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Mechanisms of damage to sperm structure in mice on the zinc-deficient diet
Bo Sun1, Jing Ma2, Junsheng Liu1
1Graduate School of Hebei Medical University, Shijiazhuang 050017, China.
Background:
Zinc (Zn)is an essential trace element for spermatogenesis and its deficiency causes abnormal spermatogenesis.
Objective:
The present study was conducted to examine the mechanisms by which Zn-deficient diet impairs sperm morphology and its reversibility.
Methods:
30 SPF grade male Kunming (KM) mice were randomly divided into three groups, 10 mice per group. Zn-normal diet group (ZN group) was given Zn-normal diet（Zn content= 30 mg/kg）for 8 weeks. Zn-deficienct diet group (ZD group) was given Zn-deficienct diet（Zn content< 1 mg/kg）for 8 weeks. Zn-deficient and Zn-normal diet group（ZDN group）was given 4 weeks Zn-deficienct diet followed by 4 weeks Zn-normal diet. After 8 weeks, the overnight fasted mice were sacrificed, and blood and organs were collected for further analysis.
Results:
The experimental results showed that Zn-deficienct diet leads to increased abnormal morphology sperm and testicular oxidative stress.The rate of abnormal morphology sperm, chromomycin A3(CMA3), DNA fragmentation index (DFI), malondialdehyde (MDA) were significantly increased, and a-kinase anchor protein 4(AKAP4), dynein axonemal heavy chain 1(DNAH1), sperm associated antigen 6(SPAG6), cilia and flagella associated protein 44(CFAP44), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), total antioxidant capacity (T-AOC), nuclear factor erythroid 2-related factor (NRF2), NAD(P)H:quinone oxidoreductase 1(NQO1)and heme oxygenase 1(HO1) were significantly decreased in the ZD group mice. While the changes in above indicators caused by Zn-deficient diet were significantly alleviated in the ZDN group.
Conclusion:
It was concluded that Zn-deficient diet causes abnormal morphology sperm and testicular oxidative stress in male mice. Abnormal morphology sperm caused by Zn-deficient diet are reversible, and Zn-normal diet can alleviate them.
Insights
Zinc deficiency in male mice significantly increases abnormal sperm morphology and oxidative stress. These effects are reversible with a zinc-normal diet, highlighting the importance of zinc for reproductive health.
Area of Science:
- Reproductive Biology
- Trace Element Metabolism
- Oxidative Stress Research
Background:
- Zinc (Zn) is crucial for spermatogenesis.
- Zinc deficiency leads to impaired sperm production and function.
Purpose of the Study:
- To investigate how a zinc-deficient diet affects sperm morphology.
- To determine the reversibility of diet-induced sperm abnormalities.
Main Methods:
- Male Kunming mice were divided into three groups: normal zinc diet, deficient zinc diet, and deficient followed by normal zinc diet.
- Diets were administered for 8 weeks, with one group receiving a switch from deficient to normal zinc diet after 4 weeks.
- Sperm morphology, oxidative stress markers, and key protein levels were analyzed.
Main Results:
- Zinc deficiency significantly increased abnormal sperm morphology, DNA fragmentation (DFI), and oxidative stress markers (MDA).
- Levels of essential sperm proteins (AKAP4, DNAH1, SPAG6, CFAP44) and antioxidant enzymes (GSH-PX, SOD, T-AOC) were significantly reduced.
- Reintroduction of a normal zinc diet (ZDN group) significantly alleviated these negative effects.
Conclusions:
- Zinc deficiency causes abnormal sperm morphology and testicular oxidative stress in male mice.
- Diet-induced sperm abnormalities are reversible upon restoring adequate zinc intake.
- Adequate zinc nutrition is essential for maintaining sperm quality and mitigating oxidative damage.
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