FIGURE 4.7 Covalent derivatives from malondialdehyde and proteins (A) or DNA (B).

It may also react with DNA bases and cause mutagenic lesions, consisting of large insertions and deletions at GC base pairs, by reaction with guanine amino groups to give the oxopropenyl derivatives 4.6 which are finally cyclized to pyrimido-purine derivatives 4.7, known as MidG adducts (Fig. 4.7B).3 For many years, there has been insufficient evidence for the implication of lipid peroxidation in the antitumor effects of radical-generating drugs like the anthracyclines, but recent studies have shown the involvement of MDA in DNA damage.4 In proliferating cells, the formation of M1dG adducts is accompanied by cell cycle arrest and inhibition of cyclin-associated kinase activities. It has been proved that antitumor compounds of the anthracyclin group, at low concentrations, increase MDA-depen-dent DNA oxopropenylation several fold,5 establishing a potential link between antitumor drug-dependent generation of ROS, induction of lipid peroxidation, and DNA damage.6

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