Maternal exposure to di-n-butyl phthalate (DBP) induces renal fibrosis in adult rat offspring
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Yi-Ping Zhu1,*, Lei Chen1,*, Xing-jie Wang1,*, Qi-Heng Jiang3,*, Xiao-Yu Bei1, Wen-Lan Sun2, Shu-Jie Xia1, Jun-Tao Jiang1
1Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China
2Department of Geriatrics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China
3Medical Services Section, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China
*These authors contributed equally to this work
Jun-Tao Jiang, email: firstname.lastname@example.org
Shu-Jie Xia, email: email@example.com
Keywords: renal fibrosis, kidney dysplasia, di-n-butyl phthalate (DBP), oxidative stress, environmental endocrine-disrupting compounds (EEDs)
Received: November 30, 2016 Accepted: March 01, 2017 Published: March 10, 2017
This study was to determine the impact of maternal exposure to di-n-butyl phthalate (DBP) on renal development and fibrosis in adult offspring. Pregnant rats received DBP at a dose of 850 mg/kg BW/day by oral perfusion during gestational days 14–18. In DBP exposed newborn offspring, gross observation and histopathological examination revealed the dysplasia of kidney. The expression of genes related to renal development was also changed. In DBP exposed adult offspring, histopathological examination and Masson’s trichrome staining revealed the pathological changes of renal fibrosis. Furthermore, higher expression levels of transforming growth factor- β (TGF-β) and alpha-smooth muscle actin (α-SMA) were also detected. In vitro studies reveal that DBP promoted the activation of NRK49F cells and G2/M arrest in NRK52E cells at a sublethal dose. The effect of DBP on these cell lines was linked to the generation of oxidative stress. In addition, DBP induced oxidative stress in both renal fibroblasts and tubular epithelial cells, whereas vitamin C ameliorated the changes caused by DBP. In conclusion, our results showed that prenatal exposure to DBP may generate oxidative stress in both renal fibroblasts and tubular epithelial cells, leading to kidney dysplasia and renal fibrosis.
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