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实验动物体内α,β-不饱和醛的吸收、代谢及尿排泄。与通过膳食摄入热应激富含多不饱和脂肪酸的烹饪油引发心血管疾病的相关性。

In vivo absorption, metabolism, and urinary excretion of alpha,beta-unsaturated aldehydes in experimental animals. Relevance to the development of cardiovascular diseases by the dietary ingestion of thermally stressed polyunsaturate-rich culinary oils.

作者信息

Grootveld M, Atherton M D, Sheerin A N, Hawkes J, Blake D R, Richens T E, Silwood C J, Lynch E, Claxson A W

机构信息

The Inflammation Research Group, St. Bartholomews and the Royal London Hospitals School of Medicine and Dentistry, London E1 2AD, United Kingdom.

出版信息

J Clin Invest. 1998 Mar 15;101(6):1210-8. doi: 10.1172/JCI1314.

Abstract

Thermal stressing of polyunsaturated fatty acid (PUFA)- rich culinary oils according to routine frying or cooking practices generates high levels of cytotoxic aldehydic products (predominantly trans-2-alkenals, trans,trans-alka-2,4-dienals, cis,trans-alka-2, 4-dienals, and n-alkanals), species arising from the fragmentation of conjugated hydroperoxydiene precursors. In this investigation we demonstrate that typical trans-2-alkenal compounds known to be produced from the thermally induced autoxidation of PUFAs are readily absorbed from the gut into the systemic circulation in vivo, metabolized (primarily via the addition of glutathione across their electrophilic carbon-carbon double bonds), and excreted in the urine as C-3 mercapturate conjugates in rats. Since such aldehydic products are damaging to human health, the results obtained from our investigations indicate that the dietary ingestion of thermally, autoxidatively stressed PUFA-rich culinary oils promotes the induction, development, and progression of cardiovascular diseases.

摘要

根据常规油炸或烹饪方式对富含多不饱和脂肪酸(PUFA)的食用油进行热应激处理,会产生大量具有细胞毒性的醛类产物(主要是反式-2-烯醛、反,反-链-2,4-二烯醛、顺,反-链-2,4-二烯醛和正链烷醛),这些物质源自共轭氢过氧化二烯前体的裂解。在本研究中,我们证明了已知由PUFA热诱导自氧化产生的典型反式-2-烯醛化合物在体内很容易从肠道吸收进入体循环,经过代谢(主要是通过在其亲电碳-碳双键上添加谷胱甘肽),并以C-3巯基尿酸盐共轭物的形式在大鼠尿液中排泄。由于此类醛类产物对人体健康有害,我们的研究结果表明,通过饮食摄入经过热自氧化应激处理的富含PUFA的食用油会促进心血管疾病的诱发、发展和进展。

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