Department of Toxicology and Nutritional Science, School of Public Health, Nanjing Medical University, 818 East Tianyuan Rd, Jiangning, Nanjing, Jiangsu, 211166, China.
Research Centre for Bone and Stem Cells, Department of Human Anatomy, Key Laboratory for Aging & Disease, The State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
J Hazard Mater. 2020 Jul 15;394:122549. doi: 10.1016/j.jhazmat.2020.122549. Epub 2020 Apr 10.
Bisphenol S is considered as a safer alternative to bisphenol A. In the present study, we used murine macrophages to investigate the effects of BPS exposure on oxidative stress and inflammatory response as well as the underlying mechanism. Cells were exposed to BPS at various concentrations for short period of times. Results showed that 10 M BPS triggered oxidative stress by increasing ROS/RNS production, increased the levels of oxidant enzyme NOX1/2, and decreased the levels of antioxidant enzymes SOD1/2, CAT and GSH-Px. 10 M BPS exposure significantly induced the production of proinflammatory mediators. Activation of the NLRP3 inflammasome, TLR4, and MAPK pathways was involved in this process. Furthermore, we illustrated that NAC pretreatment diminished these effects triggered by BPS exposure. Collectively, our data suggested that BPS at a dose relevant to human serum concentration induced oxidative stress and inflammatory response in macrophages. These novel findings shed light on the concerns regarding the potential adverse effects of BPS exposure that requires further careful attention.
双酚 S 被认为是双酚 A 的更安全替代品。在本研究中，我们使用小鼠巨噬细胞来研究 BPS 暴露对氧化应激和炎症反应的影响及其潜在机制。细胞短时间暴露于不同浓度的 BPS 中。结果表明，10μM 的 BPS 通过增加 ROS/RNS 的产生引发氧化应激，增加氧化酶 NOX1/2 的水平，降低抗氧化酶 SOD1/2、CAT 和 GSH-Px 的水平。10μM 的 BPS 暴露显著诱导促炎介质的产生。NLRP3 炎性小体、TLR4 和 MAPK 途径的激活参与了这一过程。此外，我们表明，NAC 预处理可减轻 BPS 暴露引起的这些作用。总之，我们的数据表明，与人类血清浓度相关剂量的 BPS 诱导巨噬细胞中的氧化应激和炎症反应。这些新发现引起了对 BPS 暴露潜在不良影响的关注，需要进一步谨慎关注。
