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The mechanism of acrolein-induced lipid peroxidation is unknown. This study found that acrolein and its glutathione adduct, glutathionylpropionaldehyde, induce oxygen radical formation. These oxygen radicals may be responsible for the induction of lipid peroxidation by acrolein. The enzymes xanthine oxidase and aldehyde dehydrogenase were found to interact with glutathionylpropionaldehyde to produce O2.- and HO(.). Acrolein was oxidized by xanthine oxidase to produce acroleinyl radical and O2(.-). Aldehyde dehydrogenase metabolized acrolein to form O2.- but not acroleinyl radical. The fact that glutathionylpropionaldehyde is a more potent stimulator of oxygen radical formation than acrolein indicates that glutathionylpropionaldehyde is a toxic metabolite of acrolein and may be responsible for some of the in vivo toxicity of acrolein.

Many diseases and aging may be associated with oxidative stress in the brain. However, the effects of oxidative stress in the brain should be more clearly described, especially in terms of effects on brain reduced glutathione (GSH). This issue was addressed by intracerebroventricular injection of a direct-acting oxidative stress inducing agent, tert-butylhydroperoxide. Oxidized glutathione (GSSG) levels in the brain increased by as much as 90-fold during tert-butylhydroperoxide-induced oxidative stress. At the same time, brain GSH levels decreased. The brain appears to retain GSSG and not reduce it or export it efficiently. Vitamin E levels in the striatum increased during tert-butylhydroperoxide-induced oxidative stress. Aging alters the ability of the brain to detoxify an oxidative stress, in that 8-month-old mice retain GSSG in their brains much more than 2-month-old mice. Eight-month-old mice were much more susceptible to tert-butylhydroperoxide-induced toxicity than 2-month-old mice. This may indicate that aging makes the brain more susceptible to oxidative damage.

The involvement of oxygen radicals in the pathogenesis of Parkinson's disease has been suggested for some time. This article reviews the evidence supporting the involvement of oxygen radicals in the disease process in the brain. This includes a discussion of iron, lipid peroxidation, peroxidase, catalase, superoxide dismutase, and glutathione levels in the brain. In addition, various theories of induction of Parkinson's disease are discussed in relation to the possible involvement of oxygen radicals. These theories include the environmental toxin theory, the dopamine turnover theory, and the cerebral blood flow theory.

The molecular sieve oxygen generating system (MSOG) is currently being considered as a replacement for liquid and gaseous stores on aircraft for the supply of aviator's breathing oxygen. Incorporation of onboard oxygen generation in aircraft not only increases system safety but also minimizes logistic requirements. However, a unique characteristic of the MSOG is that it concentrates not only oxygen but also argon in the process of removing nitrogen from engine bleed air. Maximum concentrations produced by present systems are in the order of 95% oxygen and 5% argon. These results have precipitated numerous questions relating to the physiological effects of argon in the product breathing gas. This report reviews the current literature concerning argon as a minor constituent (less than 10%) in gas breathing systems and recommends studies prior to human compatibility testing of the molecule sieve oxygen generating systems.

The effects of dietary vitamin E deficiency on mouse cerebral membrane order and oxygen reactive species were studied. Quantitation of vitamin E levels in several brain regions showed greatest deficiencies in striatum and cerebellum, followed by substantia nigra, and cortex. Vitamin E deficiency increased central-core membrane order in cerebral P2 fraction, but was without effect in the superficial hydrophilic membrane domain. Oxygen radical formation was studied using the probe 2',7'-dichlorofluorescein diacetate. Basal generation rates of oxygen reactive species were 2.5-fold higher when compared to control animals. While hepatic levels of vitamin E are much more reduced than brain levels, in deficient mice, the rate of oxygen radical formation in the liver was unaltered. This implies an special susceptibility of the brain to deficiency of this lipophilic antioxidant vitamin. Data demonstrate that endogenous levels of free radical scavengers, such as vitamin E, may play an important role in maintaining basal oxygen radical levels and membrane integrity. The dietary vitamin E depletion paradigm suggests that a relation exists between elevated levels of oxygen radicals and more rigid hydrophobic central-cores in cerebral membranes, effects that may play a role in mechanisms underlying the neuropathologic lesions observed following vitamin E deficiency.

A 95% oxygen-5% argon breathing mixture produced by a molecular sieve generator was shown to be similar to a 95% O2-5% N2 mixture for breathing during 1-h exposures at 7,620 m (25,000 ft) or 10,972 m (35,000 ft), as determined by the detection of proportionate numbers of intravascular bubbles in the pulmonary artery of dogs. Comparable results were obtained with 95% O2-5% He or 100% O2. The partial pressures of a 5% mixture at 7,620 and 10,972 m were 14.1 and 8.6 torr, respectively, and were apparently low enough so that the nonmetabolizable gases did not result in differences in the incidence of intravascular bubble formation or decompression sickness. Argon at the 10% level showed a nonsignificant trend to produce more bubbles. Individual susceptibility or resistance to form bubbles was observed with the different gases. Denitrogenation with either 5 or 10% mixtures of the inert gases was quite effective, as shown by a reduction in the number of intravascular bubbles detected.