thiobarbituric-acid and Heart-Diseases

Ozone is a strong oxidizing agent, and in many locations it is a major atmospheric pollutant. It is phytotoxic and an important cause of lung dysfunction in humans. Recently, a significant association has been established between total atmospheric oxidants, of which ozone is one, and daily cardiovascular mortality rates. In this article, we show that exposure of rats to ozone for 5 days, in a concentration found in major urban centers, results in an increased concentration of thiobarbituric acid-reactive material (an indicator of lipid peroxidation) in heart and brain tissue as well as elevated activity of catalase and glutathione peroxidase (enzymic scavengers of peroxides) in these tissues. We examined the heart anatomically and found evidence of extracellular and intracellular edema. These findings indicate that the heart and brain are damaged by a concentration of ozone present in major urban centers; they may have important implications for chronic illness and degenerative processes in humans.

Topics: Animals; Brain Diseases; Catalase; Glutathione Peroxidase; Heart Diseases; Lipid Peroxidation; Male; Microscopy, Electron; Ozone; Rats; Rats, Inbred Strains; Thiobarbiturates

Ascorbic acid (AH2) is a potential scavenger of superoxide radical and singlet oxygen. In the guinea pig, marginal AH2 deficiency results in intracellular oxidative damage in the cardiac tissue as evidenced by lipid peroxidation, formation of fluorescent pigment and loss of structural integrity of the microsomal membranes. The oxidative damage does not occur due to lack of enzymatic scavengers of reactive oxygen species such as superoxide dismutase, catalase and glutathione peroxidase. Also, glutathione transferase activity is not decreased in AH2 deficiency. Lipid peroxidation, fluorescent pigment formation and protein modification disappear after AH2 therapy. These results, if extra-polated to human beings, would indicate that chronic subclinical AH2 deficiency may result in progressive oxidative damage which in the long run may lead to permanent degenerative diseases in the heart.

Topics: Animals; Ascorbic Acid Deficiency; Free Radical Scavengers; Guinea Pigs; Heart Diseases; Intracellular Membranes; Lipid Peroxidation; Male; Microsomes; Thiobarbiturates

Endurance training by swimming (219-229 h) resulted in a significant protection against hypoxia/reoxygenation-induced injuries in Langendorff-perfused rat hearts. The protection was manifested as improved flow characteristics and a smaller release of creatine kinase into the perfusate. The concentration of thiobarbituric acid reactive substances (TBARS) was lower in the trained than in the respective control hearts. The trained hearts also showed a lower reoxygenation-induced increase in TBARS. The myocardium of the right ventricle and that of the left subepimyocardium were the most affected by reoxygenation. The swimming program induced a decrease in the activities of catalase and glutathione reductase in all parts of the myocardium measured. A decrease in vitamin E concentration in the subendomyocardium of the left ventricle and an increase in the activity of thioredoxin reductase also occurred. An increase in the concentration of reduced glutathione due to training was also observed, especially in the left subepimyocardium, whereas the glutathione disulfide concentration and the activity of superoxide dismutase were unaffected. The activity of glucose 6-phosphate dehydrogenase increased in the right ventricle. The results suggest both the importance of cellular redox state and the role of a lower degree of enzymatic antioxidants in training-induced protection against ischemic injuries.

Topics: Animals; Glucosephosphate Dehydrogenase; Glutathione; Heart Diseases; Hypoxia; Lipid Peroxidation; Male; Myocardium; Oxygen; Physical Conditioning, Animal; Physical Endurance; Rats; Rats, Inbred Strains; Superoxide Dismutase; Swimming; Thiobarbiturates