ABSTRACT
Zearalenone (ZEA), a nonsteroidal estrogenic mycotoxin, is known to cause testicular toxicity in animals. In the present study, the effects of ZEA on spermatogenesis and possible mechanisms involved in germ cell injury were examined in rats. Ten-week-old Sprague-Dawley rats were treated with 5 mg/kg i.p. of ZEA and euthanized 3, 6, 12, 24 or 48 h after treatment. Histopathologically, spermatogonia and spermatocytes were found to be affected selectively. They were TUNEL-positive and found to be primarily in spermatogenic stages I-VI tubules from 6 h after dosing, increasing gradually until 12 h and then gradually decreasing. Western blot analysis revealed an increase in Fas and Fas ligand (Fas-L) protein levels in the ZEA-treated rats. However, the estrogen receptor (ER)alpha expression was not changed during the study. Collectively, our data suggest that acute exposure of ZEA induces apoptosis in germ cells of male rats and that this toxicity of ZEA is partially mediated through modulation of Fas and Fas-L systems, though ERalpha may not play a significant role.
Subject(s)
Animals , Male , Rats , fas Receptor/immunology , Apoptosis/drug effects , Estrogens, Non-Steroidal/toxicity , Fas Ligand Protein/immunology , Histocytochemistry , Immunoblotting , In Situ Nick-End Labeling , Random Allocation , Rats, Sprague-Dawley , Spermatocytes/cytology , Spermatogenesis/drug effects , Spermatogonia/drug effects , Testis/cytology , Zearalenone/toxicityABSTRACT
Effect of arsenic was studied on the testicular tissue of Swiss albino mice. Sodium-meta-arsenite (NaAsO2) was administered to adult mice (25 +/- 30 g) at a dose level of 30 mg/L and 40 mg/L through drinking water for 30, 45 and 60 days. After the treatment, the testicular organ was removed, weighed and processed for histopathological observation. No change in the body weight was recorded in treated groups after arsenic exposure but significant decrease in the relative testicular weight was observed in comparison with the control. The result showed that arsenic-treated mice exhibited dose dependent gradual reductions in seminiferous tubular diameter and various gametogenic cell population i.e. resting spermatocyte, pachytene spermatocyte and step-7-spermatid except spermatogonia. Leydig cell atrophy was significantly increased in dose dependent manner indicating a definite effect of arsenic on the spermatogenesis in mice. These observations were supported by gradual reduction in Leydig cell population in the above treated groups. In conclusion, the above results confirm the toxic effect of arsenic in testis of mice.
Subject(s)
Animals , Arsenites/toxicity , Body Weight/drug effects , Leydig Cells/drug effects , Male , Mice , Organ Size/drug effects , Sodium Compounds/toxicity , Sperm Count , Spermatogenesis/drug effects , Spermatogonia/drug effects , Testicular Diseases/chemically induced , Testis/pathology , Tissue FixationABSTRACT
Administration of graded doses of nicotine (0.2 mg, 0.4 mg and 0.6 mg/100 g body weight) for 15 days to the adult mice reduced the weight of testis, number of spermatocytes and spermatids, but increased the number of spermatogonia which may be due to reduced conversion to subsequent stages. There is a high cholesterol content and Sudanophilic lipid accumulation in the treated testis. The weight of accessory sex organs which is dependent on androgens produced by the testis is also reduced. These changes are brought because of the non-availability of pituitary gonadotrophins essential for initiation and completion of spermatogenesis and steroidogenesis in the testis due to the administration of nicotine, which being CNS depressor might have caused inhibition in the neural stimulus essential for release of pituitary gonadotrophins.