Influence of lead and zinc on rat male reproduction at ‘biochemical and histopathological levels’

✍ Scribed by N. Batra; B. Nehru; M. P. Bansal

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 272 KB
• Volume: 21
• Category: Article
• ISSN: 0260-437X
• DOI: 10.1002/jat.796

✦ Synopsis

Abstract

Sequential lead accumulation and biochemical and histopathological changes were observed in rat testis and epididymis after oral administration at varied doses of lead (10, 50 and 200 mg kg^−1^ body wt.) for 3 months and also following the concomitant administration of lead with zinc (1 mg kg^−1^ body wt. +50 mg Pb kg^−1^ body wt.). Accumulation of lead in both testis and epididymis increased with dose. The concomitant administration of zinc reduced the lead levels. Similarly, dose‐related changes were seen in the activities of the enzymes alkaline phosphatase and Na^+^–K^+^‐ATPase, which decreased with increased dose of lead. A significant improvement in the activities of these enzymes was seen in the groups given both lead and zinc. Histologically, discernible changes were noticed only at higher doses (50 and 200 mg kg^−1^ body wt.), which included disorganization and disruption of spermatogenesis with accumulation of immature cells in lumen of tubule. At higher doses of lead, complete arrest of spermatogenesis was seen and a significant decrease in germ cell layer population was evident. Even in epididymis, the histoarchitecture was disrupted only at higher doses of lead both in the caput and corpus regions. The changes included damage of basement membrane, disorganization of epithelium and vacuolization of cells. The tubules were found almost empty, indicating arrest of spermatogenesis. However, with concomitant administration of lead and zinc both testis and epididymis presented a near‐normal picture, indicating the protective role of zinc. Hence, the data indicate that the protective effect of zinc on lead toxicity was mediated largely by significant competition between lead and zinc or due to reduction of the available binding sites. Copyright © 2001 John Wiley & Sons, Ltd.