Testicular androgen binding protein in zinc deficient rats

Abstract

Zinc deficiency in rats and humans is characterized by an increase in serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) and decrease in serum testosterone level and spermatogenesis. The possibility that an abnormality in the androgen binding protein may be responsible for decreased spermatogenesis in zinc deficiency was investigated. White male rats weighing approximately 220 gm were allotted to three groups: zinc-deficiency (Zn-D), Pair-fed (PF), and Ad-libitum fed controls (Ad-Lib). Androgen binding protein (ABP), total protein, testosterone, and dihydrotestosterone (DHT) were assayed in testicular cytosol by established techniques. Testosterone, DHT, and DHT binding protein sites per pair of testes were reduced in Zn-D in comparison to PF and Ad-Lib controls (p<.02). The results were not significantly different when expressed in terms of per mg of protein. Serum testosterone and DHT, testicular weights, and zinc in tibia and testes were decreased in Zn-D animals in comparison to both controls (p<.02). In conclusion our studies show that androgen protein binding sites and steroidogenesis were not affected by zinc deficiency, rather the major effect was on testicular growth. Inasmuch as zinc is known to play an important role in DNA and protein synthesis, zinc deficiency may affect adversely cell division and restrict testicular growth.