Studies on the Inactivation of Cortisol-4-[ ¹⁴C] in the Lenses of Liver-Impaired Rats

Abstract

Changes in inactivation mechanisms of cortisol, such as cortisol-binding by protein or sulphate and glucuronide conjugation in the lenses of normal and liver-impaired rats, have been studied in order to determine the role of liver in the pathogenesis of steroid cataracts. The cortisol-binding capacity of the rat lens decreased when the liver was impaired by intraperitoneal administration of carbon tetrachloride. Sulphate conjugation of cortisol-4-[¹⁴C] showed similar results, however, no significant difference was found in glucuronide conjugation. These results indicate that there is a close relationship between inactivation of steroid hormone in the lens and liver function, and that liver dysfunction in patients receiving long-term oral corticoid therapy plays an important role in causing the onset of steroid cataracts.