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膳食晚期糖基化终末产物对人类健康构成风险——并非如此!

Dietary ALEs are a risk to human health--NOT!

作者信息

Baynes John W

机构信息

Department of Chemistry and Biochemistry, University of South Carolina, Columbia 29208, USA.

出版信息

Mol Nutr Food Res. 2007 Sep;51(9):1102-6. doi: 10.1002/mnfr.200600287.

DOI:10.1002/mnfr.200600287
PMID:17854007
Abstract

Advanced lipoxidation end-products (ALEs) are formed by reaction of protein with lipid-derived reactive peroxyl and carbonyl compounds produced during food processing and cooking. There is concern that ALEs may induce damage in the gastrointestinal tract, affecting gut health, or enter the body and promote vascular inflammation and tissue damage. However, there is no direct evidence that ALE-proteins are a source of damage in the intestines or that they are transported into the circulation and cause pathology. Modification of proteins by ALEs impedes their digestion, and reactive ALEs released by gastrointestinal proteases would react with proteins or peptides in the gut, limiting their absorption. There are also potent enzymatic mechanisms for detoxifying ALEs or their precursors prior to their entry into the circulation. If ALEs gain access to the circulation, a battery of protective enzymes in tissue provides a second level of defense. These enzymes may be induced in intestinal epithelia and liver by low doses of ALEs, and adaptive responses would provide enhanced protection against future exposure to ALEs. Overall, except in persons with compromised organ function, e. g., vascular, hepatic, or renal diseases, there is little evidence that food ALEs will have any significant pathological effects.

摘要

晚期糖基化终末产物(ALEs)是由蛋白质与食品加工和烹饪过程中产生的脂质衍生的活性过氧和羰基化合物反应形成的。人们担心ALEs可能会在胃肠道中造成损害,影响肠道健康,或者进入人体并促进血管炎症和组织损伤。然而,没有直接证据表明ALEs修饰的蛋白质是肠道损伤的来源,或者它们会进入血液循环并导致病变。ALEs对蛋白质的修饰会阻碍其消化,胃肠道蛋白酶释放的活性ALEs会与肠道中的蛋白质或肽发生反应,限制它们的吸收。在ALEs进入血液循环之前,也有强大的酶促机制对其或其前体进行解毒。如果ALEs进入血液循环,组织中的一系列保护酶会提供第二道防线。低剂量的ALEs可诱导肠道上皮和肝脏中的这些酶,适应性反应将增强对未来接触ALEs的保护。总体而言,除了器官功能受损的人,如患有血管、肝脏或肾脏疾病的人,几乎没有证据表明食物中的ALEs会产生任何显著的病理影响。

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