Is Superoxide an Initiator of Microsomal Lipid Peroxidation?

Plasma malondialdehyde levels and opiate withdrawal signs observed in rats treated with morphine plus naloxone: effects of α‐lipoic acid administration

“…In addition, we found that injecting naloxone in rats receiving morphine further increases plasma MDA levels, probably as a result of the stimulation of toxic oxygen species leading to greater MDA production [15].…”

“…It lowered MDA levels in the groups receiving morphine or morphine and naloxone in comparison with those observed in the corresponding groups not treated with LA. As LA is a powerful peroxide scavenger, it may decrease or prevent the interactions between ROS and polyunsaturated fatty acids, and thus affect MDA production [15].…”

Effect of rutin and its copper complex on superoxide formation and lipid peroxidation in rat liver microsomes

“…Later on, Morehouse et al [5]doubted the importance of superoxide participation in the initiation of microsomal lipid peroxidation because the superoxide production measured via the reduction of acetylated cytochrome c was only about 1.5% of the total microsomal NADPH‐dependent reduction activity. However, the use of much more sensitive and specific assays of superoxide production such as the spin‐trapping technique [11]and lucigenin‐amplified chemiluminescence (CL) [12]supported the earlier data indicating the participation of superoxide in lipid peroxidation. The latest data confirm an important role of superoxide in the initiation of in vivo lipid peroxidation [13–16].…”

Inhibitory Action of Oren-gedoku-to Extract on Enzymatic Lipid Peroxidation in Rat Liver Microsomes.

“…[8][9][10] It has been indicated that oxygen free radicals such as superoxide radical, hydroxyl radical, and singlet oxygen participate in enzymatic lipid peroxidation in rat liver microsomes. [27][28][29][30][31][32][33][34] We have observed that when the effects of superoxide dismutase, catalase, hydroxyl radical scavengers such as mannitol, sodium formate, and dimethylthiourea, and singlet oxygen quenchers such as histidine, diazabicyclooctane, and diphenylfuran, on enzymatic lipid peroxidation in rat liver microsomes used in the present study are examined, singlet oxygen quenchers inhibit peroxidation by more than 90%, while superoxide dismutase, catalase, and hydroxyl radical scavengers inhibit it by less than 20% (unpublished data). These results are consistent with those reported by Wright et al 34) who have proposed the involvement of singlet oxygen in the initiation of enzymatic lipid peroxidation in rat liver microsomes.…”