Environmental Toxicology & Bioremediation Laboratory, Department of Zoology, University of Lucknow, Lucknow 226007, India.
Environmental Toxicology & Bioremediation Laboratory, Department of Zoology, University of Lucknow, Lucknow 226007, India.
Comp Biochem Physiol C Toxicol Pharmacol. 2021 Jul;245:109032. doi: 10.1016/j.cbpc.2021.109032. Epub 2021 Mar 17.
Sub-lethal exposure of dichlorvos induces oxidative stress, consequent genetic instability and apoptosis coupled with impairments in biochemical, histopathological and transcription of genes in Channa punctatus. Exposure of 5% (0.041 mg/L; E2) and 10% (0.082 mg/L; E3) of 96 h-LC of dichlorvos significantly (p < 0.05) elevated the reactive oxygen species (ROS) generation and activities of SOD and CAT, as compared to control (E1) after 30 d. The maximum reduction in reduced glutathione (GSH) was recorded in the liver (18.53 ± 0.81 μg/mg of protein) and kidney (19.32 ± 0.97 μg/mg of protein); while the total protein contents were also found reduced, 278.38 ± 8.40 μg/mL (liver) and 248.44 ± 7.28 μg/mL (kidney), after 30 days in E3, in comparison to respective controls. Further, significant (p < 0.05) induction in micronuclei (MN) and apoptotic cells (AC), in a dose- and exposure-based manner were also recorded. Moreover, a significant (p < 0.05) up-regulation of p53 (2.51-fold in liver), bax (2.03-fold in liver; 1.99-fold in kidney) and casp3a (2.26-fold in liver; 2.10-fold in kidney) together with an elevated expression of cat (1.73-fold in liver; 1.12-fold in kidney), p53 (1.27-fold in kidney) and apaf-1 (1.72-fold in liver) in fish exposed to higher dose of dichlorvos for 30 d evidently reflects geno-toxicological potential of referenced pesticide. Disturbed biochemical and molecular parameters evince that the fish experienced oxidative stress as is further supported by prominent pathological observations in liver and kidney. Findings are, thus, helpful in organ-specific molecular scanning against aquatic toxicants like dichlorvos.
亚致死浓度敌敌畏暴露会诱导氧化应激，继而导致遗传不稳定性和细胞凋亡，并伴有比目鱼生化、组织病理学和基因转录损伤。与对照组（E1）相比，暴露于 5%（0.041mg/L；E2）和 10%（0.082mg/L；E3）96h-LC 敌敌畏 30d 后，活性氧（ROS）生成和 SOD、CAT 活性显著升高（p<0.05）。肝脏（18.53±0.81μg/mg 蛋白）和肾脏（19.32±0.97μg/mg 蛋白）中还原型谷胱甘肽（GSH）的最大减少量；而总蛋白含量也有所降低，E3 组分别为 278.38±8.40μg/mL（肝脏）和 248.44±7.28μg/mL（肾脏），与各自的对照组相比。此外，还记录到微核（MN）和凋亡细胞（AC）以剂量和暴露为基础的显著诱导（p<0.05）。此外，p53（肝脏中 2.51 倍）、bax（肝脏中 2.03 倍；肾脏中 1.99 倍）和 casp3a（肝脏中 2.26 倍；肾脏中 2.10 倍）的显著上调（p<0.05）以及 cat（肝脏中 1.73 倍；肾脏中 1.12 倍）、p53（肾脏中 1.27 倍）和 apaf-1（肝脏中 1.72 倍）的表达升高，这些都明显反映了参考农药的遗传毒性潜力。受干扰的生化和分子参数表明，鱼类经历了氧化应激，这进一步得到肝脏和肾脏明显的病理观察的支持。这些发现有助于针对敌敌畏等水生毒物进行特定器官的分子扫描。
