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Exposure to Endosulfan can result in male infertility due to testicular atrophy and reduced sperm count

View Article: PubMed Central - PubMed

ABSTRACT

Endosulfan (ES) is a widely used organochlorine pesticide and is speculated to be detrimental to human health. However, very little is known about mechanism of its genotoxicity. Using mouse model system, we show that exposure to ES affected physiology and cellular architecture of organs and tissues. Among all organs, damage to testes was extensive and it resulted in death of different testicular-cell populations. We find that the damage in testes resulted in qualitative and quantitative defects during spermatogenesis in a time-dependent manner, increasing epididymal reactive oxygen species levels, affecting sperm chromatin integrity. This further culminated in reduced number of epididymal sperms and actively motile sperms. Finally, we show that ES exposure affected fertility in male but not in female mice. Therefore, we demonstrate that ES exerts pathophysiological changes in mice, induces testicular atrophy, affects spermatogenesis, reduces quantity and vigour of epididymal sperm and leads to infertility in males.

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Quantitative analyses of epididymal sperms on Endosulfan exposure. (a–d) Analyses of epididymal sperm collected from ES-treated mice (3 mg/kg) at various time points (11, 26 and 36 days) after treatment completion (n=9 and 10 for control and treated, respectively) showing total sperm count (a), actively motile sperms (b), sluggish motile sperms (c) and non-motile sperms (d). NS, not significant.
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fig6: Quantitative analyses of epididymal sperms on Endosulfan exposure. (a–d) Analyses of epididymal sperm collected from ES-treated mice (3 mg/kg) at various time points (11, 26 and 36 days) after treatment completion (n=9 and 10 for control and treated, respectively) showing total sperm count (a), actively motile sperms (b), sluggish motile sperms (c) and non-motile sperms (d). NS, not significant.

Mentions: To check the effects of spermatogenesis-dependent testicular-cell depletion on epididymal sperm following treatment with ES (3 mg/kg, 11, 26 and 36 day), clinical analysis of epididymal sperm was carried out post-ES treatment. The time points were selected based on the completion of the mating windows used in the experiment explained below. We found a reduction in epididymal sperm count on day 11 post treatment. The difference was prominent and significant when the sperm count was taken on day 26 and 36 post-ES treatment, suggesting that effect of ES on spermatogenesis contributed to a dramatically reduced sperm count (Figure 6a). Although there was no increase in sluggish motile sperms, significant reduction in actively motile sperms and increase in non-motile sperms was observed particularly on day 26, a probable consequence of testicular-cell damage and death (Figures 6b-d). These results suggest that the epididymal sperm number and quality were severely compromised on ES treatment.


Exposure to Endosulfan can result in male infertility due to testicular atrophy and reduced sperm count
Quantitative analyses of epididymal sperms on Endosulfan exposure. (a–d) Analyses of epididymal sperm collected from ES-treated mice (3 mg/kg) at various time points (11, 26 and 36 days) after treatment completion (n=9 and 10 for control and treated, respectively) showing total sperm count (a), actively motile sperms (b), sluggish motile sperms (c) and non-motile sperms (d). NS, not significant.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4979443&req=5

fig6: Quantitative analyses of epididymal sperms on Endosulfan exposure. (a–d) Analyses of epididymal sperm collected from ES-treated mice (3 mg/kg) at various time points (11, 26 and 36 days) after treatment completion (n=9 and 10 for control and treated, respectively) showing total sperm count (a), actively motile sperms (b), sluggish motile sperms (c) and non-motile sperms (d). NS, not significant.
Mentions: To check the effects of spermatogenesis-dependent testicular-cell depletion on epididymal sperm following treatment with ES (3 mg/kg, 11, 26 and 36 day), clinical analysis of epididymal sperm was carried out post-ES treatment. The time points were selected based on the completion of the mating windows used in the experiment explained below. We found a reduction in epididymal sperm count on day 11 post treatment. The difference was prominent and significant when the sperm count was taken on day 26 and 36 post-ES treatment, suggesting that effect of ES on spermatogenesis contributed to a dramatically reduced sperm count (Figure 6a). Although there was no increase in sluggish motile sperms, significant reduction in actively motile sperms and increase in non-motile sperms was observed particularly on day 26, a probable consequence of testicular-cell damage and death (Figures 6b-d). These results suggest that the epididymal sperm number and quality were severely compromised on ES treatment.

View Article: PubMed Central - PubMed

ABSTRACT

Endosulfan (ES) is a widely used organochlorine pesticide and is speculated to be detrimental to human health. However, very little is known about mechanism of its genotoxicity. Using mouse model system, we show that exposure to ES affected physiology and cellular architecture of organs and tissues. Among all organs, damage to testes was extensive and it resulted in death of different testicular-cell populations. We find that the damage in testes resulted in qualitative and quantitative defects during spermatogenesis in a time-dependent manner, increasing epididymal reactive oxygen species levels, affecting sperm chromatin integrity. This further culminated in reduced number of epididymal sperms and actively motile sperms. Finally, we show that ES exposure affected fertility in male but not in female mice. Therefore, we demonstrate that ES exerts pathophysiological changes in mice, induces testicular atrophy, affects spermatogenesis, reduces quantity and vigour of epididymal sperm and leads to infertility in males.

No MeSH data available.


Related in: MedlinePlus