Oxidative atmospheric pollutants represent a significant source of stress to both terrestrial plants and animals. The biosurfaces of plants and surface-living organisms are directly exposed to these pollutant stresses. These surfaces, including respiratory tract surfaces, contain integrated antioxidant systems that would be expected to provide a primary defense against environmental threats caused by atmospheric reactive oxygen species. When the biosurface antioxidant defenses are overwhelmed, oxidative stress to the cellular components of the exposed biosurfaces can be expected, inducing inflammatory, adaptive, injurious, and reparative processes. Studies of mutants and/or transformed plants and insects, with specific alterations in key components of antioxidant defense systems, offer opportunities to dissect the complex systems that maintain surface defenses against environmental oxidants. In this article, we use a comparative approach to consider interactions of atmospheric oxidant pollutants with selected biosystems, with focus on O3 as the pollutant; plants, flies, skin, and lungs as the exposed biosystems; and nonenzymatic micronutrient antioxidants as significant contributors to overall antioxidant defense strategies of these varied biosystems. Parallelisms among several living organisms, with regard to their protective strategies against environmental atmospheric oxidants, are presented.

Atmospheric pollutants represent an important source of oxidative and nitrosative stress to both terrestrial plants and to animals. The exposed biosurfaces of plants and animals are directly exposed to these pollutant stresses. Not surprisingly, living organisms have developed complex integrated extracellular and intracellular defense systems against stresses related to reactive oxygen and nitrogen species (ROS, RNS), including O3 and NO2. Plant and animal epithelial surfaces and respiratory tract surfaces contain antioxidants that would be expected to provide defense against environmental stress caused by ambient ROS and RNS, thus ameliorating their injurious effects on more delicate underlying cellular constituents. Parallelisms among these surfaces with regard to their antioxidant constituents and environmental oxidants are presented. The reactive substances at these biosurfaces not only represent an important protective system against oxidizing environments, but products of their reactions with ROS/RNS may also serve as biomarkers of environmental oxidative stress. Moreover, the reaction products may also induce injury to underlying cells or cause cell activation, resulting in production of proinflammatory substances including cytokines. In this review we discuss antioxidant defense systems against environmental toxins in plant cell wall/apoplastic fluids, dead keratinized cells/interstitial fluids of stratum corneum (the outermost skin layer), and mucus/respiratory tract lining fluids.

Allergic asthma is a complex immunologically mediated disease associated with increased oxidative stress and altered antioxidant defenses. It was hypothesized that α-tocopherol (α-T) decreases oxidative stress and therefore its absence may influence allergic inflammatory process, a pathobiology known to be accompanied by oxidative stress. Therefore, selected parameters of allergic asthma sensitization and inflammation were evaluated following ovalbumin sensitization and re-challenge of α-T transfer protein (TTP) knock-out mice (TTP^−/−) that have greatly reduced lung α-T levels (e.g.<5%) compared to their litter mate controls (TTP^+/+). Results showed that severe α-T deficiency result in a blunted lung expression of IL-5 mRNA and IL-5 protein and plasma IgE levels compared with TTP^+/+ mice following immune sensitization and rechallenge, although lung lavage eosinophil levels were comparable in both genomic strains. It is concluded that the initial stimulation of immune responses by the TTP^−/− mice were generally blunted compared to the TTP^+/+ mice, thus diminishing some aspects of subsequent allergic inflammatory processes.