A study of vitamin B12 protection in experimental thyrotoxicosis in the rat

Abstract

Effects of experimentally induced hyperthyroidism in rats and protection by vitamin B12 were investigated. It was observed that thyrotoxicosis results in a vitamin B12 deficiency in blood and in liver and its mitochondrial fraction. In thyrotoxicosis there is no interference in the intestinal vitamin B12 absorption, which appears to depend mainly on the vitamin B12 status of the animal. The depletion of liver and blood glutathione closely follows the fall in tissue vitamin B12 levels. The incorporation of administered cysteine into liver glutathione is also decreased in thyrotoxicosis. There is an increased accumulation of fat in liver and its centrifugally separated fractions, particularly the supernatant. A slight drop in total choline content is seen in all fractions; however, phospholipid content does not undergo significant alterations, those observed being limited to the soluble fraction. An increased mitochondrial adenosine triphosphatase and an altered distribution of other soluble phosphatases in liver also suggest damage to the cellular particles in the thyrotoxic animal. A considerable increase in non-protein nitrogen and free amino acids occurs in the liver and plasma of hyperthyroid animals. The protective action of vitamin B12 is reflected in a correction of the various metabolic derangements observed in thyrotoxicosis. The observations are discussed with special reference to the significance of sulfhydryl compounds in the maintenance of normal mitochondrial properties.