William A. Pryor

Bio: William A. Pryor is an academic researcher from Louisiana State University. The author has contributed to research in topics: Radical & Peroxynitrite. The author has an hindex of 47, co-authored 79 publications receiving 10594 citations.

Free-radical chemistry of cigarette smoke and its toxicological implications.

Abstract: Cigarette smoke contains two very different populations of free radicals, one in the tar and one in the gas phase. The tar phase contains several relatively stable free radicals; we have identified the principal radical as a quinone/hydroquinone (Q/QH2) complex held in the tarry matrix. We suggest that this Q/QH2 polymer is an active redox system that is capable of reducing molecular oxygen to produce superoxide, eventually leading to hydrogen peroxide and hydroxyl radicals. In addition, we have shown that the principal radical in tar reacts with DNA in vitro, possibly by covalent binding. The gas phase of cigarette smoke contains small oxygen- and carbon-centered radicals that are much more reactive than are the tar-phase radicals. These gas-phase radicals do not arise in the flame, but rather are produced in a steady state by the oxidation of NO to NO2, which then reacts with reactive species in smoke such as isoprene. We suggest that these radicals and the metastable products derived from these radical reactions may be responsible for the inactivation of alpha 1-proteinase inhibitor by fresh smoke. Cigarette smoke oxidizes thiols to disulfides; we suggest the active oxidants are NO and NO2. The effects of smoke on lipid peroxidation are complex, and this is discussed. We also discuss the toxicological implications for the radicals in smoke in terms of a number of radical-mediated disease processes, including emphysema and cancer.

Oxy-radicals and related species: their formation, lifetimes, and reactions.

Abstract: In this brief overview I will review some of the ways in which free radicals and related highly reactive species are produced in biological systems. I will discuss the reactivities and lifetimes of these species, and also will briefly list some pathological conditions and chronic diseases in which these species may be involved. The rich variety of the species of interest in free radical biology is notewor­ thy. Table 1 lists species that have been implicated in various physiological and pathological processes; some of these are neutral radicals, some are radical ions, and some are molecules that contain an even number of electrons and, therefore, are not free radicals. As we shall see, radicals differ greatly in their stabilities; one of the radicals listed in Table 1, nitrogen dioxide, is sufficiently stable to reach ppm levels in polluted urban air. What name can be used to encompass the species listed in Table I? A phrase that is finding increased use in free radical biology is "partially reduced oxygen products." However, even this broad title is unsatisfactory since some of the species in Table 1 contain oxygen atoms at the same oxidation level as elemental oxygen (e.g. ozone and singlet oxygen). The property that these species share is that they have the potential to cause radical reactions to occur in biological systems. Some of these species are radicals and therefore react by radical processes; others react to produce molecules that can decompose to form radicals (e.g. singlet oxygen leads to hydroperoxides). However, these species need not always react via free radical pathways. For example, ozone, hydrogen

Autoxidation of polyunsaturated fatty acids: II. A suggested mechanism for the formation of TBA-reactive materials from prostaglandin-like endoperoxides.

Abstract: The nature and mechanism of formation of the thiobarbituric acid (TBA)-reactive material produced in the autoxidation of polyunsaturated fatty acids (PUFA) or their esters has been studied. On the basis of chemical studies and

Free radical biology and medicine: it's a gas, man!

Abstract: We review gases that can affect oxidative stress and that themselves may be radicals. We discuss O2 toxicity, invoking superoxide, hydrogen peroxide, and the hydroxyl radical. We also discuss super...

Role of free radicals in the toxicity of airborne fine particulate matter.

Abstract: Exposure to airborne fine particles (PM2.5) is implicated in excess of 50 000 yearly deaths in the USA as well as a number of chronic respiratory illnesses. Despite intense interest in the toxicity of PM2.5, the mechanisms by which it causes illnesses are poorly understood. Since the principal source of airborne fine particles is combustion and combustion sources generate free radicals, we suspected that PM2.5 may contain radicals. Using electron paramagnetic resonance (EPR), we examined samples of PM2.5 and found large quantities of radicals with characteristics similar to semiquinone radicals. Semiquinone radicals are known to undergo redox cycling and ultimately produce biologically damaging hydroxyl radicals. Aqueous extracts of PM2.5 samples induced damage to DNA in human cells and supercoiled phage DNA. PM2.5-mediated DNA damage was abolished by superoxide dismutase, catalase, and deferoxamine, implicating superoxide radical, hydrogen peroxide, and the hydroxyl radical in the reactions inducing DNA damage.

Apparent hydroxyl radical production by peroxynitrite: implications for endothelial injury from nitric oxide and superoxide.

Abstract: Superoxide dismutase reduces injury in many disease processes, implicating superoxide anion radical (O2-.) as a toxic species in vivo. A critical target of superoxide may be nitric oxide (NO.) produced by endothelium, macrophages, neutrophils, and brain synaptosomes. Superoxide and NO. are known to rapidly react to form the stable peroxynitrite anion (ONOO-). We have shown that peroxynitrite has a pKa of 7.49 +/- 0.06 at 37 degrees C and rapidly decomposes once protonated with a half-life of 1.9 sec at pH 7.4. Peroxynitrite decomposition generates a strong oxidant with reactivity similar to hydroxyl radical, as assessed by the oxidation of deoxyribose or dimethyl sulfoxide. Product yields indicative of hydroxyl radical were 5.1 +/- 0.1% and 24.3 +/- 1.0%, respectively, of added peroxynitrite. Product formation was not affected by the metal chelator diethyltriaminepentaacetic acid, suggesting that iron was not required to catalyze oxidation. In contrast, desferrioxamine was a potent, competitive inhibitor of peroxynitrite-initiated oxidation because of a direct reaction between desferrioxamine and peroxynitrite rather than by iron chelation. We propose that superoxide dismutase may protect vascular tissue stimulated to produce superoxide and NO. under pathological conditions by preventing the formation of peroxynitrite.

The Chemistry behind Antioxidant Capacity Assays

Abstract: This review summarizes the multifaceted aspects of antioxidants and the basic kinetic models of inhibited autoxidation and analyzes the chemical principles of antioxidant capacity assays. Depending upon the reactions involved, these assays can roughly be classified into two types: assays based on hydrogen atom transfer (HAT) reactions and assays based on electron transfer (ET). The majority of HAT-based assays apply a competitive reaction scheme, in which antioxidant and substrate compete for thermally generated peroxyl radicals through the decomposition of azo compounds. These assays include inhibition of induced low-density lipoprotein autoxidation, oxygen radical absorbance capacity (ORAC), total radical trapping antioxidant parameter (TRAP), and crocin bleaching assays. ET-based assays measure the capacity of an antioxidant in the reduction of an oxidant, which changes color when reduced. The degree of color change is correlated with the sample's antioxidant concentrations. ET-based assays include th...