Lumeng L, Lin R C
Department of Medicine, Indiana University School of Medicine, Indianapolis.
Ann N Y Acad Sci. 1991;625:793-801. doi: 10.1111/j.1749-6632.1991.tb33921.x.
With the use of antibodies that can recognize acetaldehyde adducts and the application of various immunological techniques, several protein-AAs have now been shown to form in vivo during chronic alcohol ingestion. These protein-AAs include the 37-kDa liver protein-AA, the CytP450IIE1-AA, hemoglobin-AA, two serum protein-AAs with molecular weights of 50 kDa and 103 kDa, and collagen type I protein-AA in liver. If acetaldehyde is the agent responsible for alcoholic liver injury, acetaldehyde toxicity in chronic alcohol ingestion must be linked to the ability of acetaldehyde to form adducts with proteins and perhaps other macromolecules. This is at least one mechanism of acetaldehyde-mediated liver injury. For proteins that serve critical functions, acetaldehyde adduct formation may alter their functions and thereby produce organ damage. Acetaldehyde adduct formation can also elicit humoral or cytotoxic immune responses and these responses may also lead to organ injury.
通过使用能够识别乙醛加合物的抗体以及应用各种免疫技术，现已表明在长期摄入酒精期间，体内会形成几种蛋白质-乙醛加合物。这些蛋白质-乙醛加合物包括37 kDa的肝脏蛋白质-乙醛加合物、细胞色素P450IIE1-乙醛加合物、血红蛋白-乙醛加合物、两种分子量分别为50 kDa和103 kDa的血清蛋白质-乙醛加合物以及肝脏中的I型胶原蛋白-乙醛加合物。如果乙醛是导致酒精性肝损伤的介质，那么长期摄入酒精时乙醛的毒性必定与乙醛和蛋白质以及可能与其他大分子形成加合物的能力有关。这至少是乙醛介导的肝损伤机制之一。对于发挥关键功能的蛋白质，乙醛加合物的形成可能会改变其功能，从而导致器官损伤。乙醛加合物的形成还可引发体液或细胞毒性免疫反应，而这些反应也可能导致器官损伤。
