Erciyes University Faculty of Pharmacy, Department of Pharmaceutical Toxicology, Kayseri, Turkey.
Hacettepe University Faculty of Pharmacy, Department of Pharmaceutical Toxicology, Ankara, Turkey.
Arh Hig Rada Toksikol. 2022 Jul 7;73(2):148-157. doi: 10.2478/aiht-2022-73-3629.
The aim of this study was to investigate oxidative stress induced by perfluorooctanoic acid (PFOA) in the brain and liver tissues of Balb/c mice as well as protective effects of taurine and coenzyme Q (CoQ) in both organs. For this purpose, animals were treated with PFOA (15 and 30 mg/kg) orally and their lipid peroxidation, total glutathione levels (GSH), and antioxidant enzyme activities measured and both tissues analysed for histopathological changes. Our results showed a dose-dependent decrease in body weight and increase in relative brain and liver weights, PFOA-induced lipid peroxidation and reduced glutathione peroxidase (GPx) activity in the brain tissue, and changes in GSH levels, GPx, superoxide dismutase (Cu-Zn SOD), and catalase (CAT) activities in the liver tissue. Pre-treatment with taurine or CoQ provided protection against PFOA-induced Cu-Zn SOD reduction in the liver tissue. Our findings evidence the depleting effect of PFOA on antioxidative systems and confirm that PFOA exerts its (neuro)toxicity through oxidative stress, but further research is needed to identify the exact toxicity mechanisms, especially in the brain.
本研究旨在探讨全氟辛酸(PFOA)在 Balb/c 小鼠脑和肝组织中诱导的氧化应激,以及牛磺酸和辅酶 Q(CoQ)在这两个器官中的保护作用。为此,动物经口给予 PFOA(15 和 30mg/kg),并测量其脂质过氧化、总谷胱甘肽水平(GSH)和抗氧化酶活性,同时分析两个组织的组织病理学变化。结果表明,体重呈剂量依赖性下降,脑和肝的相对重量增加,PFOA 诱导脑组织脂质过氧化和谷胱甘肽过氧化物酶(GPx)活性降低,肝组织 GSH 水平、GPx、超氧化物歧化酶(Cu-Zn SOD)和过氧化氢酶(CAT)活性改变。牛磺酸或 CoQ 的预处理可防止 PFOA 诱导肝组织 Cu-Zn SOD 减少。我们的研究结果证明了 PFOA 对抗氧化系统的消耗作用,并证实 PFOA 通过氧化应激发挥其(神经)毒性,但需要进一步研究以确定确切的毒性机制,特别是在大脑中。