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Abstract <p>Activation of lipid peroxidation (LPO) in the mitochondria of rat H9c2 cardiomyoblasts and human fibroblasts by the cystine transport inhibitor erastin or glutathione peroxidase 4 inhibitor RSL3 was accompanied by rapid (18&#xa0;h) accumulation of lipofuscin. The mitochondria-targeted antioxidant SkQ1 and redox mediator methylene blue, which prevents the formation of reactive oxygen species (ROS) in the mitochondrial respiratory chain complex&#xa0;I, blocked both mitochondrial LPO and lipofuscin accumulation. These data indicate that mitochondrial LPO serves as a driving force for the accelerated accumulation of lipofuscin in cells. Rapid (24&#xa0;h) lipofuscin formation was observed in isolated heart mitochondria in the presence of iron ions. It was significantly accelerated by ROS generated in the respiratory chain complex&#xa0;I and blocked by SkQ1. The question of whether oxidized components of mitochondria serve as a source for lipofuscin formation in cells remains open. The results obtained suggest possible application of mitochondria-targeted compounds in the treatment of diseases associated with excessive lipofuscin accumulation.</p>

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Mitochondrial Lipid Peroxidation Initiates Rapid Accumulation of Lipofuscin in Cultured Cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月23日

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  • He Huan,
  • Alisa A. Panteleeva,
  • Ruben A. Simonyan,
  • Armine V. Avetisyan,
  • Konstantin G. Lyamzaev,
  • Boris V. Chernyak

摘要

Abstract

Activation of lipid peroxidation (LPO) in the mitochondria of rat H9c2 cardiomyoblasts and human fibroblasts by the cystine transport inhibitor erastin or glutathione peroxidase 4 inhibitor RSL3 was accompanied by rapid (18 h) accumulation of lipofuscin. The mitochondria-targeted antioxidant SkQ1 and redox mediator methylene blue, which prevents the formation of reactive oxygen species (ROS) in the mitochondrial respiratory chain complex I, blocked both mitochondrial LPO and lipofuscin accumulation. These data indicate that mitochondrial LPO serves as a driving force for the accelerated accumulation of lipofuscin in cells. Rapid (24 h) lipofuscin formation was observed in isolated heart mitochondria in the presence of iron ions. It was significantly accelerated by ROS generated in the respiratory chain complex I and blocked by SkQ1. The question of whether oxidized components of mitochondria serve as a source for lipofuscin formation in cells remains open. The results obtained suggest possible application of mitochondria-targeted compounds in the treatment of diseases associated with excessive lipofuscin accumulation.