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Effects of Subchronic Steroid Therapy on Vitamin E-Deficient Rats

Summary Experiments were carried out to determine the effectiveness of steroid therapy in vitamin E-deficiency, as measured by autohemolysis of isolated RBC's, body-weight gain, serum creatine phosphokinase activity, and stabilization or labilization of isolated hepatic lysosomes. Results of such experiments would indicate whether triam-cinolone acetonide could supplant vitamin E in vitamin E-deficiency states via its ability to stabilize various membranes. Autohemolysis induced by vitamin E-deficiency could not be prevented by daily administration of triamcinolone. Daily dosages of 0.1 and 0.4 mg/kg (ip) triamcinolone given concomitantly with replacement vitamin E (at sufficient dosages to reverse the autohemolysis) resulted in an increased autohemolysis. No changes in lysosomal membrane fragility were noted when hepatic lysosomes were obtained from vitamin E-deficient rats. Treatment of vitamin E-deficient rats with triamcinolone resulted in a greater attenuation of body-weight gain. Creatine phosphokinase levels were not augmented in vitamin E-deficient rats. Vitamin E-deficient rats supplemented with vitamin E and treated with triamcinolone, manifested an increase in creatine phosphokinase. It was therefore concluded that although triamcinolone and vitamin E possess a common ability to stabilize membranes and proteins, their mechanisms must be different since triamcinolone could not substitute for vitamin E in a deficiency state. Indeed, triamcinolone was found to be more toxic in the absence of vitamin E.