We report here the results of a study performed on the livers of rats intoxicated with CCl4 in order to investigate the dependence of 23Na n.m.r. parameters on specific cell alterations. In this connection, CCl4 represents a useful probe, since the hepatocellular damaging effects induced by this aliphatic halocarbon have been extensively investigated. The t1relaxationtimes of intracellular sodium ion under physiological conditions in the presence of the paramagnetic shift reagent dysprosium tripolyphosphate were investigated. The significant increase of t1 in the livers of rats intoxicated with CCl4 with respect to the t1relaxationtimes of normal rats was studied. Evidence is given that neither liver cell necrosis nor fat accumulation nor proliferative processes affected the observed t1 lengthening. However, when t1relaxationtimes were measured in the livers of vitamin E-treated rats subsequently intoxicated with CCl4 a significant shortening of t1 with respect to the times measured in intoxicated rats was observed. We report the results of the present study, taking into consideration that peroxidation of microsomal lipids is the key factor in the CCl4-induced liver injury process and that vitamin E exerts an antioxidant action against CCl4-induced microsomal lipidperoxidation.
Evidence for carbon tetrachloride-induced lipid peroxidation in vivo by 23Na relaxation times t1
BANNI, SEBASTIANO;SCANO, PAOLA;
1987-01-01
Abstract
We report here the results of a study performed on the livers of rats intoxicated with CCl4 in order to investigate the dependence of 23Na n.m.r. parameters on specific cell alterations. In this connection, CCl4 represents a useful probe, since the hepatocellular damaging effects induced by this aliphatic halocarbon have been extensively investigated. The t1relaxationtimes of intracellular sodium ion under physiological conditions in the presence of the paramagnetic shift reagent dysprosium tripolyphosphate were investigated. The significant increase of t1 in the livers of rats intoxicated with CCl4 with respect to the t1relaxationtimes of normal rats was studied. Evidence is given that neither liver cell necrosis nor fat accumulation nor proliferative processes affected the observed t1 lengthening. However, when t1relaxationtimes were measured in the livers of vitamin E-treated rats subsequently intoxicated with CCl4 a significant shortening of t1 with respect to the times measured in intoxicated rats was observed. We report the results of the present study, taking into consideration that peroxidation of microsomal lipids is the key factor in the CCl4-induced liver injury process and that vitamin E exerts an antioxidant action against CCl4-induced microsomal lipidperoxidation.
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