More than 6000 residents of Latvia were involved in recovery work in Chernobyl. They were healthy men exposed to substantial ionizing radiation (0.01-0.5 Gy). Now, these recovery workers suffer from "postradiation syndrome": dizziness and poor memory, headache, local pains, and so forth. The biochemical mechanism of "postradiation syndrome" has not been completely established. In this Phase I study, we have investigated how exposure to radiation impacts antioxidative defense and trace element concentrations in the blood of recovery workers. Thirty-five patients with postradiation syndrome (men, age range 33-50 yr) and 15 healthy men similar in age as control subjects were studied for the effects on plasma chemiluminescence, the activity of antioxidant enzymes, and the concentration of ceruloplasmin and concentrations of selenium (Se), zinc (Zn), and copper (Cu) in blood. The results revealed that plasma chemiluminescence was significantly increased (3.5-fold to 5.5-fold), the activity of catalase in erythrocytes was significantly elevated, and the activity of glutathione peroxidase in plasma was significantly reduced in examined patients. Concentrations of Zn and Cu were significantly higher and the concentration of Se was lower in these patients. We conclude that the patients exposed to ionizing radiation have diminished blood antioxidant defense associated with pronounced Se deficiency and imbalance of Zn and Cu.

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Threatened abortion at the early critical terms of gestation is characterized by drastic changes in the antioxidant status of the blood: activation of the pentose phosphate pathway of energy metabolism in erythrocytes and intensification of lipid peroxidation in erythrocytes and plasma.

Using an experimental ischemia-reperfusion model it is found that combined treatment with a-tocopherol and panthenol markedly increases the content of endogenous antioxidant tocopherol during total ischemia and reperfusion, i.e., it improves the antioxidant state of the postischemized myocardium, thus preventing possible damage caused by stepped-up production of active oxygen forms during reoxygenation.