Akademik Veri Yönetim Sistemi
Turkish Journal of Biochemistry, cilt.36, sa.4, ss.283-289, 2011 (SCI-Expanded)
Objectives: The aim of the present study was to investigate the relation between brain damage induced by carbon tetrachloride and superoxide dismutase, catalase, glutathione pero-xidase, and glutathione S-transferase enzyme activities. Also, the other aim was to evaluate the effect of stobadine on this metabolism. We particularly choose brain tissue as an experimental model because it contains reach polyunsaturated fatty acids which is one of the most important targets of the free radicals. Another important reason for choosing brain as a model is the limited studies with brain tissue damaged with carbon tetrachloride that compared to numerous ones with hepatic tissue. Methods: Rats were randomly separated into four experimental groups as control (n=10), stobadine (n=10), carbon tetrachloride (n=10), carbon tetrachloride+ stobadine (n=10). Results: Carbon tetrachloride administration reduced superoxide dismutase, catalase, glu-tathione peroxidase, and glutathione S-transferase enzyme activities. Catalase, superoxide dismutase and glutathione S-transferase enzyme activities of the carbon tetrachloride+ stobadine group nearly approached the levels of the control group. On the contrary, glutathione peroxidase activity could not access the normal levels. Histopathologic results showed that carbon tetrachloride induced morphologic damage and edema in the brain cells. In spite of limited improvement in the carbon tetrachloride + stobadine group we found eosinophilia and edemas at the neurons and neuroglial cells, respectively. Conclusions: It could be suggested that glutathione peroxidase enzyme can be more important antioxidant enzyme to protect brain cells against the oxygen or carbon tetrachloride based free radicals. The authors do not have a conflict of interest.