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Abstract
The present study investigates the effect of dietary zinc deficiency on testes of Wistar rats. Pre-pubertal rats (40–50 g) were divided into three groups of 10 each viz. zinc control (ZC) and pair fed (PF) [100 ppm zinc diet] and zinc deficient (ZD) [1 ppm zinc diet]. Experiments were set for 2- and 4-weeks. Pre-pubertal rats fed zinc deficient diet for 2- and 4-weeks exhibited significant ( P < 0.05) decrease in diet consumption when compared with their respective control groups. Parallel to the reduced diet consumption, a significant ( P < 0.05) decrease in body and testicular weight of ZD animals was also observed. These observations indicate that the zinc deficiency reduces diet consumption and growth of the animals. Histological studies revealed degeneration in testes of ZD rats as evident by decreased seminiferous tubular diameter and Leydig cell nuclear diameter. Decreased Leydig cell nuclear diameter is responsible for disruption of the biochemical function of Leydig cell. Testicular atrophy (viz. wavy tunica propria, karyolysis, pyknosis, karyorhexis, apoptotic bodies, multinucleated giant cells, few sperms in the lumen, atrophied Leydig cells and accumulation of oedematous fluid in the interstitium) accompanied by significant loss of germ/somatic cells (viz. Type A and Type B spermatogonia, leptotene, zygotene, pachytene spermatocytes, Golgi, cap and acrosome spermatids, Sertoli and Leydig cell) was evident in ZD groups. The degeneration was severe after 4-weeks of zinc deficiency. These observations provide evidence that the functional and morphological changes in testes are probably due to zinc deficiency. Further, the increased oedematous fluid in the interstitial region is due to the cellular death. Impairment of spermatogenesis can be attributed to the direct action of zinc on testes or indirectly from Leydig cell degeneration indicating that zinc is a critical component for maintenance of both mitotic and meiotic stages of spermatogenesis.
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