Exposure to automobile exhaust-derived PM2.5 induces spermatogenesis dysfunction by damaging UPRmt of prepubertal rats
Automobile exhaust-derived particulate matter 2.5 (PM2.5) can cause spermatogenic cell damage, potentially resulting in male infertility. This study uses male prepubertal Sprague Dawley (SD) rats to explore the molecular mechanisms by which automobile exhaust-derived PM2.5 causes spermatogenic cell...
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Elsevier
2022-10-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651322009277 |
| _version_ | 1818023341625180160 |
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| author | Cao Wang Xiang Liu Zhen Shu Jia Yin Mingchen Xiao Yaya Ai Peng Zhao Zhen Luo Bin Liu |
| author_facet | Cao Wang Xiang Liu Zhen Shu Jia Yin Mingchen Xiao Yaya Ai Peng Zhao Zhen Luo Bin Liu |
| author_sort | Cao Wang |
| collection | DOAJ |
| description | Automobile exhaust-derived particulate matter 2.5 (PM2.5) can cause spermatogenic cell damage, potentially resulting in male infertility. This study uses male prepubertal Sprague Dawley (SD) rats to explore the molecular mechanisms by which automobile exhaust-derived PM2.5 causes spermatogenic cell damage and induces spermatogenesis dysfunction during sexual maturity by disrupting the mitochondrial unfolded protein response (UPRmt) in spermatogenic cells. Male prepubertal SD rats were randomly divided into four groups: control (intratracheal instillation of normal saline), low-dose PM2.5 (5 mg/kg), high-dose PM2.5 (10 mg/kg), and PM2.5 10 mg/kg +Vit (100 mg/kg of vitamin C and 50 mg/kg of vitamin E). The rats were treated for four weeks, with five consecutive treatment days and two non-treatment days, followed by cohabitation. Testicular and epididymal tissues were harvested for analysis. The mitochondria in spermatogenic cells were observed under an electron microscope. UPRmt-, oxidative stress-, and apoptosis-related markers in spermatogenic cells were examined. Spermatogenic cell numbers and conception rate declined significantly with increasing PM2.5 dose, with their mitochondria becoming vacuolated, swollen, and degenerated to varying degrees. The apoptosis of spermatogenic cells was abnormally enhanced in PM2.5 exposed groups compared to the control group. Spermatogenic cell numbers of conception rate gradually recovered, mitochondrial damage in spermatogenic cells was alleviated, and spermatogenic cell apoptosis was significantly reduced after vitamin intervention. In addition, protein levels of superoxide dismutase 1 (Sod1), nuclear factor erythroid 2-related factor 2 (Nrf2), and B-cell lymphoma 2 (Bcl-2) were significantly lower, while those of Bcl2-associated X apoptosis regulator (Bax), cleaved caspase 3 (Casp3), and cytochrome c (Cyt-c) and malondialdehyde (MDA) levels were significantly higher in the high-dose PM2.5 group than in the control group. The levels of UPRmt-related proteins C/EBP homologous protein (Chop), heat shock protein 60 (Hsp60), and activating transcription factors 4 (Atf4) and 5 (Atf5) were higher in the low-dose PM2.5 group, lower in the high-dose PM2.5 group, and gradually recovered in PM2.5 10 mg/kg +Vit group. Our results show that exposure to automobile exhaust-derived PM2.5 induces oxidative stress responses, leads to post-sexual maturation UPRmt dysfunction and mitochondrial impairment, and abnormally enhances spermatogenic cell apoptosis in prepubertal rats, resulting in male infertility. |
| first_indexed | 2024-12-10T03:42:47Z |
| format | Article |
| id | doaj.art-1361883e7bc64d1fbe71b046be2e429f |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-12-10T03:42:47Z |
| publishDate | 2022-10-01 |
| publisher | Elsevier |
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| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-1361883e7bc64d1fbe71b046be2e429f2022-12-22T02:03:30ZengElsevierEcotoxicology and Environmental Safety0147-65132022-10-01245114087Exposure to automobile exhaust-derived PM2.5 induces spermatogenesis dysfunction by damaging UPRmt of prepubertal ratsCao Wang0Xiang Liu1Zhen Shu2Jia Yin3Mingchen Xiao4Yaya Ai5Peng Zhao6Zhen Luo7Bin Liu8Guizhou Children's Hospital, Zunyi, Guizhou Province, China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou Province, ChinaGuizhou Children's Hospital, Zunyi, Guizhou Province, China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou Province, ChinaGuizhou Children's Hospital, Zunyi, Guizhou Province, China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou Province, ChinaGuizhou Children's Hospital, Zunyi, Guizhou Province, China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou Province, ChinaGuizhou Children's Hospital, Zunyi, Guizhou Province, China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou Province, ChinaGuizhou