Liver Lipid Peroxide Levels in Carbon Tetrachloride Poisoning.

The protective action of Vit. E in carbon tetrachloride poisoning has been shown by histological means in rat liver (1). Vit. E is also known to be a lipid antioxidant. On these bases it was suggested that Vit. E functioned in this form of poisoning to protect the cellular lipid from oxidation “hypothetically'”called forth by carbon tetrachloride or its metabolites. It has also been shown that early in carbon tetrachloride poisoning there is a dislocation of ribosomes from lipoprotein membranes, and impairment of protein synthesis by the liver (2,3). The possibility that formation of lipid peroxides in the lipoprotein membranes may play a part in these changes was submitted to test. Methods and materials. Male Sprague-Dawley rats were fasted for 16–18 hours prior to experimentation. The animals were intubated without anesthesia and 0.50 cc carbon tetrachloride (C.P.) per 100 grams body weight dissolved in an equal volume of mineral oil was administered by gastric tube. Control animals received only mineral oil. At 3 hours the animals were dispatched by a sharp blow to the head and the liver quickly isolated and weighed in ice cold distilled water. The tissue was minced and homogenized in a teflon pestled apparatus in 4 volumes of distilled water at 0°C. The homogenates were quickly frozen in an acetone dryice mixture and stored at −30°C before analysis. Aliquots of homogenate were analyzed for lipid peroxide by the thiobarbituric acid method (4). Results and discussion. The results appear in Table I. The peroxide content of livers of untreated, non-fasted animals is arbitrarily set at 100%. There is no difference in control and experimental animals in regard to the amount of lipid peroxides in hepatic tissue at the 3-hour time period, when there are demonstrable morphologic alterations in the ergastoplasm and when there is clearly demonstrable depression of protein synthesis.