急性双酚 A 暴露引发蚯蚓超氧化物-一氧化氮失衡和免疫能力受损

B. O. Turra, I. D. da Cruz, N. A. C. Bonotto, C. F. Teixeira, M. Mastella, Wellington Claudino Ferreira, I. Jung, E. A. S. Musachio, M. Prigol, F. Barbisan
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引用次数: 0

摘要

双酚 A(BPA)是一种干扰内分泌的分子,与多种非传染性慢性疾病的风险有关。我们推测,双酚 A 会引发氧化改变,改变免疫能力,导致生理机能失调。为了评估双酚 A 对氧化和免疫系统的影响,我们在含有不同浓度双酚 A 的培养基中饲养了加利福尼亚蚯蚓 24 小时和 72 小时。我们用蚯蚓的体腔细胞来评估双酚 A 对氧化指标、细胞增殖和凋亡的影响,并通过酵母暴露试验和免疫反应相关基因的调控来研究双酚 A 对免疫能力的影响。低浓度的双酚 A 诱导腹膜细胞增殖、超氧化物/氧化氮水平失衡、微核频率升高和细胞凋亡。双酚 A 还诱导 Amp1 基因过表达和低效率捕获死亡酵母。DNA 损伤与先天性免疫代谢变化之间的联系可能与双酚 A 的作用有关,而双酚 A 与生理紊乱和非传染性慢性疾病的风险有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Acute Bisphenol-A exposure triggers superoxide-nitric oxide imbalance and immunocompetence impairment of Eisenia fetida earthworm
Bisphenol-A (BPA) is an endocrine-disrupting molecule associated with the risk of several non-transmissible chronic diseases. We postulated that BPA triggers oxidative alterations, altering immunocompetence and contributing to physiological dysfunction. To evaluate the effects of BPA on the oxidative and immune system, Californian earthworms were reared in a culture medium containing different BPA concentrations for 24 and 72 h. Coelomocytes were used to evaluate the effects of BPA on oxidative markers, cellular proliferation, and apoptosis, and immunocompetence effects were investigated by yeast-exposure assay and the modulation of genes related to immune response. Low BPA concentrations induced coelomocyte proliferation, imbalanced superoxide/NO levels, higher micronucleus frequency, and apoptosis. BPA also induced Amp1 gene overexpression and a low efficiency of dead yeast capture. The association between DNA damage and changes in innate immune metabolism could be related to the action of BPA, which is associated with the risk of physiological disturbances and non-transmissible chronic diseases.
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