Kamila Sreejata, Dey Koushik Kumar, Das Tanmoy, Chattopadhyay Ansuman
Department of Zoology, Visva-Bharati, Santiniketan, West Bengal 731235, India.
Department of Zoology, Visva-Bharati, Santiniketan, West Bengal 731235, India.
Environ Toxicol Pharmacol. 2025 Mar;114:104640. doi: 10.1016/j.etap.2025.104640. Epub 2025 Jan 16.
The present study investigated the individual and mixture effects of Arsenic (As) and Chromium (Cr) at their environmental concentrations in zebrafish (Danio rerio). After 15, 30 and 60 days of exposure, increased frequencies of erythrocytic nuclear abnormalities (ENAs) were noticed. After 60 days of exposure, DNA damage was observed in liver and base excision DNA repair (BER) and mismatch DNA repair (MMR) pathways were studied to know the cellular responses. Altered expression of BER (ogg1, apex1, creb1, polb) and MMR (mlh1, msh2, msh6) genes indicated inhibition of DNA repair. Downregulation of tumor suppressor genes (p53 and brca2) occurred in mixture group. Downregulation of bax, caspase9 and decreased bax/bcl2 ratio indicated prevention of intrinsic apoptotic pathway in treated groups. Results indicated As and Cr-induced predisposition to genomic instability and carcinogenesis in zebrafish. Overall, this study confirmed the additive genotoxic effects of As and Cr in zebrafish erythrocytes and in liver after chronic exposure.
本研究调查了环境浓度下砷(As)和铬(Cr)对斑马鱼(Danio rerio)的个体及混合效应。暴露15天、30天和60天后,观察到红细胞核异常(ENA)频率增加。暴露60天后,在肝脏中观察到DNA损伤,并研究了碱基切除DNA修复(BER)和错配DNA修复(MMR)途径以了解细胞反应。BER(ogg1、apex1、creb1、polb)和MMR(mlh1、msh2、msh6)基因的表达改变表明DNA修复受到抑制。混合组中肿瘤抑制基因(p53和brca2)发生下调。bax、caspase9的下调以及bax/bcl2比值的降低表明处理组中内在凋亡途径受到抑制。结果表明,砷和铬可导致斑马鱼基因组不稳定和致癌倾向。总体而言,本研究证实了慢性暴露后砷和铬对斑马鱼红细胞和肝脏具有相加的遗传毒性效应。