@article {4717,
	title = {Arsenic species that cause release of iron from ferritin and generation of activated oxygen},
	journal = {Archives of Biochemistry and Biophysics},
	volume = {382},
	number = {2},
	year = {2000},
	note = {ISI Document Delivery No.: 367PNTimes Cited: 90Cited Reference Count: 61},
	month = {Oct},
	pages = {195-202},
	type = {Article},
	abstract = {The in vitro effects of four different species of arsenic (arsenate, arsenite, monomethylarsonic acid, and dimethylarsinic acid) in mobilizing iron from horse spleen ferritin under aerobic and anaerobic conditions were investigated. Dimethylarsinic acid (DMA((V))) and dimethylarsinous acid (DMA((III))) significantly released iron from horse spleen ferritin either with or without the presence of ascorbic acid, a strong synergistic agent. Ascorbic acid-mediated iron release was time-dependent as well as both (DMA((III))) and ferritin concentration-dependent. Iron release from ferritin by DMA((III)) alone or with ascorbic acid was not significantly inhibited by superoxide dismutase (150 or 300 units/ml). However, the iron release was greater under anaerobic conditions (nitrogen gas), which indicates direct chemical reduction of iron from ferritin by DMA((III)), with or without ascorbic acid. Both DMA((V)) and DMA((III)) released iron from both horse spleen and human liver ferritin. Further, the release of ferritin-iron by DMA((III)) with ascorbic acid catalyzed bleomycin-dependent degradation of calf thymus DNA. These results indicate that exogenous methylated arsenic species and endogenous ascorbic acid can cause (a) the release of iron from ferritin, (b) the iron-dependent formation of reactive oxygen species, and (c) DNA damage. This reactive oxygen species pathway could be a mechanism of action of arsenic carcinogenesis in man. (C) 2000 Academic Press.},
	keywords = {arsenic, ascorbic acid, BIOCHEMICAL PARAMETERS, DAMAGE, DIMETHYLARSINIC ACID, DNA-DAMAGE, ferritin, FREE-RADICALS, INORGANIC ARSENICS, iron, LIPID-PEROXIDATION, MAIN METABOLITE, OXIDATIVE, oxygen species, REACTIVE, reactive oxygen, VITAMIN-C},
	isbn = {0003-9861},
	url = {<Go to ISI>://000090070800005},
	author = {Ahmad, S. and Kitchin, K. T. and Cullen, W. R.}
}
@article {4199,
	title = {Active oxygen species formation in synaptosomes exposed to an aluminum chelator},
	journal = {Neurotoxicology and Teratology},
	volume = {20},
	number = {3},
	year = {1998},
	note = {ISI Document Delivery No.: ZU241Times Cited: 4Cited Reference Count: 37},
	month = {May-Jun},
	pages = {317-320},
	type = {Article},
	abstract = {This study evaluates the potential of two chelators, 1,2-dimethyl-3-hydroxypyridine-4-one (Hdpp) and 1-n-butyl-2-methyl-3-hydroxypyridin-4-one (Hnbp), to modulate cerebral rates of free radical production. The fluorometric assay for 2{\textquoteright},7{\textquoteright}-dichlorofluorescein, which is formed by oxidation of a nonfluorescent precursor (2{\textquoteright},7{\textquoteright}-dichlorofluorescin diacetate), was used to assay reactive oxygen species (ROS) production. The chelator Hdpp alone and the aluminum complexes of each chelator, Al(dpp)(3) and Al(nbp)(3), all inhibited basal rates of generation of ROS within a rat cerebral synaptosomal fraction. In the presence of an iron salt (1 mu M FeSO4), a major enhancement of syn aptosomal ROS formation was apparent. However, with the addition of an equimolar concentration of Hdpp, Al(dpp)(3), or Al(nbp)(3), this stimulation was completely abolished. The N-substituted-3-hydroxy-4-pyridinones have been proposed to be of clinical utility for the removal of iron or aluminum from tissues. The clinical potential of this class of chelator may be enhanced by their ability to inhibit iron-related oxidative events. (C) 1998 Elsevier Science Inc.},
	keywords = {3-HYDROXY-4-PYRIDINONES, aluminum, ALZHEIMERS-DISEASE, CHELATOR, COMPLEXES, DEFEROXAMINE, DESFERRIOXAMINE, Free Radicals, hydroxypyridinones, iron, LIPID-PEROXIDATION, metal chelation, NEUROFIBRILLARY TANGLES, QUANTITATION, RATS, reactive oxygen species},
	isbn = {0892-0362},
	url = {<Go to ISI>://000074176500011},
	author = {Bondy, S. C. and Tseng, H. and Orvig, Chris}
}
