Related Experiment Video
Updated: Jan 20, 2026
Studying Chronic Exposure of Mice to Ultraviolet B Radiation
Published on: August 19, 2025
Chronic Copper Exposure Induces Hypospermatogenesis in Mice by Increasing Apoptosis Without Affecting Testosterone
Hanming Chen1, Zhenlong Kang1, Na Qiao1
1College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
Abstract:
Chronic copper exposure impaired spermatogenesis in adult male mice. The aim of this study was to determine whether chronic copper exposure can induce apoptosis of testicular cell and hypospermatogenesis via disturbing testosterone synthesis in adult male mice. In the present study, sixty CD-1 male mice were randomly divided into four groups, and were continuously administered for 8 weeks by oral gavage with copper sulfate at a dose of 0, 25, 100, and 150 mg/kg/day, respectively. We determined the content of serum and testicular copper, testicular coefficient, testicular histopathology, sperm count and motility, the mRNA and protein levels of Caspase-3, Bax, and Bcl-2, Leydig cell count, testosterone content, testosterone synthetase, and testosterone synthesis-related genes. The results showed that the copper levels in serum increased in a dose-dependent manner, and the copper levels in testes were significantly related to serum copper levels. Male mice given copper sulfate 100 and 150 dosage groups showed significant decreased in sperm motility and sperm number as well as increased in testes damage, and there was no significant change in testicular coefficient in the four groups. The mRNA levels of Bcl-2 decreased and Caspase-3 increased in 150 dosage group, and Bax increased in two higher dosage groups. Meanwhile, Caspase-3 and Bax proteins increased in 150 dosage group, and Bcl-2 protein decreased in three copper treatment groups. Nevertheless, there were no differences on the levels of testosterone content and testosterone synthetase of 3β-HSD, 17β-HSD, 17α-Hyd, and 20α-Hyd, mRNA levels of Cyp11a1, Cyp17a1, and Star, and quantity of Leydig cells in four groups. Overall, these data showed that chronic copper exposure led to copper residues in the testes, and the doses of 100 and 150 mg/kg/day copper sulfate may induce hypospermatogenesis by increasing apoptosis without affecting testosterone secretion.
Insights
Chronic copper exposure in male mice led to testicular damage and reduced sperm count. This occurred through increased cell apoptosis, not by affecting testosterone synthesis.
Area of Science:
- Reproductive Toxicology
- Environmental Health
- Cell Biology
Background:
- Chronic copper exposure is a concern for male reproductive health.
- Copper accumulation in testes may impair spermatogenesis.
- The specific mechanisms, particularly apoptosis and testosterone synthesis, require elucidation.
Purpose of the Study:
- To investigate the effects of chronic copper sulfate exposure on spermatogenesis in adult male mice.
- To determine if copper exposure induces testicular cell apoptosis and hypospermatogenesis.
- To assess the impact of copper on testosterone synthesis pathways.
Main Methods:
- Adult male mice were exposed to varying doses of copper sulfate (0, 25, 100, 150 mg/kg/day) for 8 weeks.
- Evaluated serum/testicular copper, testicular histopathology, sperm parameters, and apoptosis markers (Caspase-3, Bax, Bcl-2).
- Assessed Leydig cell counts and key genes/enzymes involved in testosterone synthesis.
Main Results:
- Copper levels increased dose-dependently in serum and testes.
- Higher copper doses (100, 150 mg/kg/day) significantly reduced sperm count/motility and increased testicular damage.
- Apoptosis markers (Bax, Caspase-3) increased, while Bcl-2 decreased, without altering testosterone levels or Leydig cell counts.
Conclusions:
- Chronic copper exposure leads to copper accumulation in testes.
- Copper-induced hypospermatogenesis in mice is mediated by increased testicular cell apoptosis.
- Testosterone synthesis pathways remain unaffected by the tested copper doses.
Related Concept Videos
01:26Testosterone: Functions and Regulation
01:30Apoptosis
01:25Increased Body Temperature
01:17Increased pulse rate
Many factors can elevate the risk of developing tachycardia. These include advanced age, a family history of arrhythmias, and an...
01:25Hormones Secreted by the Stomach
Each of these hormones secreted by different enteroendocrine cells plays a unique role in digestion. Here are a few examples:
01:26Pancreatic Juice and Secretion
When acidic chyme from the stomach enters the duodenum, it triggers the release of secretin, a hormone that prompts pancreatic juice secretion. After a fatty meal, cholecystokinin, another hormone, stimulates gallbladder contraction and enhances enzyme-rich...