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Mercaptans Decrease Selenium-Dependent Glutathione Peroxidase Activity in the Chick¹

Steven D. Mercurio^* and Gerald F. Combs, Jr.^*,,

^* Department of Poultry and Avian Sciences Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853

A variety of mercaptans, especially the ß-mercaptocarboxylic acids, inhibited the selenium (Se)-dependent glutathione peroxidase (SeGSHpx) activity of chick liver postmitochondrial supernatant or cytosol and of purified bovine erythrocyte SeGSHpx. The effects of mercaptans and a glutathione analogue on Se utilization were determined by subcutaneous injection of test compounds into vitamin E–deficient chicks fed diets containing 0.1 ppm Se (as Na₂SeO₃) at times when > 50% of vitamin E– and Se-deficient chicks showed the vitamin E–, Se-deficiency disease exudative diathesis (ED). D-(–)-Penicillamine hydrochloride (the positive control model compound), sodium ß-mercaptopyruvate, t-butyl mercaptan and S-methylglutathione (nonmercaptan glutathione analogue) decreased SeGSHpx activity in chick liver postmitchondrial supernatants within 24 h of injection and increased the incidence of ED within 4 d. Other mercaptans tested did not increase ED incidence or affect liver, kidney or plasma SeGSHpx activities. Although mercaptosuccinic acid, N-(2-mercaptopropionyl)glycine and sodium thioglycolate each strongly inhibited SeGSHpx in vitro, each also significantly increased chick mortality in the dosage range tested; therefore, their effects on SeGSHpx in vivo could not be evaluated. It appears that the ß-mercaptocarboxylic acids, mercaptans with a high degree of steric hinderance in close proximity to the thiol group and a close structural analogue of glutathione are capable of altering selenium status in chicks.

KEY WORDS: • mercaptans • glutathione peroxidase • selenium • exudative diathesis

¹ Supported in part by grants from the USDA (Human Nutrition Program Grant No. CRCR-11829) and the USPHS (Grant No. GM 30677).

Manuscript received 2 June 1986. Revision accepted 11 December 1986.