Department of Zoology, University of Lucknow, Lucknow-226007, India.
Department of Zoology, DBS College, CSJM University, Kanpur, India.
Fish Physiol Biochem. 2022 Oct;48(5):1299-1313. doi: 10.1007/s10695-022-01119-8. Epub 2022 Sep 7.
Chromium has been detected in various water bodies as a harmful metallic stressor to aquatic organisms. This study aimed to investigate the mechanism associated with autophagy, oxidative stress, and genotoxicity after chromium (Cr) exposure (1/20th of 96 h-LC50, 1/10th of 96 h-LC50, and 1/5th of 96 h-LC50 of Cr) of common food fish Channa punctatus. The mRNA levels of autophagy-related genes ATG5, LC3, GABARAP, and mTOR were assessed in the liver and kidney tissue of fish. An upregulation of ATG5, LC3, and GABARAP was observed in both liver and kidney tissue samples, while mTOR showed transcriptional downregulation in both the tissue samples. This depicts autophagic vesicle formation due to stress signals. All the studied oxidative stress markers SOD, CAT, GSH, GR, and GPx showed an increase in the activity level of treated groups in a dose-dependent manner. Particularly, SOD and CAT have shown a significant elevation in activity level. ROS levels in blood cells increased significantly (p < 0.05) in all the treated groups (groups II, III, and IV) in a time-dependent manner as compared to the control (group I). There was a significant induction in MN frequency in all the treated groups. The highest frequency of micronuclei induced by Cr was recorded in group IV after 28 days of exposure period. Collectively, it can be concluded that the information about Cr-induced oxidative stress-mediated autophagy in vital organs of fish Channa punctatus remains largely obscure hitherto; to fill the aforesaid gap, this study was undertaken, which gives a snapshot for the mechanisms of autophagy induced by Cr in fish. HIGHLIGHTS: • Chronic exposure to Cr induces eco-toxicological manifestations in a fish Channa punctatus. • Altered transcriptional profile of autophagy-related genes suggests autophagic vesicle formation due to stress signals. • Increased activity levels of oxidative stress biomarkers reveal that Cr annihilates antioxidative defense system in fish. • Genotoxicity due to chromium exposure is evident by increased frequency of MN in red blood cells of fish. • The information presented in this study is helpful to get an insight into the mechanism of Cr-induced oxidative stress-mediated induction of autophagy in the liver and kidney of Channa punctatus.
铬在各种水体中被检测到，是一种对水生生物有害的金属应激物。本研究旨在研究在暴露于铬（Cr）后（Cr 的 96 小时 LC50 的 1/20、1/10 和 1/5）对食用鱼 Channa punctatus 的肝和肾组织中与自噬、氧化应激和遗传毒性相关的机制。评估了自噬相关基因 ATG5、LC3、GABARAP 和 mTOR 在鱼肝脏和肾脏组织中的 mRNA 水平。在肝和肾组织样本中均观察到 ATG5、LC3 和 GABARAP 的上调，而 mTOR 在两种组织样本中均表现出转录下调。这描述了由于应激信号导致自噬小泡的形成。所有研究的氧化应激标志物 SOD、CAT、GSH、GR 和 GPx 的活性水平在处理组中均呈剂量依赖性增加。特别是 SOD 和 CAT 的活性水平显著升高。血细胞中的 ROS 水平在所有处理组（第二、三和四组）中均呈时间依赖性显著升高（与对照组（第一组）相比）。在所有处理组中，MN 频率均显著升高。在暴露期 28 天后，Cr 诱导的微核频率最高。综上所述，可以得出结论，迄今为止，有关 Cr 诱导的鱼类重要器官中氧化应激介导的自噬的信息在很大程度上仍然不清楚；为了填补上述空白，进行了这项研究，该研究为 Cr 诱导鱼类自噬的机制提供了一个快照。 要点： • 慢性暴露于 Cr 会在鱼类 Channa punctatus 中引起生态毒性表现。 • 自噬相关基因的转录谱改变表明由于应激信号导致自噬小泡的形成。 • 氧化应激生物标志物活性水平的增加表明 Cr 破坏了鱼类的抗氧化防御系统。 • 由于铬暴露导致的遗传毒性，在鱼类红细胞中的 MN 频率增加。 • 本研究提供的信息有助于深入了解 Cr 诱导的氧化应激介导的 Channa punctatus 肝和肾自噬的机制。
