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Updated: Mar 20, 2026
Phosphopeptide Analysis of Rodent Epididymal Spermatozoa
Published on: December 30, 2014
Cadmium inhibits mouse sperm motility through inducing tyrosine phosphorylation in a specific subset of proteins
Lirui Wang1, Yuhua Li1, Jieli Fu1
1Shanghai Key Lab of Veterinary Biotechnology, School of Agriculture and Biology, Shanghai Jiaotong University, Shanghai 200240, China.
Abstract:
Cadmium (Cd) has been reported to impair male fertility, primarily by disrupting sperm motility, but the underlying molecular mechanism remains unclear. Here we investigated the effects of Cd on sperm motility, tyrosine phosphorylation, AMP-activated protein kinase (AMPK) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity, and ATP levels in vitro. Our results demonstrated that Cd inhibited sperm motility, GAPDH activity, AMPK activity and ATP production, and induced tyrosine phosphorylation of 55-57KDa proteins. Importantly, all the parameters affected by Cd were restored to normal levels when incubated with 10μM Cd in the presence of 30μM ethylene diamine tetraacetic acid (EDTA). Interestingly, changes of tyrosine phosphorylation levels of 55-57KDa proteins are completely contrary to that of other parameters. These results suggest that Cd-induced tyrosine phosphorylation of 55-57KDa proteins might act as an engine to block intracellular energy metabolism and thus decrease sperm motility.
Insights
Cadmium exposure impairs male fertility by reducing sperm motility and energy production. This study suggests cadmium-induced protein tyrosine phosphorylation disrupts cellular energy metabolism, decreasing sperm function.
Area of Science:
- Reproductive Biology
- Environmental Toxicology
- Biochemistry
Background:
- Cadmium (Cd) is a toxic metal known to negatively impact male reproductive health.
- Impaired sperm motility is a key consequence of cadmium exposure, but the molecular mechanisms are not fully understood.
Purpose of the Study:
- To investigate the effects of cadmium on sperm motility, tyrosine phosphorylation, AMP-activated protein kinase (AMPK) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity, and ATP levels in vitro.
- To elucidate the molecular mechanisms underlying cadmium-induced male infertility.
Main Methods:
- In vitro assessment of sperm motility, tyrosine phosphorylation, AMPK and GAPDH activity, and ATP levels following cadmium exposure.
- Evaluation of the protective effect of ethylene diamine tetraacetic acid (EDTA) against cadmium toxicity.
Main Results:
- Cadmium significantly inhibited sperm motility, GAPDH activity, AMPK activity, and ATP production.
- Cadmium exposure induced tyrosine phosphorylation of 55-57KDa proteins, with changes contrary to other measured parameters.
- Ethylene diamine tetraacetic acid (EDTA) successfully restored all cadmium-affected parameters to normal levels.
Conclusions:
- Cadmium impairs male fertility by disrupting sperm motility and intracellular energy metabolism.
- Cadmium-induced tyrosine phosphorylation of specific proteins may be a key mechanism blocking energy production and reducing sperm function.
- EDTA can mitigate cadmium's adverse effects on sperm parameters, suggesting chelation as a potential therapeutic strategy.
