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Sulforaphane attenuates di‐N‐butylphthalate‐induced reproductive damage in pubertal mice: Involvement of the Nrf2‐antioxidant system
Author(s) -
Jiang Xuping,
Tang Jingyuan,
Xu Zhen,
Han Peng,
Qin Zhiqiang,
Yang Chengdi,
Wang Shangqian,
Tang Min,
Wang Wei,
Qin Chao,
Xu Yang,
Shen Baixin,
Zhou Weimin,
Zhang Wei
Publication year - 2017
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22413
Subject(s) - sulforaphane , oxidative stress , spermatogenesis , reproductive toxicity , downregulation and upregulation , medicine , endocrinology , sperm , antioxidant , andrology , toxicity , apoptosis , chemistry , stimulation , biology , biochemistry , gene
di‐N‐butylphthalate (DBP) is a ubiquitous environmental pollutant used for plastic coating and in the cosmetics industry. It has toxic effects on body health, especially the male reproductive system. Here, we investigated the effects of DBP on the male reproductive system of pubertal mice and explored the protective role of sulforaphane (SFN). The results showed that DBP significantly reduced the anogenital distance, testicular weight, sperm count and motility, and plasma and testicular testosterone levels and significantly increased the oxidative stress, sperm abnormalities, and testicular cell apoptosis. SFN supplementation ameliorated these effects. After DBP stimulation, the transcription factor nuclear factor erythroid‐related factor 2 (Nrf2) was adaptively increased together with its target genes, such as HO‐1 and NQO1. Upregulation of Nrf2 by SFN reduced the DBP‐mediated intracellular oxidative toxicity and also increased testosterone secretion and spermatogenesis, which were decreased by DBP. These findings indicate that SFN can attenuate DBP‐induced reproductive damage in pubertal mice via Nrf2‐associated pathways.