Vitamin C supplementation rescued meiotic arrest of spermatocytes in Balb/c mice exposed to BDE-209
Deca-brominated diphenyl ether (BDE-209) is a ubiquitous industrial chemical as brominated flame retardant (BFRs). Exposure to BDE-209 has been clearly associated with male reproductive disorders. However, the meiotic arrest mechanism of spermatocytes exposed to BDE-209 is still unclear. The present...
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Elsevier
2022-09-01
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author | Taifa Zhang Huan He Yu Wei Wenfeng Geng Jinxia Zhai |
author_facet | Taifa Zhang Huan He Yu Wei Wenfeng Geng Jinxia Zhai |
author_sort | Taifa Zhang |
collection | DOAJ |
description | Deca-brominated diphenyl ether (BDE-209) is a ubiquitous industrial chemical as brominated flame retardant (BFRs). Exposure to BDE-209 has been clearly associated with male reproductive disorders. However, the meiotic arrest mechanism of spermatocytes exposed to BDE-209 is still unclear. The present work aimed to explore the protective effect of vitamin C on BDE-209-induced meiotic arrest of spermatocytes and its possible mechanism. Vitamin C (100 mg/kg BW) was administered to BDE-209-exposed (80 mg/kg BW) male Balb/c mice once daily by intraperitoneal injection for 2 weeks. Our results showed that vitamin C played male reproductive protection effects as showed by attenuated BDE-209-induced testicular damage, and reduced sperm abnormality rate. Vitamin C also attenuated BDE-209-induced increase in SOD and MDA in testes and GC-2 spd cells. Moreover, vitamin C promoted meiotic prophase in BDE-209-induced mice, with suppressed γ-H2AX, restored DMC1, RAD51, and crossover marker MLH1 levels, and prevented BDE-209-induced DNA impairment. In addition, vitamin C supplementation also interfered with BDE-209-induced upregulation of testicular H3K4me3 through inhibition of KDM5s capacity and decreasing ferrous ion concentration. Furthermore, ferrous sulfate pretreatment could partially restore the expression of H3K4me3 via maintaining the concentration of ferrous ions. Taken together, vitamin C exerts a potential therapeutic agent for preventing BDE-209-induced reproductive toxicity with meiotic arrest, which is attributed to its antioxidant and electron donor properties, as well as, modulation of ferrous ion levels and demethylation of H3K4me3. |
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spelling | doaj.art-b4cf259eed864962819626a67889666c2022-12-22T03:44:42ZengElsevierEcotoxicology and Environmental Safety0147-65132022-09-01242113846Vitamin C supplementation rescued meiotic arrest of spermatocytes in Balb/c mice exposed to BDE-209Taifa Zhang0Huan He1Yu Wei2Wenfeng Geng3Jinxia Zhai4Department of Occupational and Environmental Health, School of Public Health, Anhui Medical University, Meishan Rd 81, Hefei 230032, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Anhui Medical University, Meishan Rd 81, Hefei 230032, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Anhui Medical University, Meishan Rd 81, Hefei 230032, ChinaDepartment of Occupational and Environmental Health, School of Public Health, Anhui Medical University, Meishan Rd 81, Hefei 230032, ChinaCorresponding author.; Department of Occupational and Environmental Health, School of Public Health, Anhui Medical University, Meishan Rd 81, Hefei 230032, ChinaDeca-brominated diphenyl ether (BDE-209) is a ubiquitous industrial chemical as brominated flame retardant (BFRs). Exposure to BDE-209 has been clearly associated with male reproductive disorders. However, the meiotic arrest mechanism of spermatocytes exposed to BDE-209 is still unclear. The present work aimed to explore the protective effect of vitamin C on BDE-209-induced meiotic arrest of spermatocytes and its possible mechanism. Vitamin C (100 mg/kg BW) was administered to BDE-209-exposed (80 mg/kg BW) male Balb/c mice once daily by intraperitoneal injection for 2 weeks. Our results showed that vitamin C played male reproductive protection effects as showed by attenuated BDE-209-induced testicular damage, and reduced sperm abnormality rate. Vitamin C also attenuated BDE-209-induced increase in SOD and MDA in testes and GC-2 spd cells. Moreover, vitamin C promoted meiotic prophase in BDE-209-induced mice, with suppressed γ-H2AX, restored DMC1, RAD51, and crossover marker MLH1 levels, and prevented BDE-209-induced DNA impairment. In addition, vitamin C supplementation also interfered with BDE-209-induced upregulation of testicular H3K4me3 through inhibition of KDM5s capacity and decreasing ferrous ion concentration. Furthermore, ferrous sulfate pretreatment could partially restore the expression of H3K4me3 via maintaining the concentration of ferrous ions. Taken together, vitamin C exerts a potential therapeutic agent for preventing BDE-209-induced reproductive toxicity with meiotic arrest, which is attributed to its antioxidant and electron donor properties, as well as, modulation of ferrous ion levels and demethylation of H3K4me3.http://www.sciencedirect.com/science/article/pii/S0147651322006868Decabromodiphenyl ether (BDE-209)H3K4me3Meiotic prophase IVitamin CDemethylation |
spellingShingle | Taifa Zhang Huan He Yu Wei Wenfeng Geng Jinxia Zhai Vitamin C supplementation rescued meiotic arrest of spermatocytes in Balb/c mice exposed to BDE-209 Ecotoxicology and Environmental Safety Decabromodiphenyl ether (BDE-209) H3K4me3 Meiotic prophase I Vitamin C Demethylation |
title | Vitamin C supplementation rescued meiotic arrest of spermatocytes in Balb/c mice exposed to BDE-209 |
title_full | Vitamin C supplementation rescued meiotic arrest of spermatocytes in Balb/c mice exposed to BDE-209 |
title_fullStr | Vitamin C supplementation rescued meiotic arrest of spermatocytes in Balb/c mice exposed to BDE-209 |
title_full_unstemmed | Vitamin C supplementation rescued meiotic arrest of spermatocytes in Balb/c mice exposed to BDE-209 |
title_short | Vitamin C supplementation rescued meiotic arrest of spermatocytes in Balb/c mice exposed to BDE-209 |
title_sort | vitamin c supplementation rescued meiotic arrest of spermatocytes in balb c mice exposed to bde 209 |
topic | Decabromodiphenyl ether (BDE-209) H3K4me3 Meiotic prophase I Vitamin C Demethylation |
url | http://www.sciencedirect.com/science/article/pii/S0147651322006868 |
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