Effect of Vitamin A Deficiency on Luteinizing Hormone Receptors and Adenosine 3′,5′-Monophosphate-Mediated Steroidogenesis in Rat Testicular Tissue

Abstract

Abstract

Weanling male Sprague-Dawley rats were maintained on a vitamin A (retinol)-deficient retinoic acid-supplemented diet for a period of 8 to 14 weeks. After 10 weeks, Leydig cell-enriched preparations from vitamin A-deficient animals had 45% fewer gonadotropin receptors for human luteinizing hormone (hLH). Testicular slices from vitamin A-deficient animals demonstrated decreased formation of adenosine 3′5′-monophosphate (cyclic AMP) and decreased testosterone content in response to hLH stimulation compared to vitamin A-supplemented rats (P < 0.01). Our findings suggest that changes which cause hyporesponsiveness in testosterone production from vitamin A-deficient rats can be attributed to a reduction in gonadotropin testicular receptors for hLH and a decreased cyclic AMP production. Testicular morphology was not altered during the first 10 weeks of the experiment, although, after 14 weeks on the experimental diet there was marked degeneration of tubules, cessation of spermatogenesis, and testicular atrophy.