Indian J Physiol Pharmacol 1999; 43 (2) : 247-250 GENTAMICIN INDUCED INHIBITION OF STEROIDOGENIC ENZYMES IN RAT TESTIS SARMISHTHA GHOSH* AND SHAKUNTALA DASGUPTA** *Department of Physiology, Manipal College of Medical Science, Post Box # 155, Pokhara, Nepal and ** Department of Physiology, University College of Science & Technology, 92, APC Road, Calcutta - 700 009 (Received on November 28, 1998) Abstract: Gentamicin is an aminoglyc<;Jside antibiotic, widely used for treating many gram negative bacterial infections. Though nephrotoxicity is the most highlighted side effect, it has also been found to cause an alterati6n in the phosphatase activities of testes and accessory sex organs and a decline in the sperm count. This study was designed to assess the effects of gentamicin on testicular steroidogenesis and to ascertain whether such alterations are reversible. Laboratory inbred adult, male, 'Wistar' strain rats were chosen as the experimental animal. A significant dose- dependant reduction in the activities of the two steroidogenic enzymes, accompanied with a significant decrease in ascorbic acid and elevation of level of cholesterol wa, observed. The effects were maximum at a dose of 100 mglkg, b.wt. After 15 days of withdrawal of the drug therapy the biochemical parameters namely ascorbic acid and cholesterol returned to normal levels whereas the activities of the two dehydrogenases showed a compensatory increase. This indicates that gentamicin affects the steroidogenic enzymes, causing an alteration in the formation of testosterone, which was manifested in the elevated cholesterol in the adult rat testes. However, thes alterations were reversible. Key words: gentamicin steroidogenesis hydroxysteroid dehydrogenase cholesterol ascorbic acid sperm count INTRODUCTION Gentamicin, has been reported to cause various side effects in the recipient (1). The most prevalent adverse effect is nephrotoxicity followed by ototoxicity (2). *Corresponding Author Aminoglycosides also affect the arachidonic acid metabolism in rats (3) which, in turn, is known to be involved in the hypothalamic control of ovulation (4). An alteration of testicular functions in patients with type II hyperlipoproteinemia, treated with