ArticleThe Biochemical journal2004
Relocalized redox-active lysosomal iron is an important mediator of oxidative-stress-induced DNA damage.
Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 101 citations in OpenAlex.
- Underlying Mechanism of Lysosomal Membrane Permeabilization in CNS Injury: A Literature Review.Molecular neurobiology · 2025Review
- Mechanisms of Biological Aging with Special Reference to the Skeletal Muscle.Advances in experimental medicine and biology · 2025Review
- Structural features localizing the ferroptosis inhibitor GIF-2197-r to lysosomes.RSC advances · 2023Article
- Altered iron metabolism as a target for ferroptosis induction in head and neck cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- Ferroptosis in viral infection: the unexplored possibility.Acta pharmacologica Sinica · 2022Review
- Role of endolysosome function in iron metabolism and brain carcinogenesis.Seminars in cancer biology · 2021Review
- The epigenetic and morphogenetic effects of molecular oxygen and its derived reactive species in development.Free radical biology & medicine · 2021Article
- Outcomes of Deferoxamine Action on HInternational journal of molecular sciences · 2021Article
- Dysregulated iron metabolism in C. elegans catp-6/ATP13A2 mutant impairs mitochondrial function.Neurobiology of disease · 2020Article
- Chiral polymer modified nanoparticles selectively induce autophagy of cancer cells for tumor ablation.Journal of nanobiotechnology · 2018Article
- Oxidant-induced autophagy and ferritin degradation contribute to epithelial-mesenchymal transition through lysosomal iron.Journal of inflammation research · 2017Article
- CLIC5: a novel ETV6 target gene in childhood acute lymphoblastic leukemia.Haematologica · 2016Article
- Artesunate induces cell death in human cancer cells via enhancing lysosomal function and lysosomal degradation of ferritin.The Journal of biological chemistry · 2014Article
- The anticancer agent di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone (Dp44mT) overcomes prosurvival autophagy by two mechanisms: persistent induction of autophagosome synthesis and impairment of lysosomal integrity.The Journal of biological chemistry · 2014Article
- Oxidative stress, redox signaling, and autophagy: cell death versus survival.Antioxidants & redox signaling · 2014Review
- Disruption of clathrin-mediated trafficking causes centrosome overduplication and senescence.Traffic (Copenhagen, Denmark) · 2014Article
- Noxa couples lysosomal membrane permeabilization and apoptosis during oxidative stress.Free radical biology & medicine · 2013Article
- Radiation protection following nuclear power accidents: a survey of putative mechanisms involved in the radioprotective actions of taurine during and after radiation exposure.Microbial ecology in health and disease · 2012Article
- Chelation of lysosomal iron protects dopaminergic SH-SY5Y neuroblastoma cells from hydrogen peroxide toxicity by precluding autophagy and Akt dephosphorylation.Toxicological sciences : an official journal of the Society of Toxicology · 2011Article
- Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson's, Huntington's, Alzheimer's, prions, bactericides, chemical toxicology and others as examples.Archives of toxicology · 2010Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative damage to nuclear DNA is known to involve site-specific Fenton-type chemistry catalysed by redox-active iron or copper in the immediate vicinity of DNA. However, the presence of transition metals in the nucleus has not been shown convincingly. Recently, it was proposed that a major part of the cellular pool of loose iron is confined within the acidic vacuolar compartment [Yu, Persson, Eaton and Brunk (2003) Free Radical Biol. Med. 34, 1243-1252; Persson, Yu, Tirosh, Eaton and Brunk (2003) Free Radical Biol. Med. 34, 1295-1305]. Consequently, rupture of secondary lysosomes, as well as subsequent relocation of labile iron to the nucleus, could be an important intermediary step in the generation of oxidative damage to DNA. To test this concept we employed the potent iron chelator DFO (desferrioxamine) conjugated with starch to form an HMM-DFO (high-molecular-mass DFO complex). The HMM-DFO complex will enter cells only via fluid-phase endocytosis and remain within the acidic vacuolar compartment, thereby chelating redox-active iron exclusively inside the endosomal/lysosomal compartment. Both free DFO and HMM-DFO equally protected lysosomal-membrane integrity against H2O2-induced oxidative disruption. More importantly, both forms of DFO prevented H2O2-induced strand breaks in nuclear DNA, including telomeres. To exclude the possibility that lysosomal hydrolases, rather than iron, caused the observed DNA damage, limited lysosomal rupture was induced using the lysosomotropic detergent O-methyl-serine dodecylamine hydrochloride; subsequently, hardly any DNA damage was found. These observations suggest that rapid oxidative damage to cellular DNA is minimal in the absence of redox-active iron and that oxidant-mediated DNA damage, observed in normal cells, is mainly derived from intralysosomal iron translocated to the nucleus after lysosomal rupture.
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