To elucidate the mechanism of protective effects of the selenium, antioxidant system was monitored during the hepatic carcinogenesis. Sprague Dawley rats were subjected to chemical heptocarcinogenic procedure according to the Solt-Farber model
treted
with diethylnitrosamine(DEN), acetylaminofluorene(AAF) and selenium(Se) before and after partial hepatectomy(PH). Biochemical analysis of oxygen radicals, superoxide dismutase(SOD), glutathione peroxidase(GSHPx) and glutathione S-transferase(GST)
at the
scheduled hepatic putative preneoplastic lesions by placental from of glutathione S-transferase(GST-P) antibody were carried out. Experimental group were divided into four groups; G1(DEN only(, G2(DEN+ Se), G3(DEN+AAF) and G4(DEN+ AAF +Se) and
control
G(PH only).
Superoxide radicals were increased in the early stage of carcinogenesis, followed by progressive decrease without significant effects by selenium, Cu, Zn SOD, Mn-SOD and peroxidase were significantly suppressed during carcinogenesis which were
reversingly increased by selenium, Hydroxyl radicals were increased in the early stage of carcinogenesis followed by progressive decrease with significant decreasing effect by selenium. Glutathioe peroxidase was not changed during the whole stage
of
carcinogenesis, though selenium treatment increased it significantly. Glutathioe S-transferase was significantly increased during carcinogenesis, but its expression was not affected by selenium treatment. From these results, it can be concluded
that
major protective roles of the selenium on the hepatic carcinogenesis are conducted mainly through glutathione peroxidase and partially by superoxide dismutase.
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