Reversal of respiratory decline in necrotic liver degeneration by intraportal tocopherols.

Necrotic liver degeneration is produced in rats by diets deficient in vitamin E, cystine, and Factor 3 (1). During the latent phase of the disease, several weeks before the onset of acute hepatic necrosis, a defect in oxidative metabolism has been demonstrated in livers of animals on such diets. oxygen consumption of histologically unaffected liver slices breaks down after a brief initial period of normal respiration (2). This decline of 02 uptake is associated with an impaired utilization of acetate-Cl4 for lipogenesis, ketogenesis, and CO2 formation (3). The agents preventing hepatic necrosis, vitamin E, cystine, or Factor 3, also forestall the respiratory lesion effectively when supplemented to the diet. The addition in vitro of cr-tocopherol to liver slices from deficient rats, either as an emulsion or in water-soluble form, has no significant effect on the metabolic lesion.’ However, preliminary studies showed that injection of emulsions of dl-a-tocopherol into the portal vein caused the almost immediate disappearance of the defect (4). The present report describes this phenomenon; the relative potencies of several forms of oc-tocopherol and of the other tocopherols (p-, y-, and S-) are compared. Both c+ and y-tocopherol were found to be quite potent in their ability to reverse the metabolic lesion upon intraportal injection; ,& and b-tocopherol were much less so.