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Cypermethrin inhibits Leydig cell development and function in pubertal rats.

Shijun Li1, Yun Wang1, Cheng Zou2

  • 1Institute of Life Sciences, Wenzhou University, Wenzhou, China.

Environmental Toxicology
|February 1, 2022
PubMed
Summary
This summary is machine-generated.

Cypermethrin insecticide exposure harms Leydig cell development and function in male rats during late puberty. This endocrine disruptor impacts testosterone production and increases oxidative stress, affecting male reproductive health.

Keywords:
Leydig cellscypermethrinoxidative stresssteroidogenesistestosterone

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Area of Science:

  • Endocrinology
  • Reproductive Toxicology
  • Environmental Health

Background:

  • Cypermethrin, a widely used pyrethroid insecticide, is suspected of causing endocrine disruption in the male reproductive system.
  • The specific impact of cypermethrin on Leydig cell development and function during late puberty remains largely uninvestigated.

Purpose of the Study:

  • To investigate the effects of cypermethrin exposure on Leydig cell development and function in male rats during late puberty.
  • To elucidate the underlying mechanisms by which cypermethrin may disrupt Leydig cell activity.

Main Methods:

  • Male Sprague-Dawley rats (postnatal day 35) were administered varying doses of cypermethrin (0, 12.5, 25, 50 mg/kg/day) until postnatal day 49.
  • Serum hormone levels (testosterone, LH, FSH), Leydig and Sertoli cell markers (CYP11A1, SOX9), gene and protein expression (Lhcgr, Star, Cyp11a1, Cyp17a1, Dhh, Amh), oxidative stress markers (malondialdehyde, Sod1, Sod2), reactive oxygen species (ROS), and mitochondrial membrane potential were assessed.
  • In vitro studies using primary Leydig cells were conducted to evaluate ROS generation and mitochondrial function.

Main Results:

  • Cypermethrin exposure (50 mg/kg) significantly reduced serum testosterone and Leydig cell number (CYP11A1-positive), while increasing luteinizing hormone.
  • Down-regulation of key Leydig cell genes and proteins (Lhcgr, Star, Cyp11a1, Cyp17a1) and up-regulation of Sertoli cell markers (Dhh, Amh) were observed.
  • Increased oxidative stress (malondialdehyde, ROS) and impaired mitochondrial function were evident in cypermethrin-treated rats and Leydig cells.

Conclusions:

  • Cypermethrin inhibits Leydig cell development and function in male rats during late puberty.
  • The disruption involves down-regulation of steroidogenic genes, increased oxidative stress, and mitochondrial dysfunction.
  • These findings highlight cypermethrin's potential as an endocrine disruptor affecting male reproductive health.