Zinc oxide nanoparticles cause hepatotoxicity in rare minnow (Gobiocypris rarus) via ROS-mediated oxidative stress and apoptosis activation and inhibition of lipid peroxidation
文献类型： 外文期刊
作者： Su, Liangxia 1 ; Li, Huanhuan 1 ; Wang, Jiahuan 1 ; Wu, Jinming 2 ; Wan, Jing 1 ; He, Yongfeng 3 ; Liu, Jun 1 ;
作者机构： 1.Wuhan Polytech Univ, Engn Res Ctr Feed Prot Resources Agr By Prod, Hubei Key Lab Anim Nutr & Feed Sci, Minist Educ, Wuhan, Peoples R China
2.Chinese Acad Fishery Sci, Yangtze River Fisheries Res Inst, Key Lab Freshwater Biodivers Conservat, Minist Agr & Rural Affairs China, Wuhan 430223, Peoples R China
3.Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan, Hubei, Peoples R China
关键词： Zinc oxide nanoparticle; Liver injuries; Gobiocypris rarus; ROS-mediated oxidative stress and apoptosis; Lipid metabolism
期刊名称：AQUACULTURE REPORTS （ 影响因子：3.7； 五年影响因子：4.0 ）
ISSN： 2352-5134
年卷期： 2024 年 38 卷
页码：
收录情况： SCI
摘要： Zinc oxide nanoparticles (ZnO NPs) measuring 30 +/- 10 nm in diameter are utilized in various applications, including batteries, plastics, ceramics, cosmetics, flame retardants, and food. However, their potential impact and risk on aquatic ecosystems remain unclear. This study examined the hepatotoxic effects of dietary ZnO NPs in rare minnow. Three hundred rare minnows were fed diets containing 0 mg/kg, 20 mg/kg and 60 mg/kg of ZnO NPs for 60 days, with hepatotoxicity assessments at 15-day intervals. The histological data showed that ZnO NPs severely damage liver tissues, causing cytoplasmic vacuolization and irregular or missing nuclei. The treatment groups showed a significant rise in the liver injury index (P < 0.05). Moreover, there was a notable increase in zinc accumulation in the ZnO NPs groups compared to the control group (P < 0.05). ZnO NPs also reduced body weight and hepato-somatic index (HSI) in rare minnows. The enzyme activity results showed elevated levels of reactive oxygen species (ROS), total cholesterol (T-CHO), triglyceride (TG), acetyl Coa carboxylase (ACC), and fatty acid synthase (FAS) in the ZnO NPs fed groups, while total antioxidant capacity (TAOC) and malondialdehyde (MDA) decreased. Further investigation found that accumulation of ZnO NPs in the liver tissues up-regulated the levels of genes related to antioxidant (mn-sod, cat and nf-kappa b), pro-apoptotic (bax) and lipogenesis (gpat3, dgat1a and dgat1b), while down-regulating genes associated with lipid catabolism (cpt1 and tpi1). These findings suggest that dietary ZnO NPs cause hepatotoxicity by inducing oxidative stress through ROS, triggering apoptosis, and inhibiting lipid peroxidation. The results indicate that ZnO NPs may pose a significant threat to aquatic animals and ecosystems.
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