Children's Hospital, Zunyi, Guizhou Province, China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou Province, ChinaGuizhou Children's Hospital, Zunyi, Guizhou Province, China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou Province, ChinaGuizhou Children's Hospital, Zunyi, Guizhou Province, China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou Province, ChinaGuizhou Children's Hospital, Zunyi, Guizhou Province, China; Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou Province, China; Correspondence to: Department of Pediatric Surgery, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi 563000, China.Automobile exhaust-derived particulate matter 2.5 (PM2.5) can cause spermatogenic cell damage, potentially resulting in male infertility. This study uses male prepubertal Sprague Dawley (SD) rats to explore the molecular mechanisms by which automobile exhaust-derived PM2.5 causes spermatogenic cell damage and induces spermatogenesis dysfunction during sexual maturity by disrupting the mitochondrial unfolded protein response (UPRmt) in spermatogenic cells. Male prepubertal SD rats were randomly divided into four groups: control (intratracheal instillation of normal saline), low-dose PM2.5 (5 mg/kg), high-dose PM2.5 (10 mg/kg), and PM2.5 10 mg/kg +Vit (100 mg/kg of vitamin C and 50 mg/kg of vitamin E). The rats were treated for four weeks, with five consecutive treatment days and two non-treatment days, followed by cohabitation. Testicular and epididymal tissues were harvested for analysis. The mitochondria in spermatogenic cells were observed under an electron microscope. UPRmt-, oxidative stress-, and apoptosis-related markers in spermatogenic cells were examined. Spermatogenic cell numbers and conception rate declined significantly with increasing PM2.5 dose, with their mitochondria becoming vacuolated, swollen, and degenerated to varying degrees. The apoptosis of spermatogenic cells was abnormally enhanced in PM2.5 exposed groups compared to the control group. Spermatogenic cell numbers of conception rate gradually recovered, mitochondrial damage in spermatogenic cells was alleviated, and spermatogenic cell apoptosis was significantly reduced after vitamin intervention. In addition, protein levels of superoxide dismutase 1 (Sod1), nuclear factor erythroid 2-related factor 2 (Nrf2), and B-cell lymphoma 2 (Bcl-2) were significantly lower, while those of Bcl2-associated X apoptosis regulator (Bax), cleaved caspase 3 (Casp3), and cytochrome c (Cyt-c) and malondialdehyde (MDA) levels were significantly higher in the high-dose PM2.5 group than in the control group. The levels of UPRmt-related proteins C/EBP homologous protein (Chop), heat shock protein 60 (Hsp60), and activating transcription factors 4 (Atf4) and 5 (Atf5) were higher in the low-dose PM2.5 group, lower in the high-dose PM2.5 group, and gradually recovered in PM2.5 10 mg/kg +Vit group. Our results show that exposure to automobile exhaust-derived PM2.5 induces oxidative stress responses, leads to post-sexual maturation UPRmt dysfunction and mitochondrial impairment, and abnormally enhances spermatogenic cell apoptosis in prepubertal rats, resulting in male infertility.http://www.sciencedirect.com/science/article/pii/S0147651322009277PM2.5Mitochondrial unfolded protein response (UPRmt)Prepubertal exposureSpermatogenic cellsApoptosis |
| spellingShingle | Cao Wang Xiang Liu Zhen Shu Jia Yin Mingchen Xiao Yaya Ai Peng Zhao Zhen Luo Bin Liu Exposure to automobile exhaust-derived PM2.5 induces spermatogenesis dysfunction by damaging UPRmt of prepubertal rats Ecotoxicology and Environmental Safety PM2.5 Mitochondrial unfolded protein response (UPRmt) Prepubertal exposure Spermatogenic cells Apoptosis |
| title | Exposure to automobile exhaust-derived PM2.5 induces spermatogenesis dysfunction by damaging UPRmt of prepubertal rats |
| title_full | Exposure to automobile exhaust-derived PM2.5 induces spermatogenesis dysfunction by damaging UPRmt of prepubertal rats |
| title_fullStr | Exposure to automobile exhaust-derived PM2.5 induces spermatogenesis dysfunction by damaging UPRmt of prepubertal rats |
| title_full_unstemmed | Exposure to automobile exhaust-derived PM2.5 induces spermatogenesis dysfunction by damaging UPRmt of prepubertal rats |
| title_short | Exposure to automobile exhaust-derived PM2.5 induces spermatogenesis dysfunction by damaging UPRmt of prepubertal rats |
| title_sort | exposure to automobile exhaust derived pm2 5 induces spermatogenesis dysfunction by damaging uprmt of prepubertal rats |
| topic | PM2.5 Mitochondrial unfolded protein response (UPRmt) Prepubertal exposure Spermatogenic cells Apoptosis |
| url | http://www.sciencedirect.com/science/article/pii/S0147651322009277 |
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