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DNA strand scission by Fe(III) 2‐methylaminopyridine complex and hydrogen peroxide
Author(s) -
ElSayed Ibrahim H.,
ElMasry Samir A.
Publication year - 2003
Publication title -
biotechnology and applied biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.468
H-Index - 70
eISSN - 1470-8744
pISSN - 0885-4513
DOI - 10.1042/ba20030047
Subject(s) - hydrogen peroxide , dna , chemistry , superoxide dismutase , sodium azide , mutagenesis , dna damage , bond cleavage , stereochemistry , biochemistry , microbiology and biotechnology , enzyme , biology , mutation , gene , catalysis
Oxidative DNA damage is involved in mutagenesis, carcinogenesis, aging, radiation effects and also in the action of several anticancer drugs. Accumulated evidence indicates that iron may play an important role in these processes. The conversion of the closed circular double‐stranded supercoiled plasmid pcDNA3 into the nicked circular and linear forms was used to investigate DNA nicking induced by the reactions of an iron complex of 2‐methylaminopyridine (L), which exhibited a pronounced superoxide dismutase‐mimetic activity and antitumour activity with H 2 O 2 . Hence the dose–response curve for the [FeL 2 Cl 2 ]Cl·H 2 O‐mediated H 2 O 2 ‐dependent DNA nicking was studied. For a fixed concentration of [FeL 2 Cl 2 ]Cl·H 2 O (25 μM), the concentration of H 2 O 2 producing a maximum extent of DNA nicking was 100 μM. The effects of these two constituents are synergistic. The biological antioxidants such as glycerol, sodium azide and superoxide dismutase significantly inhibited DNA breakage induced by [FeL 2 Cl 2 ]Cl·H 2 O and hydrogen peroxide.