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Biomedical subjects

J S Bus

Publications and source records attributed to J S Bus.

At least 55 records · Page 3Linked to original sources
PubMed1982

Mechanisms of superoxide radical-mediated toxicity.

Free radicals generated from metabolism of foreign compounds can have extremely detrimental consequences on cell function and survival. Due to their high reactivity, free radicals may potentially perturb a wide spectrum of important cellular macromolecules such as nucleic acids, proteins, lipids and polysaccharides. Recently, the toxicity of several xenobiotics has been suggested to be mediated by formation of free radicals derived from reduction of molecular oxygen, forming superoxide anion (O(2)) and hydroxyl radical (OH .). For example, the pulmonary toxicity of the bipyridylium herbicide paraquat has been attributed to an enzymatically catalyzed one-electron redox cycling of the parent molecule, resulting in generation of O(2). Examples of other compounds that are subject to redox cycling with associated O(2) formation are those agents containing quinone or aromatic nitro structural elements. An important aspect of free-radical-mediated toxicity is that it is moderated by several cellular defense mechanisms including superoxide dismutase, catalase, glutathione peroxidase, vitamin E and reduced glutathione. Thus, toxicity mediated by free radical generation may not occur unless defense mechanisms are overwhelmed by radical production.

Cell Membrane↗
PubMed1979

Simultaneous determination of n-hexane, 2-hexanone and 2,5-hexanedione in biological tissues by gas chromatography mass spectrometry.

A quantitative method is reported for the determination of n-hexane, 2-hexanone and 2,5-hexanedione in biological tissues by stable isotope dilution using gas chromatography mass spectrometry. n-[2H14]Hexane, 2-[2H5]hexanone and 2,5-[2H10]hexanedione are used as the isotopic diluents. After tissue homogenization and extraction of the three compounds in the presence of the deuterated internal standards, analysis is carried out in a single gas chromatographic injection by selected ion monitoring. Principal advantages of the technique are the ease of sample handling, rapidity of analysis and low limits of detection. The methodology is used to determine the organ distribution, pharmacokinetics and metabolism of n-hexane to 2-hexanone and 2,5-hexanedione in rats following inhalation exposure.

Animals↗
PubMed1978

Biochemical and physiologic changes in lungs of rats exposed to a cadmium chloride aerosol.

The purpose of this study was to examine the in vivo effects of acute exposure to a cadmium chloride aerosol on the activity of pulmonary enzymes and selected physiologic parameters that are altered by exposure to oxidant agents. Male rats were exposed for 1 hour to 0.5 per cent aerosol of cadmium chloride. At 1,5, and 11 days after exposure to cadmium chloride, exposed rats compared to control rats (data expressed as per cent of control values) had lung-to-body weight ratios of 192, 174, and 140 per cent; lung glucose-6-phosphate dehydrogenase activities of 90, 107, and 135 per cent; lung superoxide dismutase activities of 96, 101, and 132 per cent; tidal volumes of 62, 63, and 89 per cent; respiratory frequencies of 170, 145, and 108 per cent; and lung weight-specific static deflation volumes at 30 cm water of 30, 13, and 31 per cent. A zero-order clearance of cadmium from whole lung was observed, with a half-time of 27.4 days. Light microscopic examination of lung tissue revealed initial pulmonary edema on day 1 that progressed to interstitial pneumonitis on day 5, with some recovery by 11 days after exposure. The cadmium induced biochemical, physiologic, and pathologic alterations were similar to the responses observed in lungs of rats exposed to a wide variety of pulmonary irritants; thus, the changes observed may represent a nonspecific response to tissue injury.

Aerosols↗
PubMed1976

Paraquat toxicity: proposed mechanism of action involving lipid peroxidation.

The purpose of this study was to investigate the hypothesis that paraquat pulmonary toxicity results from cyclic reduction-oxidation of paraquat with sequential generation of superoxide radicals and singlet oxygen and initiation of lipid peroxidation. In vitro mouse lung microsomes catalyzed an NADPH-dependent, single-electron reduction of paraquat. Incubation of paraquat with NADPH, NADPH-cytochrome c reductase, and purified microsomal lipid increased malondialdehyde production is a concentration dependent manner. Addition of either superoxide dismutase or a single oxygen trapping agent 1,3-dipheylisobenzo furan inhibited paraquat stimulated lipid peroxidation. In vivo, pretreatment of mice with phenobarbital decreased paraquat toxicity, possibly by competing for electrons which might otherwise reduce paraquat. In contrast, paraquat toxicity in mice was increased by exposure to 100% oxygen and by deficiencies of the antioxidants selenium, vitamin E, or reduced glutahione (GSH). Paraquat, given IP to mice, at 30 mg/kg, decreased concentrations of the water-soluble antioxidant GSH in liver and lipid soluble antioxidants in lung. Oxygen-tolerant rats, which hae increased activities of pulmonary enzymes which combat lipid peroxidation, were also tolerant to lethal doses of paraquat as indicated by an increased paraquat LT50. Furthermore, rats chronically exposed to 100 ppm paraquat in the water had elevated pulmonary activities of glucose-6-phosphate dehydrogenase and GSH reductase. These results were consistent with the hypothesis that lipid peroxidation is involved in the toxicity of paraquat.

Anaerobiosis↗