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Impact of lead toxicity on male rat reproduction at “hormonal and histopathological levels”
47
Citations
25
References
2010
Year
SpermatogenesisFertilityToxic EffectsFemale Reproductive FunctionSemen AnalysisReproductive Biology“ HormonalReproductive EndocrinologyLead PoisoningDrinking WaterToxicologyReproductive MedicineMale InfertilityPublic HealthInfertilityAndrologyMale Rat ReproductionEndocrine ResearchExperimental ToxicologyEndocrinologyPharmacologyBlood Pb LevelEndocrine DisruptorsPhysiologyMedicineLead ToxicityReproductive Hormone
The mechanisms of lead (Pb) toxicity involved in the pathogenesis of spermatogenesis have not been clearly elucidated. Thereby, the present work was conducted to investigate the toxic effects of Pb on the pituitary-testicular axis, and endocrine and exocrine testicular functions. Two groups of male Wister rats (30 days old), each consisting of 15 rats, were used. The first group received sodium acetate (control group), while the second group received drinking water containing 0.1% lead acetate (PbAc) (PbAc-treated group) for successive 60 days. At the end of the experiment, the toxic effects of Pb were assessed on the basis of metal, hormonal, and histopathological evaluations. In PbAc-exposed rats, blood Pb level exceeded 22 µg dL−1 with a simultaneous drop in plasma testosterone, follicle stimulating hormone, and luteinizing hormone levels by 46%. Collectively, the secretion of testosterone by Leydig cells and epididymal sperm count were reduced by 34 and 13%, respectively. Morphologically, the degeneration of germinal epithelium and sloughing of germ cells into the lumen, and fewer individual pyknotic germ cells of seminiferous tubules were seen. In conclusion, it appears that the hypothalamic-pituitary axis is the major target of Pb. However, the direct toxic action of Pb on the interstitial and Sertoli cells cannot be excluded.
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