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双酚 A 诱导的抗氧化剂失衡和细胞因子改变导致罗非鱼幼虫发育期间的免疫抑制。

Bisphenol-A induced antioxidants imbalance and cytokines alteration leading to immune suppression during larval development of Labeo rohita.

机构信息

Department of Zoology, GC University, Lahore, Pakistan.

Department of Physiology and Cell Biology, University of Health Sciences, Lahore, Pakistan.

出版信息

Environ Sci Pollut Res Int. 2020 Jul;27(21):26800-26809. doi: 10.1007/s11356-020-08959-y. Epub 2020 May 7.

DOI:10.1007/s11356-020-08959-y
PMID:32382907
Abstract

Recently, the oxidative stress and immunotoxicity biomarkers have been extensively used in embryotoxicity using fish embryos as promising models especially after exposure to chemical-like environmental estrogens. Bisphenol-A (BPA) is an estrogenic endocrine disruptor and is ubiquitous in the aquatic environment. Larvae of Labeo rohita were exposed to low concentrations of BPA (10, 100, 1000 μg/l) for 21 days. Innate immune system, antioxidants parameters, and developmental alterations were used as biomarkers. Exposure to BPA caused developmental abnormalities including un-inflated swim bladder, delayed yolk sac absorption, spinal curvature, and edema of pericardium. Lipid peroxidation increased and activity of catalase (p < 0.05), superoxide dismutase (p < 0.05), and glutathione peroxidase (p < 0.01) decreased after exposure to BPA. Level of reduced glutathione also decreased (p < 0.05) in BPA-exposed group. Lower expression of tumor necrosis factor-α (p < 0.05) and interferon-γ (p < 0.001) was observed in BPA-exposed groups while expression of interleukin-10 increased (p < 0.05) in larvae exposed to 10 μg/l BPA. Moreover, exposure of BPA caused a concentration-dependent increase in expression of heat shock protein 70 (p < 0.05). The present study showed that the exposure to BPA in early life stages of Labeo rohita caused oxidative stress and suppress NF-κB signaling pathway leading to immunosuppression. The results presented here demonstrate the cross talk between heat shock protein 70 and cytokines expression.

摘要

最近,氧化应激和免疫毒性生物标志物已被广泛用于鱼类胚胎的胚胎毒性研究,尤其是在接触类似化学的环境雌激素后。双酚 A(BPA)是一种雌激素内分泌干扰物,广泛存在于水生环境中。罗非鱼幼鱼在低浓度 BPA(10、100、1000μg/l)中暴露 21 天。使用先天免疫系统、抗氧化参数和发育变化作为生物标志物。BPA 暴露导致发育异常,包括未充气的鳔、卵黄囊吸收延迟、脊柱弯曲和心包水肿。暴露于 BPA 后,脂质过氧化增加,过氧化氢酶(p<0.05)、超氧化物歧化酶(p<0.05)和谷胱甘肽过氧化物酶(p<0.01)的活性降低。还原型谷胱甘肽水平也降低(p<0.05)。BPA 暴露组肿瘤坏死因子-α(p<0.05)和干扰素-γ(p<0.001)的表达降低,而白细胞介素-10的表达在暴露于 10μg/l BPA 的幼鱼中增加(p<0.05)。此外,BPA 暴露导致热休克蛋白 70(HSP70)的表达呈浓度依赖性增加(p<0.05)。本研究表明,BPA 在罗非鱼早期生活阶段的暴露会导致氧化应激和抑制 NF-κB 信号通路,从而导致免疫抑制。这里呈现的结果表明热休克蛋白 70 和细胞因子表达之间存在串扰。

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