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.

of apoptosis is an efficient method of treating cancer. [7] Triterpenoids represent a diverse class of natural products. Recently, pentacyclic triterpenoids have been described to induce apoptosis in different cell types. [8] Lantana camara L.

This study evaluated the role of selenium (0.5 ppm selenium/kg diet) and vitamin E (200 mg alpha-tocopherol/kg diet) on spermatogenesis after scrotal hyperthermia (42 °C, 30 min) in six different groups of male Balb/c mice; Control, Heat shock, Selenium, Selenium+heat shock, Vitamin E and Vitamin E+heat shock. Markers of the stress responses, hypoxia and oxidative stress, were evaluated in testis after the hyperthermic shock. Hyperthermia caused an elevated mRNA expression of hypoxia-inducible factor-1 alpha, haem oxygenase-1 (HMOX-1) and also glutathione peroxidase activity and reactive oxygen species (ROS). Apoptosis was evaluated by TUNEL assay and further by mRNA expression of Bcl-2, caspase 3, 8, 9, bid and AKT. TUNEL assay showed significant increase in apoptotic index of spermatogenic cells, whereas decrease in mRNA expression of Bcl-2, AKT and increase in caspase 3, 8, 9 and Bid in heat-shock group were observed. A significant decrease in sperm motility was also seen in heat-shock group in comparison with control group. These observations clearly indicate the development of oxidative stress and apoptosis after hyperthermia. Further analysis in Selenium+heat shock and Vitamin E+heat shock groups showed protective behaviour as compared to effects in heat-shock group which could be of therapeutic interest in future studies.

The present study was designed to elucidate the mechanisms accounting for disruption of the normal function of the testis exposed to various levels of Pb. Three different doses of Pb (10, 50, 200 mg Pb/kg body weight per d) were given orally to male Portan rats (groups 2, 3, 4). Zn (1 mg Zn/kg body weight per d) was also given with Pb (50 mg Pb/kg body weight per d) in group 5. Treatments continued for 3 months. Plasma luteinizing hormone and follicle-stimulating hormone concentrations were found to be decreased in Pb-exposed rats. This was in turn reflected in the appreciable decline in fertility status. In cell kinetic studies, significant declines in various cell populations (preleptotene, pachytene, young (step 7) spermatids and mature (step 19) spermatids) were seen. However, in group 5 after Zn supplementation, hormone levels, cell numbers and fertility status were found to be close to normal. It is concluded that Pb might act at maturation level to cause conspicuous degenerative changes in the testis; Zn supplementation protected against these effects.

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