Is superoxide an initiator of microsomal lipid peroxidation?

The effects of "pro-oxidant" quinones, doxorubicin, Fe(3+)-ADP-doxorubicin complex, and menadione, as well as of free radical scavengers possessing superoxide-dismuting activities, Fe(3+)-rutin and Cu(2+)-rutin, on superoxide production and lipid peroxidation in rat liver microsomes have been studied. All quinone compounds efficiently suppressed lucigenin-dependent chemiluminescence produced in NADPH-dependent microsomal lipid peroxidation, but exhibited different effects on cytochrome c reduction: doxorubicin and Fe(3+)-ADP-doxorubicin weakly inhibited and menadione enhanced it. In accord with previous findings, menadione inhibited malondialdehyde (MDA) formation in microsomes, while Fe3-ADP-doxorubicin enhanced it.

Mechanism of the interaction of superoxide ion and ascorbate with anthracycline antibiotics.

The interaction of superoxide ion and ascorbate anion with anthracycline antibiotics (adriamycin and aclacinimycin A) as well as with their Fe3+ complexes has been studied in aprotic and protic media. It was found that both superoxide and ascorbate reduce anthracyclines to deoxyaglycons via a one-electron transfer mechanism under all conditions studied. The reaction of ascorbate anion with adriamycin and aclacinomycin A in aqueous solution proceeded only in the presence of Fe3+ ions; it is supposed that an active catalytic species was Fe3+ adriamycin.

[Mechanism of the interaction of the anticancer antibiotic adriamycin (doxorubicin) with the anion radical O2].

Interaction of the O2. anion radical with adriamycin in water-acetonitrile mixtures was studied by UV-spectroscopy. It was shown that with changing of the water content in the reaction mixture from 0 to 90 per cent O2.