Enantioselective endocrine-disrupting effects of bifenthrin on hormone synthesis in rat ovarian cells

Liu, J; Yang, Y; Zhuang, S; Yang, Y; Li, F; Liu, W

HERO ID

1401875

Reference Type

Journal Article

Year

2011

Language

English

PMID

21871944

HERO ID 1401875
In Press No
Year 2011
Title Enantioselective endocrine-disrupting effects of bifenthrin on hormone synthesis in rat ovarian cells
Authors Liu, J; Yang, Y; Zhuang, S; Yang, Y; Li, F; Liu, W
Journal Toxicology
Volume 290
Issue 1
Page Numbers 42-49
Abstract Bifenthrin (BF), a broad-spectrum and widely used synthetic pyrethroid, is a typical chiral pesticide. More attention is being paid to the health risk assessment of the enantioselective toxicity of BF isomers. In this study, we used rat ovarian granulosa cells as in vitro model to investigate effects of BF enantiomers on the biosynthesis of two hormones, progesterone and prostaglandin E2 (PGE2), which are critical for mammalian reproduction. We showed that 1S-cis-BF, but not 1R-cis-BF significantly decreased the secretion of progesterone and PGE2 in granulosa cells. 1S-isomer of BF reduced the expression of genes P450scc, StAR, PBR and DBI, as well as COX-2, which are involved in regulating the rate-limiting steps of progesterone or PGE2 biosynthesis. The transcriptional activation of StAR and COX-2 promoter were disrupted by 1S-cis-BF. Furthermore, activity of protein kinase C (PKC), an important signaling mediator of progesterone and PGE2 synthesis, was differentially inhibited by 1S-cis-BF. The data of molecular docking revealed that one hydrogen bond was formed between 1S-cis-BF and PKC protein. In conclusion, we firstly reported in this study the enantioselective disrupting effects of BF isomers on progesterone and PGE2 synthesis via PKC pathway in rat ovarian cells. Our findings suggest that the enantioselective toxicity of chiral pesticides should be considered for evaluating mammalian reproductive health, a toxicologic endpoint of great concern in health risk assessment.
Doi 10.1016/j.tox.2011.08.016
Pmid 21871944
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English