Persistent testicular structural and functional alterations after exposure of adult rats to atrazine
•Atrazine induced irreversible effects on testicular morphology and steroidogenesis.•3β-HSD expression was reduced in Leydig cell after atrazine exposure.•Testicular atrophy and 3β-HSD decline were pronounced after a recovery period.•Testicular macrophages positive for 3β-HSD increased after the rec...
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Veröffentlicht in: | Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2017-10, Vol.73, p.201-213 |
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Sprache: | eng |
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Zusammenfassung: | •Atrazine induced irreversible effects on testicular morphology and steroidogenesis.•3β-HSD expression was reduced in Leydig cell after atrazine exposure.•Testicular atrophy and 3β-HSD decline were pronounced after a recovery period.•Testicular macrophages positive for 3β-HSD increased after the recovery period.•Cells ED1−/ED2+, ED1+/ED2+ and ED1+/ED2− increased 89%, 76% and 42% post recovery.
Atrazine is an endocrine disruptor affecting testicular steroidogenesis, and promoting testicular atrophy and 3β-HSD reduction. However, it remains unknown whether these effects are reversible or permanent. To address this issue was the aim of this study. Exposition of rats to 200mg/kg of atrazine resulted in transient increase in testicular weight, seminiferous tubules dilation and atrophy, and reduction in Leydig cell 3β-HSD. Testicular atrophy and 3β-HSD reduction were more pronounced after the recovery period of 75days. There was increase in aromatase expression after long-term exposure but it returned to control level after recovery. Moreover, there was increase in ED1−/ED2+, ED1+/ED2+ and ED1+/ED2− macrophages, in the recovery group. These macrophages were positive for 3β-HSD, thereby raising possibility of their involvement in steroidogenesis. These findings further emphasize the adverse effects of atrazine on male reproduction, highlighting that testicular damages may be irreversible even after a recovery period longer than the spermatogenic cycle. |
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ISSN: | 0890-6238 1873-1708 |
DOI: | 10.1016/j.reprotox.2017.08.010 |