Components Of Antioxidant Defense System Research Articles

Protective influence of vitamin E on antioxidant defense system in the blood of rats treated with cadmium.

The effects of acute exposure to cadmium (Cd) on the blood antioxidant defense system, lipid peroxide concentration and hematological parameters, as well as the possible protective role of vitamin E were studied. Male Wistar albino rats (3 months old) were treated with cadmium (0.4 mg Cd/kg b.m., i.p., 24 h before the experiment) or with vitamin E + Cd (20 IU Vit E/kg b.m., i.m., 48 h + 0.4 mg Cd/kg b.m., i.p., 24 h before the experiment). The hematological parameters were assessed: red blood cell counts, hematocrit value and hemoglobin concentration were significantly decreased in the blood of Cd-treated rats. Intoxication with cadmium was also followed by significantly increased lipid peroxide concentrations. We also observed increased activity of antioxidant defense enzymes: copper zinc containing superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase as well as concentrations of non-enzymatic components of antioxidant defense system: reduced glutathione, vitamin C and vitamin E. Pretreatment with vitamin E exhibited a protective role on the toxic effects of cadmium on the hematological values, lipid peroxide concentration as well as on enzymatic and non-enzymatic components of antioxidant defense system.

Environmental oxidant pollutant effects on biologic systems: a focus on micronutrient antioxidant-oxidant interactions.

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.

Superoxide dismutase biosynthesis by two thermophilic bacteria.

Some high-molecular weight antioxidant defense system components of two thermophilic bacteria isolated from spa waters of Serbia (Yugoslavia) and identified as Bacillus stearothermophilus and Thermothrix sp. were studied. In addition to superoxide dismutase (SOD; EC 1.15.1.1), qualitative analyses demonstrated the presence of catalase (EC 1.11.1.6), peroxidases and oxidases in both bacterial strains. Cell-free extracts were subjected to nondenaturing polyacrylamide gel electrophoresis (PAGE) and SOD activity in the eluates of the corresponding bands was examined in the presence of several specific inhibitors. A slight decrease of SOD activity observed in the presence of 0.3 M potassium cyanide and its complete insensitivity to hydrogen peroxide (5 mM) and sodium azide (20 mM) action suggest that the enzyme occurring in the two thermophiles represents Mn SOD. A high SOD activity recorded in cell-free extracts strongly recommends these two bacterial strains as potential producers of this important antioxidant defense system component at industrial scale.

Vitamin a deficiency modifies antioxidant defenses and essential element contents in rat heart

Oxidative stress in the heart of male rats fed on a vitamin A-deficient diet for three months from 21 days of age was evaluated. Vitamin A restriction produced subclinical plasma retinol concentration (0.7 μmol/l), negligible liver retinol stores and a significant decrease of heart retinol concentration, as determined by HPLC, compared with the control group receiving the same diet with 4000 IU of vitamin A (8 mg retinol as retinyl palmitate) per kg of diet. Vitamin A-deficient rats had lower body weight than control rats. No change in the heart weights was observed. In serum of rats fed the vitamin A-deficient diet the concentrations of thiobarbituric acid-reactive substances (TBARS) and reduced glutathione (GSH) increased by ∼65% and 60%, respectively, compared with those fed on the control diet. In hearts of vitamin A-deficient rats the concentration of TBARS and the glutathione peroxidase activity significantly increased. The activity of catalase decreased by ∼30%, while the superoxide dismutase did not change. Additionally, vitamin A-deficient rats showed lower heart concentrations of the trace elements selenium, manganese and chromium. Heart iron, copper and zinc concentrations were not affected. Vitamin A deprivation for 3 months decreased the plasma and heart retinol concentrations associated with changes in non-enzymatic and enzymatic antioxidant defense system components.

Studies on lipid peroxidation in rat tissues following administration of low and moderate doses of cadmium chloride

The susceptibility to lipid peroxidation (LPO) of liver, kidneys, brain, lungs, heart, and testes was assessed in rats administered intraperitoneally with various doses of cadmium (Cd). Dose-response studies were carried out with male Long Evans rats (12-week-old; 300 ± 33 g) injected with 25, 125, 500, and 1250 μg Cd/kg as CdCl 2 and sacrificed after 24 h. In time-response studies, animals were administered with 25 and 500 μg Cd/kg as CdCl 2 and sacrificed after 2, 6, 12, 24, and 72 h. Exposure of rats to low and moderate doses of Cd by the intraperitoneal route stimulated LPO in all the tissues investigated as assessed by the measurement of thiobarbituric acid reactive substances (TBARS). Lungs and brain were the most responsive, and these tissues and liver displayed early responses following Cd exposure. Comparison of LPO to various tissue indicators (for liver: alanine aminotransferase (ALT), sorbitol dehydrogenase (SDH), alkaline phosphatase (ALP); for lungs: ALP, gamma-glutamyl transpeptidase (GGT)) suggested that low doses of Cd stimulated LPO without any evidence of acute damages. These results suggest that LPO is an early and sensitive consequence of Cd exposure as determined in various organs. Investigation of liver, lungs, and heart antioxidant defense system components (glutathione peroxidase (GPX), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PDH), superoxide dismutase (SOD)) revealed that GPX might be considered as a potential modulator of the Cd-induced LPO reaction in lungs and heart tissues.