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Trichlorfon blocks androgen synthesis and metabolism in rat immature Leydig cells
Huan Chen1, Yaoyao Dong2, Huitao Li2
1Department of Emergency, The Dingli Clinical College of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China.
Abstract:
Trichlorfon is a widely used organophosphorus insecticide. It has been reported that it has reproductive toxicity to animal models. However, whether trichlorfon affects testosterone biosynthesis and metabolism remains unclear. In this study, we explored the effects of trichlorfon on the steroidogenesis and the expression of genes in androgen biosynthetic and metabolic cascades in immature Leydig cells isolated from pubertal male rats. Immature Leydig cells were treated with trichlorfon (0.5-50 µM) for 3 h. Trichlorfon significantly inhibited total androgen output under basal condition at 5 and 50 μM, and under LH- and cAMP-stimulated conditions at 50 μM. Trichlorfon also downregulated the expression of Star, Sod2, and Gpx1 and their proteins at 5 and 50 μM and the expression of Cyp11a1, Hsd3b1, Cyp17a1, and Srd5a1 at 50 μM. Trichlorfon significantly inhibited total androgen output at 50 μM, which was partially reversed by 400 μg/ml vitamin E, which alone had no effects on androgen output. In conclusion, trichlorfon downregulates the expression of steroidogenesis-related genes and antioxidants, which leads to a decrease in androgen production in rat immature Leydig cells.
Insights
Trichlorfon insecticide exposure reduces testosterone production by downregulating key genes involved in androgen synthesis and antioxidant function in rat Leydig cells. Vitamin E partially reversed these effects.
Area of Science:
- Endocrinology
- Toxicology
- Reproductive Biology
Background:
- Trichlorfon is a common organophosphorus insecticide with known reproductive toxicity.
- Its specific impact on testosterone biosynthesis and metabolism remains largely uncharacterized.
Purpose of the Study:
- To investigate the effects of trichlorfon on steroidogenesis in rat immature Leydig cells.
- To examine trichlorfon's influence on genes within androgen biosynthesis and metabolic pathways.
Main Methods:
- Immature Leydig cells from pubertal male rats were treated with varying concentrations of trichlorfon (0.5-50 µM) for 3 hours.
- Androgen output was measured under basal, luteinizing hormone (LH), and cyclic adenosine monophosphate (cAMP)-stimulated conditions.
- Gene and protein expression of steroidogenic enzymes and antioxidants (Star, Sod2, Gpx1, Cyp11a1, Hsd3b1, Cyp17a1, Srd5a1) were analyzed.
Main Results:
- Trichlorfon significantly inhibited total androgen output at 5 and 50 µM (basal) and 50 µM (stimulated conditions).
- Expression of steroidogenic genes (Star, Cyp11a1, Hsd3b1, Cyp17a1) and antioxidant genes (Sod2, Gpx1) was downregulated by trichlorfon.
- Vitamin E partially reversed the trichlorfon-induced inhibition of androgen output.
Conclusions:
- Trichlorfon exposure decreases androgen production in rat immature Leydig cells.
- This reduction is linked to the downregulation of steroidogenesis-related genes and antioxidant enzymes.
- Findings highlight trichlorfon's potential endocrine-disrupting effects on male reproductive health.
