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. 2005 Oct;12(10):855-60.
doi: 10.1038/nsmb996. Epub 2005 Oct 2.

AlkB reverses etheno DNA lesions caused by lipid oxidation in vitro and in vivo

James C Delaney  1 , Lisa Smeester, Cintyu Wong, Lauren E Frick, Koli Taghizadeh, John S Wishnok, Catherine L Drennan, Leona D Samson, John M Essigmann
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AlkB reverses etheno DNA lesions caused by lipid oxidation in vitro and in vivo

"V体育ios版" James C Delaney et al. Nat Struct Mol Biol. 2005 Oct.

Abstract

Oxidative stress converts lipids into DNA-damaging agents. The genomic lesions formed include 1,N(6)-ethenoadenine (epsilonA) and 3,N(4)-ethenocytosine (epsilonC), in which two carbons of the lipid alkyl chain form an exocyclic adduct with a DNA base. Here we show that the newly characterized enzyme AlkB repairs epsilonA and epsilonC. The potent toxicity and mutagenicity of epsilonA in Escherichia coli lacking AlkB was reversed in AlkB(+) cells; AlkB also mitigated the effects of epsilonC. In vitro, AlkB cleaved the lipid-derived alkyl chain from DNA, causing epsilonA and epsilonC to revert to adenine and cytosine, respectively. Biochemically, epsilonA is epoxidized at the etheno bond. The epoxide is putatively hydrolyzed to a glycol, and the glycol moiety is released as glyoxal VSports手机版. These reactions show a previously unrecognized chemical versatility of AlkB. In mammals, the corresponding AlkB homologs may defend against aging, cancer and oxidative stress. .

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