Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice

Jun YIN; Junze LIU; Bing NI; Zhongwei TANG; Zhiqi GAO; Li ZHAO; Mengjie ZHANG; Dewei CHEN; Wenjuan HE; Weigong LIAO

doi:10.16016/j.1000-5404.201909114

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Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice

更新时间：2026-01-09

- Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice
- Journal of Third Military Medical University Vol. 42, Issue 6, Pages: 576-582(2020)
- 作者机构：
- 作者简介：
- 基金信息：
  
  Supported by the General Program of National Natural Science Foundation of China(81701855)
- DOI：10.16016/j.1000-5404.201909114
  CLC：
- Received：16 September 2019，
  
  Published：30 March 2020
- 稿件说明：
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Jun YIN, Junze LIU, Bing NI, et al. Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice[J]. Journal of Third Military Medical University, 2020, 42(6): 576-582.
DOI：

Jun YIN, Junze LIU, Bing NI, et al. Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice[J]. Journal of Third Military Medical University, 2020, 42(6): 576-582. DOI： 10.16016/j.1000-5404.201909114.

摘要

Abstract

Objective

To investigate the damage of seminiferous tubules in mice exposed to hypoxia and the effects of hypoxia on apoptosis of mouse spermatocytes in the seminiferous tubules.

Methods

Forty 3-week-old male Balb/c mice were randomly assigned into a normoxia group (housed in a normoxic condition at an altitude of 300 m) and 3 hypoxia groups exposed to hypoxia for 15

30 or 60 d in a hypobaric chamber simulating the condition at an altitude of 6 000 m. After hypoxic exposures

the mice were euthanized and the testicular tissues were examined for pathological changes in the seminiferous tubules using HE and TUNEL staining. A mouse spermatocyte-derived cell line

GC-2spd

was also cultured in a normoxic condition or a hypoxic condition (1% O

and 5% CO

) for 48

or 72 h

and the cell apoptosis was detected using flow cytometry and TUNEL staining and by examining LDH

caspase-3

caspase-8

and caspase-9 levels in the culture medium.

Results

The apoptotic rates of the s

permatocytes in the testicular seminiferous tubules of the mice increased significantly after hypoxic exposure for 15

30 and 60 d as compared with the apoptosis rate of (4.6±1.4)% in the normoxia group (

0.01). In cultured GC-2spd cells

hypoxic exposure for 48

60 and 72 h also significantly increased the cell apoptotic rate to (15.43±1.47)%

(44.10±14.10)% and (63.36±12.74)%

as compared with the rates of (4.18±1.40)%

(5.45%±2.30)%

and (14.47±8.21)% in the normoxia group

respectively (

0.01). Microscopically

the numbers of apoptotic spermatocytes per field were 22±3

55±5

and 82±12 in the hypoxia group at 48

60 and 72 h

respectively

significantly greater than those in the normoxia group (5±1

8±2

and 15±4

respectively;

0.01). The absolute value of LDH activity in cultured GC-2spd cells at 48 h was significantly higher in the hypoxia group than in the normoxia group (1.28±0.18

0.48±0.09

0.01); the values of caspase-3/8/9 in the hypoxia group at 48 h were 12.20±0.40

22.73±0.60

and 10.90±0.40

respectively

significantly higher than those in the normoxia group (7.67±0.45

16.20±0.56

and 7.03±0.25

respectively

0.01).

Conclusion

Exposure to hypoxia simulating the condition at an altitude of 6 000 m for 15 d can cause decreased spermatogenesis and increased apoptosis of the spermatogenic cells in mice

suggesting that spermatocyte apoptosis is one of the mechanisms by which hypobaric hypoxia reduces spermatogenesis.

关键词

Keywords

references

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