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<p>Mercuric chloride (HgCl<sub>2</sub>) contamination in aquatic environments poses significant threats to aquatic life, disrupting cellular functions and overall organism health. The impact of sublethal concentrations of HgCl<sub>2</sub> on the freshwater food fish <i>Channa punctatus</i> was examined in this 60-day study, with an emphasis on cellular and molecular reactions, specifically DNA damage and the related signaling pathways. A total of 135 fish were distributed among 3 groups and exposed to sublethal concentrations of HgCl<sub>2</sub> at 0.0 (group I), 0.039 (group II), and 0.078&#xa0;mg L<sup>−1</sup> (group III). Elevated DNA damage was observed in fish exposed to HgCl<sub>2</sub>, as quantified by the comet assay, with the highest DNA tail length in the group exposed to the highest HgCl<sub>2</sub> concentration. A significant (<i>p</i> &lt; 0.05) increase in apoptotic cells (AC), in a dose-dependent manner was also noted. Upregulation of mRNA transcripts for Ataxia telangiectasia mutated (ATM), checkpoint kinase 2 (CHK2), tumor protein (P53), and (P21) indicated enhanced apoptotic and cell cycle arrest mechanisms. The study also highlighted elevated activation of Mitogen-Activated Protein Kinase (MAPK) pathways, particularly p38 MAPK, in the liver and kidney tissues, implicating their role in mediating stress responses and inflammation. Histological analysis and SEM analysis corroborated these molecular findings, revealing significant tissue damage, including hepatic inflammation and renal tubular disorientation. Regression analysis showed strong correlations between various molecular markers in liver tissues, while kidney tissues exhibited variable responses, suggesting different regulatory mechanisms. These results underscore the comprehensive impact of HgCl<sub>2</sub> on cellular integrity and stress response pathways, providing novel insights into the tissue-specific effects of heavy metal toxicity.</p>

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Mutagenic and cellular integrity disruptions in freshwater food fish exposed to mercuric chloride contamination

  • 期刊论文

  • 发表日期：

    2025年7月21日

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  • Manoj Kumar,
  • Shefalee Singh,
  • Anamika Jain,
  • Vidyanand Tiwari,
  • Yashika Awasthi,
  • Kamlesh K. Yadav,
  • Shraddha Dwivedi,
  • Sunil P. Trivedi

摘要

Mercuric chloride (HgCl2) contamination in aquatic environments poses significant threats to aquatic life, disrupting cellular functions and overall organism health. The impact of sublethal concentrations of HgCl2 on the freshwater food fish Channa punctatus was examined in this 60-day study, with an emphasis on cellular and molecular reactions, specifically DNA damage and the related signaling pathways. A total of 135 fish were distributed among 3 groups and exposed to sublethal concentrations of HgCl2 at 0.0 (group I), 0.039 (group II), and 0.078 mg L−1 (group III). Elevated DNA damage was observed in fish exposed to HgCl2, as quantified by the comet assay, with the highest DNA tail length in the group exposed to the highest HgCl2 concentration. A significant (p < 0.05) increase in apoptotic cells (AC), in a dose-dependent manner was also noted. Upregulation of mRNA transcripts for Ataxia telangiectasia mutated (ATM), checkpoint kinase 2 (CHK2), tumor protein (P53), and (P21) indicated enhanced apoptotic and cell cycle arrest mechanisms. The study also highlighted elevated activation of Mitogen-Activated Protein Kinase (MAPK) pathways, particularly p38 MAPK, in the liver and kidney tissues, implicating their role in mediating stress responses and inflammation. Histological analysis and SEM analysis corroborated these molecular findings, revealing significant tissue damage, including hepatic inflammation and renal tubular disorientation. Regression analysis showed strong correlations between various molecular markers in liver tissues, while kidney tissues exhibited variable responses, suggesting different regulatory mechanisms. These results underscore the comprehensive impact of HgCl2 on cellular integrity and stress response pathways, providing novel insights into the tissue-specific effects of heavy metal toxicity.