NDLI: Role of the Alkali Labile Sites, Reactive Oxygen Species and Antioxidants in DNA Damage Induced by Methylated Trivalent Metabolites of Inorganic Arsenic

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Role of the Alkali Labile Sites, Reactive Oxygen Species and Antioxidants in DNA Damage Induced by Methylated Trivalent Metabolites of Inorganic Arsenic

Content Provider	Springer Nature Link
Author	Soto Reyes, Ernesto Del Razo, Luz María Valverde, Mahara Rojas, Emilio
Copyright Year	2005
Abstract	In the last decade arsenic metabolism has become an important matter of discussion. Methylation of inorganic arsenic (iAs) to monomethylarsonic acid (MMAV) and dimethylarsinic acid (DMAV) is considered to decrease arsenic toxicity. However, in addition to these pentavalent metabolites, the trivalent metabolites monomethylarsonous (MMAIII) and dimethylarsinous acid (DMAIII) have been identified recently as intermediates in the metabolic pathway of arsenic in cultured human cells. To examine the role of oxidative damage in the generation of DNA strand breaks by methylated trivalent arsenic metabolites, we treated human lymphocytes with both metabolites at non-cytotoxic concentrations. We further tested whether these effects are sensitive to modulation by the antioxidants ascorbate (Vitamin C) and selenomethionine (Se-Met). Both trivalent metabolites produced oxidative stress related DNA damage, consisting of single strand breaks and alkali-labile sites, with MMAIII being more potent at low concentrations than DMAIII. Neither MMAIII nor DMAIII induced DNA-double strand breaks. The oxidative stress response profiles of the metabolites were parallel as determined by lipid peroxidation induction. MMAIII induced peroxidation from the lowest concentration tested, while effects of DMAIII were apparent only at concentrations above 10 μM. The antioxidant Se-Met exhibited a more pronounced inhibition of trivalent arsenic metabolite-induced oxidative-DNA damage than did vitamin C. The present findings suggest that DNA damage by methylated trivalent metabolites at non-cytotoxic concentrations may be mediated by a mix of reactive oxygen and nitrogen oxidized species.
Starting Page	493
Ending Page	506
Page Count	14
File Format	PDF
ISSN	09660844
Journal	BioMetals
Volume Number	18
Issue Number	5
e-ISSN	15728773
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2005-01-01
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	arsenic trivalent genotoxicity DNA oxidative damage alkali labile sites Physical Chemistry Biochemistry
Content Type	Text
Resource Type	Article
Subject	Metals and Alloys Biochemistry, Genetics and Molecular Biology Biomaterials Agricultural and Biological Sciences

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