dose-dependent manner. It was determined that TCDD at 20 μg L-1 caused a maximum increase in biochemical parameters within 2 h (p<0.0001). The result also showed that propranolol (20 mg L-1), sodium selenite (345 mg L-1) and vitamin E (α-tocopherol, 700 mg L-1) significantly decreases TCDD hepatotoxicity. Aminotransferase enzyme activity as well as glutathione and protein content significantly changed in treatment groups as compared to the TCDD group (p<0.001). Reduction in hepatotoxicity may be attributed to prevention of lipid peroxidation, although other mechanisms may also be involved.
PDF References
How to cite this article
M. Ghazi- Khansari, M. Karami, M. Rezayat, M. Abdollahi, B. Minaie and O. Sabzevari, 2005. The Protective Effects of Antioxidants and Propranolol on Hepatotoxicity of
TCDD During Isolated Rat Liver Perfusion. International Journal of Pharmacology, 1: 336-341.
DOI: 10.3923/ijp.2005.336.341
URL: https://scialert.net/abstract/?doi=ijp.2005.336.341
DOI: 10.3923/ijp.2005.336.341
URL: https://scialert.net/abstract/?doi=ijp.2005.336.341
REFERENCES
- Kelada, F.S., 1990. Occupational intake by dermal exposure to polychlorinated dibenzo-p-dioxins and polychlorinated dibenzo-furans in pulp mill industry. Am. Ind. Hyg. Assoc. J., 51: 519-521.
Direct Link - Stohs, S.J., M.Q. Hassan and W.J. Murray, 1983. Lipid peroxidation as a possible cause of TCDD toxicity. Biochem. Biophys. Res. Commun., 111: 854-859.
CrossRefDirect Link - Pitot, H.C., T. Goldsworthy, H.A. Campbell and A. Poland, 1980. Quantitative evaluation of the promotion by 2,3,7,8-tetrachlorodibenzo-p-dioxin of hepatocarcinogenesis from diethylnitrosamine. Can. Res., 40: 3616-3620.
Direct Link - Kew, M.C., 2000. Serum aminotransferase concentration as evidence of hepatocellular damage. Lancet, 355: 591-592.
CrossRefPubMedDirect Link - Moron, M.S., J.W. Depierre and B. Mannervik, 1979. Levels of glutathione, glutathione reductase and glutathione S-transferase activities in rat lung and liver. Biochim. Biophys. Acta Gen. Subj., 582: 67-78.
CrossRefPubMedDirect Link - Ellman, G.L., 1959. Tissue sulfhydryl groups. Arch. Biochem. Biophys., 82: 70-77.
CrossRefPubMedDirect Link - Bradford, M.M., 1976. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal. Biochem., 72: 248-254.
CrossRefPubMedDirect Link - Keenan, R.E., D.J. Paustenbach, R.J. Wenning and A.H. Parsons, 1991. Pathology reevaluation of the Kociba et al., 1978, bioassay of 2,3,7,8-TCDD: Implications for risk assessment. J. Toxicol. Environ. Health, 34: 279-296.
PubMedDirect Link