Autoxidation of methyl linoleate initiated by the ozonide of allylbenzene.

Allylbenzene ozonide (ABO), a model for polyunsaturated fatty acid (PUFA) ozonides, initiates the autoxidation of methyl linoleate (18:2 ME) at 37 degrees C under 760 torr of oxygen. This process is inhibited by d-alpha-tocopherol (alpha-T) and 2,6-di-tert-butyl-4-methylphenol (BHT). The autoxidation was followed by the appearance of conjugated diene (CD), as well as by oxygen-uptake. The rates of autoxidation are proportional to the square root of ABO concentration, implying that the usual free radical autoxidation rate law is obeyed. Activation parameters for the thermal decomposition of ABO were determined under N2 in the presence of radical scavengers and found to be Ea = 28.2 +/- 0.3 kcal mol-1 and log A = 13.6 +/- 0.2; kd (37 degrees C) is calculated to be (5.1 +/- 0.3) X 10(-7) sec-1. Autoxidation data are also reported for ozonides of 18:2 ME and methyl oleate (18:1 ME).

The kinetics of the autoxidation of polyunsaturated fatty acids.

The kinetics of the autoxidation of a series of polyunsaturated fatty acids (PUFA) with increasing degrees of unsaturation and the mono-, di- and triglycerides of linoleate have been studied in homogeneous chlorobenzene solution at 37 C under 760 torr of oxygen. The autoxidations were initiated by thermal decomposition of azo initiators and followed by measuring the rate of oxygen uptake. The rate of chain initiation was determined by the induction period method using alpha-tocopherol as the chain-breaking antioxidant. The measured oxidizabilities of the PUFA are linearly dependent on the number of doubly allylic positions present in the molecule. Thus, the oxidizability of linoleate is 2.03 X 10(-2) M-1/2 sec-1/2, and the value for docosahexaenoate is five times greater, 10.15 X 10(-2) M-1/2 sec-1/2. The rate of autoxidation for all PUFA studied and for the mono- and diglyceride is proportional to the substrate concentration and to the square root of the rate of chain initiation, implying that the autoxidation of these compounds follows the usual kinetic rate law. The autoxidation of the triglyceride is more complex and does not appear to follow the same rate law at all substrate concentrations. This deviation from the usual kinetic rate expression may be due to lipid aggregation at low concentrations of the triglyceride.

Cigarette tar causes single-strand breaks in DNA.

The results of this study demonstrate, for the first time, that cigarette tar causes DNA damage. Incubation in vitro of phage PM2 DNA with aqueous extracts of cigarette tar results in the introduction of DNA single-strand breaks. The effects of protective enzymes and radical scavengers indicate the involvement of active oxygen species. Although the semiquinone components of tar reduce dioxygen forming superoxide radicals and hydrogen peroxide, our results suggest that hydroxyl radicals formed via metal catalyzed decomposition of hydrogen peroxide are ultimately responsible for the DNA lesions. Our results also suggest that the metals in tar are reduced by the semiquinone components of tar and by superoxide at comparable rates.

The metal-mediated formation of hydroxyl radical by aqueous extracts of cigarette tar.

Aqueous extracts of cigarette tar produce hydroxyl radicals that are spin trapped by 5,5-dimethyl-1-pyrroline-N-oxide. The addition of catalase almost completely inhibits and superoxide dismutase partially inhibits spin adduct formation. The addition of ethylenediamine tetraacetic acid greatly increases the amount of hydroxyl radical adduct observed; in contrast, diethylenetriamine pentaacetic acid causes complete inhibition of spin adduct formation. We suggest that the hydroxyl radical arises from the metal-mediated decomposition of hydrogen peroxide, and that hydrogen peroxide is formed from the reduction of dioxygen by the semiquinones present in the cigarette tar.