Yano E
Department of Public Health, Teikyo University School of Medicine, Tokyo, Japan.
Int Arch Occup Environ Health. 1988;61(1-2):19-23. doi: 10.1007/BF00381603.
Malondialdehyde (MDA) is a product of free-radical reaction with lipids and has been implicated in a variety of pathological processes including inflammation and carcinogenesis. In order to document the toxic reactions related to the pathogenic mechanisms of mineral fibers, asbestos and other mineral dusts were examined for their potency to produce lipid peroxidation using the thiobarbital method for MDA measurement. Human peripheral blood-derived neutrophils (PMN), guinea pig peritoneal macrophages, and guinea pig alveolar lavage cells produced MDA when treated with crocidolite asbestos. Of the various mineral dusts tested, only crocidolite showed a significant increase of MDA production. The amount of MDA produced by PMN treated with crocidolite increased with milling the fiber and with the incubation time. Both superoxide dismutase (SOD) and catalase were examined for their ability to inhibit MDA formation. At concentrations of up to 50 micrograms/10(6) cells, SOD did not inhibit the MDA formation in macrophages. However, catalase at the same concentration inhibited MDA formation in macrophages completely. A possible mechanism of MDA formation and its relationship with superoxide production are discussed.
丙二醛（MDA）是自由基与脂质反应的产物，与包括炎症和致癌作用在内的多种病理过程有关。为了记录与矿物纤维致病机制相关的毒性反应，使用硫代巴比妥酸法测定丙二醛，检测了石棉和其他矿物粉尘产生脂质过氧化的能力。用青石棉处理人外周血来源的中性粒细胞（PMN）、豚鼠腹腔巨噬细胞和豚鼠肺泡灌洗细胞时会产生丙二醛。在测试的各种矿物粉尘中，只有青石棉显示出丙二醛产量的显著增加。用青石棉处理的PMN产生的丙二醛量随纤维研磨和孵育时间的增加而增加。研究了超氧化物歧化酶（SOD）和过氧化氢酶抑制丙二醛形成的能力。在浓度高达50微克/10⁶细胞时，SOD不能抑制巨噬细胞中丙二醛的形成。然而，相同浓度的过氧化氢酶能完全抑制巨噬细胞中丙二醛形成。本文讨论了丙二醛形成的可能机制及其与超氧化物产生的关系。
