Neyfakh E A, Alimbekova A I, Ivanenko G F
Institute of Biochemical Physics, Russian Academy of Sciences, Moscow, 117977, Russia.
Biochemistry (Mosc). 1998 Aug;63(8):977-87.
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.
在切尔诺贝利核电站事故后受放射性核素污染地区居住的428名0至7岁儿童的血浆中，测定了脂过氧化级联反应（LPC）的分解代谢产物，包括二烯共轭物、酮二烯和羰基化合物，以及必需的脂质生物抗氧化剂（BAO）——维生素E和A。测定了个体外部γ辐射剂量（D）。γ辐射占总辐射负荷的90%以上，并且与所检查地区居民吸收源的辐射相关。在检查前，对一组儿童（第一组，n = 90）进行了口服多种维生素治疗（使用含有本研究中测定的BAO的制剂），该组儿童与未接受治疗的组（第二组）具有可比性。与第一组年龄匹配的亚组相比，第二组中所有LPC分解代谢产物的平均水平高两至六倍，而维生素E和A的水平低两至三倍。在第二组中，在最大区域辐射负荷下，所有分解代谢产物水平的个体变化达到了致病应激源的程度。产前暴露和生命第一年的暴露造成了最强的致病作用。BAO治疗在所有剂量（高达7 cSv）下都能使LPC和维生素（E和A）的水平强烈恢复正常，并提高受试者的辐射抗性。在低辐射剂量与所有研究代谢物与其正常水平的偏离程度之间，在p < 0.05水平上共发现了47个线性相关性（54%的方程r = 0.4至0.7，87%的方程p < 0.02）。在各种条件下发现的辐射剂量-效应相关性的多样性表明，所检查儿童中发现的病理体征是由辐射引起的。LPC系统紊乱在低剂量时就会出现，并且没有阈值效应。数据表明，这些紊乱是由于在BAO缺乏的情况下，长期暴露于低剂量强电离辐射引起的自由基链式分支LPC反应所致。
