Oxidative stress, inflammation, and steatosis elucidate the complex dynamics of HgCl2 induced liver damage in Channa punctata.

Water bodies are highly pollution-prone areas in which mercury (Hg) is considered as a major menace to aquatic organisms. However, the information about the toxicity of mercuric chloride (HgCl2) in a vital organ such as the liver of fish is still inadequate. This study aimed to assess the impact of mercuric chloride (HgCl2) exposure on the liver of Channa punctata fish over 15, 30, and 45 days, at two different concentrations (0.039 mg/L and 0.078 mg/L). Mercury is known to be a significant threat to aquatic life, and yet, information regarding its effects on fish liver remains limited. The results of this study demonstrate that exposure to HgCl2 significantly increases oxidative stress markers, such as lipid peroxidation (LPO) and protein carbonyls (PC), as well as the levels of serum glutamic-oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) in the fish. Additionally, the transcriptional and protein analysis of specific genes and molecules associated with necroptosis and inflammation, such as ABCG2, TNF α, Caspase 3, RIPK 3, IL-1ß, Caspase-1, IL-18, and RIPK1, confirm the occurrence of necroptosis and inflammation in the liver. Histopathological and ultrastructural examinations of the liver tissue further reveal a significant presence of liver steatosis. Interestingly, the upregulation of PPARα suggests that the fish's body is actively responding to counteract the effects of liver steatosis. This study provides a comprehensive analysis of oxidative stress, biochemical changes, gene expression, protein profiles, and histological findings in the liver tissue of fish exposed to mercury pollution in freshwater environments.

Copper-induced Genotoxicity, Oxidative Stress, and Alteration in Transcriptional Level of Autophagy-associated Genes in Snakehead Fish Channa punctatus.

Copper (Cu) is an essential and important trace element for some significant life processes for most organisms. However, an excessive amount of Cu can be highly toxic. The present study was conducted to elucidate the oxidative stress-induced alteration in transcriptional level of autophagy-related genes in the liver and kidney tissue of fish Channa punctatus after treatment with three different sublethal concentrations of CuSO4 for 28 days. All the studied enzymatic and non-enzymatic oxidative stress markers viz. superoxide dismutase-SOD, catalase-CAT, glutathione peroxidase-GPx, glutathione reductase-GR, and glutathione-GSH showed an increase in their activity levels in the treated groups in a dose-dependent manner. Particularly SOD and CAT have shown a significant hike in activity levels. ROS levels in blood cells increased significantly (p < 0.05) in all the treated groups, i.e., Group II-1/20th of 96 h-LC50 (0.2 mg/L), Group III-1/10th of 96 h-LC50 (0.4 mg/L), and Group IV-1/5 h of 96 h-LC50 (0.8 mg/L) of Cu2+ in a dose-dependent manner as compared to control (Group I). The upregulation in mRNA levels of autophagy-related genes Microtubule-associated protein 1 light chain 3 (LC3), Gamma-aminobutyric acid receptor-associated protein precursor (Gabarap), and Golgi-associated ATPase enhancer of 16 kDa (GATE16), autophagy-related 5 (ATG5) was observed while mammalian target of rapamycin (mTOR) showed downregulation in the liver and kidney tissue of fish. The decrease in mTOR and increase in ATG5 gene expression projects autophagic vesicle formation due to oxidative stress. There was significant induction in micronuclei (MN) frequency in all the treated groups. The highest frequency of MN induced by Cu2+ was recorded in Group IV after 28 days of the exposure period. Thus, it can be concluded that the available information about Cu2+-induced oxidative stress-mediated autophagy in the liver and kidney of fish C. punctatus remains largely unclear to date, so to fill the aforesaid gap, the present study was undertaken, which gives an insight for the mechanisms of autophagy induced by Cu2+ in fish.

Altered transcriptional levels of autophagy-related genes, induced by oxidative stress in fish Channa punctatus exposed to chromium.

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 (Cr6+) exposure (1/20th of 96 h-LC50, 1/10th of 96 h-LC50, and 1/5th of 96 h-LC50 of Cr6+) 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 Cr6+ was recorded in group IV after 28 days of exposure period. Collectively, it can be concluded that the information about Cr6+-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 Cr6+ in fish. HIGHLIGHTS: • Chronic exposure to Cr6+ 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 Cr6+ 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 Cr6+-induced oxidative stress-mediated induction of autophagy in the liver and kidney of Channa punctatus.