Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice
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...
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Editorial Office of Journal of Third Military Medical University
2020-03-01
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| Series: | Di-san junyi daxue xuebao |
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| Online Access: | http://aammt.tmmu.edu.cn/Upload/rhtml/201909114.htm |
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| author | YIN Jun LIU Junze NI Bing TANG Zhongwei GAO Zhiqi ZHAO Li ZHANG Mengjie CHEN Dewei HE Wenjuan LIAO Weigong |
| author_facet | YIN Jun LIU Junze NI Bing TANG Zhongwei GAO Zhiqi ZHAO Li ZHANG Mengjie CHEN Dewei HE Wenjuan LIAO Weigong |
| author_sort | YIN Jun |
| collection | DOAJ |
| description | 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% O2 and 5% CO2) for 48, 60, 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 spermatocytes 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 (P < 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 (P < 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; P < 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 vs 0.48±0.09, P < 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, P < 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. |
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| spelling | doaj.art-5263dcb940934bd1b421f450782c5aa22022-12-21T20:21:32ZzhoEditorial Office of Journal of Third Military Medical UniversityDi-san junyi daxue xuebao1000-54042020-03-0142657658210.16016/j.1000-5404.201909114Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in miceYIN Jun0LIU Junze1 NI Bing2TANG Zhongwei3GAO Zhiqi4ZHAO Li5ZHANG Mengjie6 CHEN Dewei7HE Wenjuan8 LIAO Weigong9Department of Pathophysiology, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Key Laboratory of High Altitude Medicine of PLA, Faculty of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, China Department of Pathophysiology, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Key Laboratory of High Altitude Medicine of PLA, Faculty of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, China Department of Pathophysiology, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Key Laboratory of High Altitude Medicine of PLA, Faculty of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, China Department of Pathophysiology, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Key Laboratory of High Altitude Medicine of PLA, Faculty of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, China Department of Pathophysiology, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Key Laboratory of High Altitude Medicine of PLA, Faculty of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, China Department of Pathophysiology, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Key Laboratory of High Altitude Medicine of PLA, Faculty of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, China Department of Pathophysiology, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Key Laboratory of High Altitude Medicine of PLA, Faculty of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, China Department of Pathophysiology, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Key Laboratory of High Altitude Medicine of PLA, Faculty of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, China Department of Pathophysiology, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Key Laboratory of High Altitude Medicine of PLA, Faculty of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, China Department of Pathophysiology, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Key Laboratory of High Altitude Medicine of PLA, Faculty of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, China 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% O2 and 5% CO2) for 48, 60, 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 spermatocytes 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 (P < 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 (P < 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; P < 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 vs 0.48±0.09, P < 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, P < 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.http://aammt.tmmu.edu.cn/Upload/rhtml/201909114.htmapoptosishypoxiaspermatocyte |
| spellingShingle | YIN Jun LIU Junze NI Bing TANG Zhongwei GAO Zhiqi ZHAO Li ZHANG Mengjie CHEN Dewei HE Wenjuan LIAO Weigong Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice Di-san junyi daxue xuebao apoptosis hypoxia spermatocyte |
| title | Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice |
| title_full | Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice |
| title_fullStr | Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice |
| title_full_unstemmed | Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice |
| title_short | Hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice |
| title_sort | hypoxia causes seminiferous tubule damage by inducing apoptosis of spermatocytes in mice |
| topic | apoptosis hypoxia spermatocyte |
| url | http://aammt.tmmu.edu.cn/Upload/rhtml/201909114.htm |
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