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Testosterone: Functions and Regulation

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The intricate hormonal interplay essential for male reproductive health begins with the release of gonadotropin-releasing hormone (GnRH) by the hypothalamus. This hormone prompts the pituitary gland to secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH). LH targets the Leydig cells in the testes, stimulating them to produce and release testosterone. In concert with testosterone, FSH acts on the Sertoli cells within the seminiferous tubules to facilitate the release of...

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TCP structure intensified the chlorpyrifos-induced decrease in testosterone synthesis via LH-LHR-PKA-CREB-Star

Jinwang Li¹, Bing Fang¹, Fazheng Ren²

¹Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.

The Science of the Total Environment

|June 3, 2020

Summary

This summary is machine-generated.

3,5,6-trichloro-2-pyridinol (TCP), a chlorpyrifos (CPF) metabolite, significantly reduces testosterone synthesis by disrupting the LH-LHR-PKA-CREB-Star pathway. This finding highlights TCP as a key contributor to CPF

Keywords:

3,5,6-Trichloro-2-pyridinol Chlorpyrifos Diethylphosphate Leydig cells Testis Testosterone synthesis

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Area of Science:

Environmental Toxicology
Endocrinology
Reproductive Science

Background:

Chlorpyrifos (CPF) is a widely used insecticide.
CPF is metabolized into diethylphosphate (DEP) and 3,5,6-trichloro-2-pyridinol (TCP).
TCP is a biomarker for CPF exposure, and both metabolites are found in human samples.

Purpose of the Study:

To determine which CPF structure (TCP or DEP) mediates the negative effects on testosterone synthesis.
To elucidate the mechanisms underlying CPF's impact on testosterone production.
To assess the role of the LH-LHR-PKA-CREB-Star pathway in CPF-induced reproductive toxicity.

Main Methods:

Exposure of rats to different doses of CPF for 20 weeks.
In vitro assessment of testosterone synthesis in isolated primary Leydig cells exposed to CPF, TCP, and DEP.
Measurement of testosterone levels, Star protein, CREB phosphorylation, and PKA phosphorylation.

Main Results:

CPF exposure significantly reduced testosterone levels in testes and Leydig cells.
TCP, but not DEP, aggravated the decrease in testosterone synthesis in Leydig cells.
CPF and TCP decreased levels of Star protein, CREB phosphorylation, and PKA phosphorylation, indicating pathway disruption.

Conclusions:

TCP is the key structure mediating CPF-induced testosterone synthesis reduction.
CPF-induced decrease in testosterone synthesis is mediated by the disruption of the LH-LHR-PKA-CREB-Star pathway.
Chemicals containing the TCP structure may act as endocrine disruptors, impacting fertility and requiring consideration in reproductive toxicity assessments.