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2 ppm臭氧暴露对大鼠肺脂质脂肪酸的影响。

Effect of 2 ppm ozone exposure on rat lung lipid fatty acids.

作者信息

Rabinowitz J L, Bassett D J

机构信息

Veterans Administration Hospital, University of Pennsylvania, Philadelphia 19104.

出版信息

Exp Lung Res. 1988;14(4):477-89. doi: 10.3109/01902148809087822.

Abstract

Based on in vitro studies, the initial damage to lung cells by ozone exposure is believed to result in part from the breakdown of lipid polyunsaturated fatty acids to aldehydes, ozonides, and peroxides. The present study measured lipid breakdown products in lungs isolated from rats pretreated with [1-14C]acetate 12 h before exposure for 4 h to either air or 2 ppm ozone. Lipid fatty acid breakdown was indicated by a 112% increase in thiobarbituric acid-reactive substances on ozone exposure and by changes in chemical and radioactive measurements of mono- and dicarboxylic acids formed by treatment of lipid fractions with hydrogen peroxide. Ozone exposure resulted in a 63% increase in recovery of short-chain fatty acids accounted for by increased recoveries of malonic acid by 37%, hexanoic acid by 47%, nonanoic acid by 118%, and azelaic acid by 107%. Recovery of glutaric acid was enhanced 15-fold by ozone exposure. Although decreases in tissue arachidonic acid could not be detected, oleic acid was significantly decreased by 36%. Recovery of radiolabel as short-chain fatty acids was increased by 65% on ozone exposure and was mainly accounted for by enhanced labeling of nonanoic and glutaric acid fractions. The failure to observe significant increases in 14C recovery in the other fractions suggested ozone-induced breakdown of unlabeled fatty acids. These results demonstrate the cleavage of unsaturated fatty acid double bonds following in vivo exposure of lungs to ozone. Breakdown of arachidonic and oleic acids was specifically identified by increased recoveries of glutaric and nonanoic acids, respectively.

摘要

基于体外研究,臭氧暴露对肺细胞的初始损伤被认为部分是由于脂质多不饱和脂肪酸分解为醛、臭氧化物和过氧化物所致。本研究测量了在暴露于空气或2 ppm臭氧4小时前12小时用[1-¹⁴C]乙酸预处理的大鼠分离肺组织中的脂质分解产物。脂质脂肪酸分解表现为臭氧暴露后硫代巴比妥酸反应性物质增加112%,以及用过氧化氢处理脂质组分形成的一元和二元羧酸的化学和放射性测量值发生变化。臭氧暴露导致短链脂肪酸回收率增加63%,这是由于丙二酸回收率增加37%、己酸增加47%、壬酸增加118%和壬二酸增加107%所致。臭氧暴露使戊二酸的回收率提高了15倍。虽然未检测到组织花生四烯酸减少,但油酸显著减少了36%。臭氧暴露使作为短链脂肪酸的放射性标记回收率增加65%,主要是由于壬酸和戊二酸组分的标记增强。在其他组分中未观察到¹⁴C回收率显著增加,这表明臭氧诱导了未标记脂肪酸的分解。这些结果证明了肺组织在体内暴露于臭氧后不饱和脂肪酸双键的断裂。分别通过戊二酸和壬酸回收率的增加特异性地鉴定了花生四烯酸和油酸的分解。

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