Mingwei Qian

TL;DR: In this paper, the authors suggest that at least part of the long-term toxicity may involve iron-mediated oxidative damage to the mitochondrial genome with an accumulation of mutational events leading to progressive mitochondrial dysfunction.

TL;DR: It is concluded that long-term damage to cells and organs in iron-overload disorders involves interactions between iron and mitochondrial reactive oxygen species resulting in cumulative damage to mtDNA, impaired synthesis of respiratory chain subunits, and respiratory dysfunction.

TL;DR: It is concluded that interactions between respiring mitochondria and O2 are primarily responsible for hyperoxic cell damage.

TL;DR: It appears that the remarkable oxygen tolerance of HeLa-80 cells derives from tighter coupling of the electron transport chain, which may act to deplete upstream electron-rich intermediates responsible for ROS generation.

TL;DR: It is concluded that chronic iron overload leads to cumulative iron-mediated damage to mitochondrial DNA and impaired synthesis of mitochondrial respiratory chain subunits and similar accumulation of damage to mtDNA may also explain the mitochondrial dysfunction observed in slowly progressing diseases such as neurodegenerative disorders.