Graduate School of Hebei Medical University, Shijiazhuang 050017, China.
Hebei Key Laboratory of Reproductive Medicine, Hebei Institute of Reproductive Health Science and Technology, Shijiazhuang 050071, China.
J Trace Elem Med Biol. 2023 Sep;79:127251. doi: 10.1016/j.jtemb.2023.127251. Epub 2023 Jun 24.
Zinc (Zn)is an essential trace element for spermatogenesis and its deficiency causes abnormal spermatogenesis.
The present study was conducted to examine the mechanisms by which Zn-deficient diet impairs sperm morphology and its reversibility.
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.
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.
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.
锌(Zn)是精子发生所必需的微量元素,其缺乏会导致精子发生异常。
本研究旨在探讨缺锌饮食损害精子形态的机制及其可逆性。
30 只 SPF 级昆明(KM)雄性小鼠随机分为 3 组,每组 10 只。锌正常饮食组(ZN 组)给予锌正常饮食(锌含量=30mg/kg)8 周。缺锌饮食组(ZD 组)给予缺锌饮食(锌含量<1mg/kg)8 周。缺锌和锌正常饮食组(ZDN 组)给予缺锌饮食 4 周,再给予锌正常饮食 4 周。8 周后,禁食过夜的小鼠被处死,采集血液和器官进行进一步分析。
实验结果表明,缺锌饮食导致精子畸形率增加和睾丸氧化应激。异常形态精子率、吖啶橙(CMA3)、DNA 片段化指数(DFI)、丙二醛(MDA)明显升高,而 a-激酶锚蛋白 4(AKAP4)、轴丝动力蛋白重链 1(DNAH1)、精子相关抗原 6(SPAG6)、纤毛和鞭毛相关蛋白 44(CFAP44)、谷胱甘肽过氧化物酶(GSH-PX)、超氧化物歧化酶(SOD)、总抗氧化能力(T-AOC)、核因子红细胞 2 相关因子(NRF2)、NAD(P)H:醌氧化还原酶 1(NQO1)和血红素加氧酶 1(HO1)明显降低。而在 ZDN 组中,缺锌饮食引起的上述指标变化明显缓解。
缺锌饮食导致雄性小鼠精子形态异常和睾丸氧化应激。缺锌饮食引起的精子形态异常是可逆的,锌正常饮食可缓解。