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General Session 4: Marine environment, ecosystem & sustainability |
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The toxic effects of bisphenol S showing immunomodulation
in fish macrophage
Monday 9th @ 1425-1445
Room 1
Wenhui Qiu, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China
Lei Hu, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China
Shuai Liu, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China
Bei Chen, State Key Laboratory of Marine Environmental Science, College of Ocean & Earth Science, Xiamen University, Xiamen, Fujian 361005, China
Ming Yang* , School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China
Ke-Jian Wang, State Key Laboratory of Marine Environmental Science, College of Ocean & Earth Science, Xiamen University, Xiamen, Fujian 361005, China
Presenter Email: mingyang@shu.edu.cn
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| Bisphenol S (BPS) has been thought as a safer substitute for bisphenol A (BPA) introduced into the industry but its observed toxic effect has been often revealed in recent years and thus causing more attention for its potential risks. The present study will use the fish primary macrophages as in vitro model to evaluate the potential immune modulatory effects of BPS associated with estrogen receptors (ERs). The alteration in level of ROS, NO, iNOS, TNOS and the expression of the immune associated genes tested in the study were used for the indicator assessment of the toxic effects of BPS. Here we demonstrate that bisphenol S exposure induced the immunotoxic effects on fish macrophage. The level of either ROS, NO, iNOS or TNOS was significantly increased upon exposure to BPS at the concentrations of 10, 100, 1000 μg/L. Correspondingly, the eight immune-associated genes tested were significantly expressed, indicating the immunomodulatory effects of BPS exposure on the related immune gene expression. It was further noted that the post challenge of LPS after the exposure of BPS (100 μg/L) significantly enhanced the mRNA expression of each immune-associated gene than that with either LPS or BPS alone, suggesting that BPS was likely to have the synergistic capability with LPS to increase the inflammatory reaction. Unlike BPA which could induce a significant increase of caspase 3 and apoptosis at the concentration of 10 μg/L, BPS induced a significant increase of caspase 3 and apoptosis at a much high concentration of 1000 μg/L, meaning the possibly slight damage to cells caused by BPS than by BPA. Furthermore, the study showed that each immune–associated gene expression upon exposure to either BPS or BPA was involved in the regulation of estrogen receptors ER and ER2, however, the involvement of these estrogen receptors in the immune regulation of toxic effects was somewhat differentiated between BPS and BPA. This study shows that even at a lower dose of BPS exposure, BPS could significantly induce the immunomodulation of those tested immune-associated genes and also generation of cellular apoptosis, thus it would be concluded that BPS, similar to BPA, was not a safer chemical to be widely used. Correspondence may be addressed to mingyang@shu.edu.cn (M.Yang) & wkjian@xmu.edu.cn (K.-J. Wang) |
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