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Journal ArticleDOI

Molecular bases of cellular iron toxicity.

John W. Eaton, +1 more
- 01 May 2002 - 
- Vol. 32, Iss: 9, pp 833-840
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TLDR
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.
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This article is published in Free Radical Biology and Medicine.The article was published on 2002-05-01. It has received 353 citations till now. The article focuses on the topics: Mitochondrion & Intracellular.

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Citations
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Mitochondrial Membrane Permeabilization in Cell Death

TL;DR: Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria, meaning that mitochondria coordinate the late stage of cellular demise.
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The role of iron and reactive oxygen species in cell death

TL;DR: The different roles of iron in triggering cell death, targets of iron-dependent ROS that mediate cell death and a new form ofIron-dependent cell death termed ferroptosis are described to suggest new therapeutic avenues to treat cancer, organ damage and degenerative disease.
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Lysosomal membrane permeabilization in cell death

TL;DR: The regulation of LMP is perturbed in cancer cells, suggesting that specific strategies for LMP induction might lead to novel therapeutic avenues.
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Biomarkers of Nutrition for Development (BOND)-Iron Review.

TL;DR: A full appreciation of folate's history as a public health issue, its biology, and an overview of available biomarkers and their interpretation across a range of clinical and population-based uses are provided.
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Abnormal lysosomal trafficking and enhanced exosomal export of cisplatin in drug-resistant human ovarian carcinoma cells

TL;DR: This study shows that the lysosomal compartment of human ovarian carcinoma cells selected for stable resistance to CDDP is markedly reduced in size, and that these cells abnormally sort some lysOSomal proteins and the putative CDDP transporters into an exosomal pathway that also exports CDDP.
References
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Journal ArticleDOI

Rapid evolution of animal mitochondrial DNA.

TL;DR: The rate of evolution of the mitochondrial genome appears to exceed that of the single-copy fraction of the nuclear genome by a factor of about 10 and is likely to be an extremely useful molecule to employ for high-resolution analysis of the evolutionary process.
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Oxidative Stress, Caloric Restriction, and Aging

TL;DR: Support for this hypothesis includes the following observations: (i) Overexpression of antioxidative enzymes retards the age-related accrual of oxidative damage and extends the maximum life-span of transgenic Drosophila melanogaster and (ii) Variations in longevity among different species inversely correlate with the rates of mitochondrial generation of the superoxide anion radical and hydrogen peroxide.
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Mitochondrial diseases in man and mouse.

TL;DR: The essential role of mitochondrial oxidative phosphorylation in cellular energy production, the generation of reactive oxygen species, and the initiation of apoptosis has suggested a number of novel mechanisms for mitochondrial pathology.
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Oxidative damage and mitochondrial decay in aging

TL;DR: Evidence supports the suggestion that age-associated accumulation of mitochondrial deficits due to oxidative damage is likely to be a major contributor to cellular, tissue, and organismal aging.
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