Abstract

We report here the results of a study performed on the livers of rats intoxicated with CCl 4 in order to investigate the dependence of 23Na n.m.r. parameters on specific cell alterations. In this connection, CCl 4 represents a useful probe, since the hepatocellular damaging effects induced by this aliphatic halocarbon have been extensively investigated. The t 1 relaxation times of intracellular sodium ion under physiological conditions in the presence of the paramagnetic shift reagent dysprosium tripolyphosphate were investigated. The significant increase of t 1 in the livers of rats intoxicated with CCl 4 with respect to the t 1 relaxation times of normal rats was studied. Evidence is given that neither liver cell necrosis nor fat accumulation nor proliferative processes affected the observed t 1 lengthening. However, when t 1 relaxation times were measured in the livers of vitamin E-treated rats subsequently intoxicated with CCl 4 a significant shortening of t 1 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 CCl 4-induced liver injury process and that vitamin E exerts an antioxidant action against CCl 4-induced microsomal lipid peroxidation.

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