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<p>Methylmercury (MeHg) can have profound effects on cells of the nervous system, leading to DNA damage, oxidative stress, neuroinflammation, and cell death. In this study, transcriptomic changes in neuronal (B103) and glial (C6) cell lines from rat (<i>Rattus norvegicus</i>) were investigated after exposure to non-lethal concentrations of MeHg. In neuronal cells, low MeHg concentration (0.1&#xa0;µM) affected signaling pathways related to protein metabolism and signal transduction, including those involving glycosylphosphatidylinositol (GPI)-anchored proteins (GPI-APs) and 3β-hydroxysteroid dehydrogenase (3β-HSD). Conversely, high MeHg concentration (2.8&#xa0;µM) primarily disrupted ion transport pathways (e.g. SLC-mediated transmembrane transport) and oxidative stress responses. In glial cells, a low concentration of MeHg (0.1&#xa0;µM) impaired the <i>Rho-GTPase</i> pathway, while a higher concentration (6.3&#xa0;µM) impaired sodium–potassium-exchange-ATPase (Na+/K+-ATPase) activity. MicroRNA profiling showed that <i>MAPK</i> signaling was impaired by MeHg in both cell lines regardless of exposure level, with the <i>mmu-miR-466</i> family consistently involved. Furthermore, ontology analysis of human phenotypes linked these transcriptomic changes to abnormalities in the nervous system and neurological development, establishing a link between MeHg exposure and disturbances in brain morphology and cognitive impairment. These findings elucidate critical molecular mechanisms underlying MeHg-induced neurotoxicity and underscore the far-reaching implications for cellular function and central nervous system health.</p>

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Effects of methylmercury exposure on the transcriptomes of cell lines from the rat central nervous system

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月6日

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  • Laís Teixeira Bonfim,
  • Carolina Koury Nassar Amorim,
  • Edivaldo Herculano Corrêa de Oliveira,
  • Wallax Augusto Silva Ferreira

摘要

Methylmercury (MeHg) can have profound effects on cells of the nervous system, leading to DNA damage, oxidative stress, neuroinflammation, and cell death. In this study, transcriptomic changes in neuronal (B103) and glial (C6) cell lines from rat (Rattus norvegicus) were investigated after exposure to non-lethal concentrations of MeHg. In neuronal cells, low MeHg concentration (0.1 µM) affected signaling pathways related to protein metabolism and signal transduction, including those involving glycosylphosphatidylinositol (GPI)-anchored proteins (GPI-APs) and 3β-hydroxysteroid dehydrogenase (3β-HSD). Conversely, high MeHg concentration (2.8 µM) primarily disrupted ion transport pathways (e.g. SLC-mediated transmembrane transport) and oxidative stress responses. In glial cells, a low concentration of MeHg (0.1 µM) impaired the Rho-GTPase pathway, while a higher concentration (6.3 µM) impaired sodium–potassium-exchange-ATPase (Na+/K+-ATPase) activity. MicroRNA profiling showed that MAPK signaling was impaired by MeHg in both cell lines regardless of exposure level, with the mmu-miR-466 family consistently involved. Furthermore, ontology analysis of human phenotypes linked these transcriptomic changes to abnormalities in the nervous system and neurological development, establishing a link between MeHg exposure and disturbances in brain morphology and cognitive impairment. These findings elucidate critical molecular mechanisms underlying MeHg-induced neurotoxicity and underscore the far-reaching implications for cellular function and central nervous system health.