Ellis Elizabeth M
Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 204 George Street, Glasgow, G1 1XW, United Kingdom.
Pharmacol Ther. 2007 Jul;115(1):13-24. doi: 10.1016/j.pharmthera.2007.03.015. Epub 2007 May 8.
Reactive aldehydes and ketones are produced as a result of oxidative stress in several disease processes. Considerable evidence is now accumulating that these reactive carbonyl products are also involved in the progression of diseases, including neurodegenerative disorders, diabetes, atherosclerosis, diabetic complications, reperfusion after ischemic injury, hypertension, and inflammation. To counter carbonyl stress, cells possess enzymes that can decrease aldehyde load. These enzymes include aldehyde dehydrogenases (ALDH), aldo-keto reductases (AKR), carbonyl reductase (CBR), and glutathione S-transferases (GST). Some of these enzymes are inducible by chemoprotective compounds via Nrf2/ARE- or AhR/XRE-dependent mechanisms. This review describes the metabolism of reactive carbonyls and discusses the potential for manipulating levels of carbonyl-metabolizing enzymes through chemical intervention.
在多种疾病进程中，氧化应激会产生反应性醛类和酮类物质。目前，大量证据表明这些反应性羰基产物也参与了包括神经退行性疾病、糖尿病、动脉粥样硬化、糖尿病并发症、缺血性损伤后的再灌注、高血压和炎症在内的疾病进展。为了应对羰基应激，细胞拥有能够降低醛负荷的酶。这些酶包括醛脱氢酶（ALDH）、醛酮还原酶（AKR）、羰基还原酶（CBR）和谷胱甘肽S-转移酶（GST）。其中一些酶可被化学保护化合物通过Nrf2/ARE或AhR/XRE依赖性机制诱导。本综述描述了反应性羰基的代谢，并讨论了通过化学干预来调控羰基代谢酶水平的可能性。
