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<p>The challenge in addressing methylmercury (MeHg) poisoning primarily lies in devising effective therapeutic strategies. In this study, we explore the potential cytoprotective effects of thiamine pyrophosphate (TPP) as a novel agent to alleviate MeHg-induced complications. Fetal fibroblast cells were exposed to 100 µM MeHg with varying concentrations of TPP (12.5–100 mM). Treated and control cells were analyzed for determination of DNA and protein contents, whereas glutathione and lipid peroxidation levels were measured as oxidative stress markers. TPP reduced the cellular lipid peroxidation and restored the intracellular glutathione levels altered by MeHg, also increasing the cell DNA content in the 12.5 mM TPP treatment group. TPP treatment led to enhanced cell survival, underscoring TPP’s capacity to alleviate MeHg toxicity by improving the antioxidant status. Further studies on additional oxidative stress markers and apoptotic pathways are necessary to fully elucidate the scope and mechanisms of TPP’s cytoprotective effects against MeHg toxicity. While the data in this trial highlight the potential of TPP as a novel therapeutic agent for individuals exposed to MeHg, clinical studies are required to confirm its protective efficacy aiming at developing future mitigation strategies.</p>

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Thiamine Mitigates the Toxicity of Methylmercury in Cultured Fetal Fibroblast Cell Lines

  • 期刊论文

  • 发表日期：

    2025年7月21日

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  • Parisa Sadighara,
  • Jamileh Salar-Amoli,
  • Abbas Barin,
  • Sher Ali,
  • Carlos Augusto Fernandes Oliveira

摘要

The challenge in addressing methylmercury (MeHg) poisoning primarily lies in devising effective therapeutic strategies. In this study, we explore the potential cytoprotective effects of thiamine pyrophosphate (TPP) as a novel agent to alleviate MeHg-induced complications. Fetal fibroblast cells were exposed to 100 µM MeHg with varying concentrations of TPP (12.5–100 mM). Treated and control cells were analyzed for determination of DNA and protein contents, whereas glutathione and lipid peroxidation levels were measured as oxidative stress markers. TPP reduced the cellular lipid peroxidation and restored the intracellular glutathione levels altered by MeHg, also increasing the cell DNA content in the 12.5 mM TPP treatment group. TPP treatment led to enhanced cell survival, underscoring TPP’s capacity to alleviate MeHg toxicity by improving the antioxidant status. Further studies on additional oxidative stress markers and apoptotic pathways are necessary to fully elucidate the scope and mechanisms of TPP’s cytoprotective effects against MeHg toxicity. While the data in this trial highlight the potential of TPP as a novel therapeutic agent for individuals exposed to MeHg, clinical studies are required to confirm its protective efficacy aiming at developing future mitigation strategies.