Radiation-induced lipoperoxidative stress in children coupled with deficit of essential antioxidants.

Catabolic products of the lipoperoxidative cascade (LPC), including diene conjugates, ketodienes, and carbonyl compounds, as well as essential lipid bioantioxidants (BAO)--vitamins E and A--were determined in blood plasma of 428 children aged 0-7 years residents of areas contaminated with radionuclides after the Chernobyl Power Plant accident. Individual external gamma-irradiation doses (D) were determined. Gamma-irradiation accounted for more than 90% of total radiation loads and correlated with irradiation from absorbed sources in residents of the areas examined. Before examination, oral multivitamin therapy (with preparations containing the BAO determined in this work) was administered to a group of children (group I, n = 90) comparable to the group receiving no therapy (group II). Group II had two to six times higher mean levels of all LPC catabolic products and two to three times lower levels of vitamins E and A in comparison to age-matched subgroups of group I. In group II, individual shifts in the levels of all catabolic products achieved pathogenic stressor magnitudes at maximal regional radiation loads. Antenatal exposure and exposure over the first year of life caused the strongest pathogenic effects. BAO therapy strongly normalized the levels of LPC and vitamins (E and A) at all doses (up to 7 cSv) and increased the radiation resistance of the subjects. A total of 47 linear correlations were found at a p < 0.05 level (r = 0.4 to 0.7 for 54% and p < 0.02 for 87% of equations) between low radiation doses and the extent of deviation of all metabolites studied from their normal levels. The multiplicity of radiation dose--effect correlations found under various conditions suggest that pathological signs found in the children examined were due to irradiation. LPC system disorders developed at low doses and displayed no threshold effect. The data suggest that these disorders resulted from free-radical chain-branched LPC reactions caused by chronic exposure to low doses of strongly ionizing radiation under conditions of BAO deficiency.