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Chronic exposure to lead induces decreased sex hormones and spermatogenesis disturbance in male Wistar rats

Konan Kouassi Martin

 Many authors have reported adverse effects of environmental pollutants on sexual function, such as tobacco pesticides and heavy metals. Exposure of heavy metals has been associated with adverse effects on development of gonads. In animals, exposure to lead could damage. Several experimental studies have reported impairment of the spermatogenesis but theme chanisms implied in the pathogenesis are not yet completely understood.

Therefore, the present study was undertaken in albino rats to investigate the effects of lead on spermatogenesis on the one hand and testicular and serum go nadotropins and testosterone levels on the other.

 

Methods: For this study, ten male pubescent rats were randomly divided in two groups (n=5 in each groups). The control group received distilled water and the experimental groups received the lead acetate solution (0.3%) while 90 consecutive days. After 90 days, the rats were euthanized. The blood and the testes were sampled for carrying out of the different tests.

Testicular cyto architecture of the benchmark groups were in typical clusters. Gatherings given 0.5% and 1.0% Lead showed extreme deteriorated storm cellar film, serious declined stretched semini ferous epithelium, not very many spermato gonium and spermatogenic cells, augmented lumen and nonattendance of Sertoli cells while the gathering regulated 1.5% Lead acetic acid derivation for 9 and 12 weeks showed deteriorated storm cellar layer, semini ferous epithelium and tubule, sloughed off germ cells, decay, serious vacuolation, presence of apoptotic cells, enlarged lumen, nonappearance of spermatogenic cells and spermatocytes, serious development capture, nonattendance of Leydig cells, putrefaction and declined interstitial space.

Discussion: Pb has been identified with a wide scope of dysfunctions physio biochemically that prompts the acceptance of oxidative pressure and arrival of receptive oxygen species, in this way assuming negative parts in testicular harm.

In the current investigation oral organization of lead acetic acid derivation on male rodents influenced the testicles and caused histological and semina-hormonal changes and it's anything but a more drawn out timeframe effectsly affected generation and sperm boundaries.

 

Critical decrease (P<0.05) in body loads saw in the gathering managed 1.0% and 1.5% of lead acetic acid derivation for a time of 6, 9 and 12 weeks were demonstrative of atrophic changes that had occurred in the testicles. This was in concurrence with (14) who announced testicular decay of rodents treated with lead acetic acid derivation. This was likewise in concurrence with (13-18) who revealed that testicular loads essentially declined in lead-treated mice and Wistar rodents contrasted with control bunches separately, accordingly featuring expanded catabolism and metabolic irregularity as one of the significant reasons for it.  Lead gathering in the male extra organs like the prostate and epididymis weakened sperm motility.  For fruitlessness in guys to be resolved, legitimate assessment of the hormonal levels is extremely helpful determinant. Lead likewise causes hormonal lopsidedness by influencing the neuroendocrine framework and upsetting the discharge of androgens from Leydig cells. The critical decrease in serum FSH, Testosterone and LH levels were evident on a portion span subordinate way. It confirmed with (16,20) who detailed that Lead acetic acid derivation effect sly affected testis steroid ogenic work, serum gonadotropin levels and testosterone levels contrasted with control. These decreases changed hormonal equilibrium and caused neuro endocrine framework disturbance.

 

Results: The results indicate hypertrophy of the testes in the exposed rats. In addition, we have observed a significant reduction in sex hormones and a highly disturbed spermatogenic process.

 

Conclusion: The present study demonstrates that lead accumulation in the blood affects male fertility by disrupting the biosynthesis of gonadotropins and testosteroneas well as the process of spermatogenesis.

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