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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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Evaluation of physiological effects of Endosulfan in mice. (a) Body weight distribution of the ES-treated animals (n=5 per group) following exposure to different doses of Endosulfan (0, 0.33, 1, 3 and 9 mg/kg body weight). Mean body weight of the group is plotted against days after the offset of treatment. (b) Graph derived from the area of the peak in HPLC profile, showing the bioavailability of ES in mice after oral ingestion of ES (3 mg/kg) against time. (c) Bar graphs indicating enzymatic activities reflective of liver and kidney function at 1 and 21 days after ES treatment (3 mg/kg, n=5). Alkaline phosphatase and Alanine aminotransferase are markers of liver function; urea and creatinine are of kidney function. IU corresponds to international unit. n=5 in all groups. (d) Bar graphs showing RBC, WBC and platelet counts at different time points (1, 11, 21, 31 days) after ES treatment (3 mg/kg) completion. NS, not significant.
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fig1: Evaluation of physiological effects of Endosulfan in mice. (a) Body weight distribution of the ES-treated animals (n=5 per group) following exposure to different doses of Endosulfan (0, 0.33, 1, 3 and 9 mg/kg body weight). Mean body weight of the group is plotted against days after the offset of treatment. (b) Graph derived from the area of the peak in HPLC profile, showing the bioavailability of ES in mice after oral ingestion of ES (3 mg/kg) against time. (c) Bar graphs indicating enzymatic activities reflective of liver and kidney function at 1 and 21 days after ES treatment (3 mg/kg, n=5). Alkaline phosphatase and Alanine aminotransferase are markers of liver function; urea and creatinine are of kidney function. IU corresponds to international unit. n=5 in all groups. (d) Bar graphs showing RBC, WBC and platelet counts at different time points (1, 11, 21, 31 days) after ES treatment (3 mg/kg) completion. NS, not significant.

Mentions: To evaluate the pathophysiological changes induced by ES exposure, we assessed various responses in mice following ES treatment. Body weight fluctuation is an important parameter in understanding the physiological effects of a compound. Body weight analyses of male and female mice following ES treatment (0, 0.33, 1, 3, 9 mg/kg) for a period of 20 days showed remarkable fluctuations in weight in a concentration-dependent manner in case of male mice, while there was no significant change in females (Figure 1a). Thus, our results suggest that male mice are more sensitive to ES as compared with females and therefore male mice were chosen for further studies.


Exposure to Endosulfan can result in male infertility due to testicular atrophy and reduced sperm count
Evaluation of physiological effects of Endosulfan in mice. (a) Body weight distribution of the ES-treated animals (n=5 per group) following exposure to different doses of Endosulfan (0, 0.33, 1, 3 and 9 mg/kg body weight). Mean body weight of the group is plotted against days after the offset of treatment. (b) Graph derived from the area of the peak in HPLC profile, showing the bioavailability of ES in mice after oral ingestion of ES (3 mg/kg) against time. (c) Bar graphs indicating enzymatic activities reflective of liver and kidney function at 1 and 21 days after ES treatment (3 mg/kg, n=5). Alkaline phosphatase and Alanine aminotransferase are markers of liver function; urea and creatinine are of kidney function. IU corresponds to international unit. n=5 in all groups. (d) Bar graphs showing RBC, WBC and platelet counts at different time points (1, 11, 21, 31 days) after ES treatment (3 mg/kg) completion. NS, not significant.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4979443&req=5

fig1: Evaluation of physiological effects of Endosulfan in mice. (a) Body weight distribution of the ES-treated animals (n=5 per group) following exposure to different doses of Endosulfan (0, 0.33, 1, 3 and 9 mg/kg body weight). Mean body weight of the group is plotted against days after the offset of treatment. (b) Graph derived from the area of the peak in HPLC profile, showing the bioavailability of ES in mice after oral ingestion of ES (3 mg/kg) against time. (c) Bar graphs indicating enzymatic activities reflective of liver and kidney function at 1 and 21 days after ES treatment (3 mg/kg, n=5). Alkaline phosphatase and Alanine aminotransferase are markers of liver function; urea and creatinine are of kidney function. IU corresponds to international unit. n=5 in all groups. (d) Bar graphs showing RBC, WBC and platelet counts at different time points (1, 11, 21, 31 days) after ES treatment (3 mg/kg) completion. NS, not significant.
Mentions: To evaluate the pathophysiological changes induced by ES exposure, we assessed various responses in mice following ES treatment. Body weight fluctuation is an important parameter in understanding the physiological effects of a compound. Body weight analyses of male and female mice following ES treatment (0, 0.33, 1, 3, 9 mg/kg) for a period of 20 days showed remarkable fluctuations in weight in a concentration-dependent manner in case of male mice, while there was no significant change in females (Figure 1a). Thus, our results suggest that male mice are more sensitive to ES as compared with females and therefore male mice were chosen for further studies.

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