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缺锌饮食对小鼠精子结构损伤的机制。

Mechanisms of damage to sperm structure in mice on the zinc-deficient diet.

机构信息

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.

出版信息

J Trace Elem Med Biol. 2023 Sep;79:127251. doi: 10.1016/j.jtemb.2023.127251. Epub 2023 Jun 24.

Abstract

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.

摘要

背景

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。

目的

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。

方法

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。

结果

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。

结论

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。

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