Environmental Health and Toxicology Laboratory, Department of Environmental Sciences, School of Life Sciences, Bharathiar University, Coimbatore, Tamil Nadu, India.
Environ Sci Pollut Res Int. 2022 Aug;29(36):54250-54263. doi: 10.1007/s11356-022-19243-6. Epub 2022 Mar 17.
Recent evidences illustrated that the release of aluminum oxide nanoparticles (AlO-NPs) into the biosphere may pose risk to the environment and cause adverse effects on living organisms including humans. The current study assessed the hepatotoxic effects of AlO-NPs on developing chicken embryo and cell culture models. Results demonstrated that AlO-NPs exposure causes histological abnormalities and increased the level of tissue damage markers (ALP, AST, and ALT) in the embryonic liver. Furthermore, increased oxidative stress (TBARS) and impaired function of antioxidant enzymes (SOD, CAT, and GPx) were also observed. Moreover, it adversely affects red blood cells (RBC) morphology, liver metabolism, and stress response gene expression (HO-1 and NQO-1). Dose-dependent ROS generation and cytotoxic response in addition to potentiating effect on tumor necrosis factor alpha (TNF-α)-induced apoptosis (caspase-3 activity) were also observed. Inhibition of p38 mitogen-activated protein kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK) pathways modulates AlO-NPs-induced apoptosis in HepG2 cells. Novel mechanisms behind embryonic hepatotoxicity, cytotoxic potentiating effects, and possible prevention strategies have been explored.
最近的证据表明，氧化铝纳米粒子（AlO-NPs）释放到生物圈中可能对环境构成风险，并对包括人类在内的生物体产生不良影响。本研究评估了 AlO-NPs 对发育中的鸡胚和细胞培养模型的肝毒性作用。结果表明，AlO-NPs 暴露导致胚胎肝脏组织学异常，并增加组织损伤标志物（碱性磷酸酶（ALP）、天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT））的水平。此外，还观察到氧化应激（TBARS）增加和抗氧化酶（SOD、CAT 和 GPx）功能受损。此外，它还会对红细胞（RBC）形态、肝脏代谢和应激反应基因表达（HO-1 和 NQO-1）产生不利影响。还观察到 ROS 的产生和细胞毒性反应呈剂量依赖性，以及对肿瘤坏死因子 alpha（TNF-α）诱导的细胞凋亡（caspase-3 活性）的增强作用。抑制丝裂原活化蛋白激酶（p38 MAPK）和 c-Jun N 端激酶（JNK）通路可调节 HepG2 细胞中 AlO-NPs 诱导的细胞凋亡。探索了胚胎肝毒性、细胞毒性增强作用的潜在预防策略以及背后的新机制。
