Radioprotective effect of 2-mercaptopropionyl glycine on radiation-induced lipid peroxidation and enzyme release in erythrocytes.

International journal of radiation biology and related studies in physics, chemistry, and medicine Pub Date : 1988-04-01 DOI:10.1080/09553008814550951

S I Ayene, R K Kale, P N Srivastava

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引用次数: 25

Abstract

gamma-Irradiation of erythrocyte suspensions resulted in lipid peroxidation and enzyme (acetylcholinesterase, AChE) release. The presence of 2-mercaptopropionyl glycine (MPG) during irradiation decreased lipid peroxidation and enzyme (acetylcholinesterase, AChE) release. The presence of 2-mercaptopropionyl glycine (MPG) during irradiation decreased lipid peroxidation and from erythrocytes of high and low concentrations was observed at 480 and 320 Gy, respectively. This implied that the extent of enzyme release is likely to be masked when only a single dose of radiation is used, unless it happens to be an optimum dose. MPG mediated inhibition of lipid peroxidation and enzyme release indicated that lipid peroxidation may induce the breakdown of the phosphatidylinositol/enzyme interaction. Further, the enzyme damage was assigned to the direct and indirect effects of radiation on the enzyme in situ.

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2-巯基丙酰甘氨酸对辐射诱导的红细胞脂质过氧化和酶释放的辐射防护作用。

γ -照射红细胞悬液导致脂质过氧化和酶(乙酰胆碱酯酶，AChE)释放。在辐照期间，2-巯基丙酰甘氨酸(MPG)的存在降低了脂质过氧化和酶(乙酰胆碱酯酶，AChE)的释放。在480 Gy和320 Gy照射下，2-巯基丙酰甘氨酸(MPG)的存在分别降低了红细胞脂质过氧化和高浓度的脂质过氧化。这意味着，如果只使用单一剂量的辐射，酶的释放程度很可能被掩盖，除非它恰好是最佳剂量。MPG介导的脂质过氧化和酶释放抑制表明，脂质过氧化可能导致磷脂酰肌醇/酶相互作用的破坏。此外，对酶的损伤归因于辐射对原位酶的直接和间接影响。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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International journal of radiation biology and related studies in physics, chemistry, and medicine

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