Zinc against advanced glycation end products

摘要

Summary Advanced glycation end products ( AGE s) are destructive compounds with pathogenic importance in age‐related chronic diseases. Zinc has antioxidant, anti‐inflammatory and anti‐apoptotic potential. This study aimed to summarize effects of zinc on AGE formation and AGE ‐induced damaging agents. Pubmed, Google scholar, Web of Sciences, and Scopus databases were searched. There was no limitation for publication date. English language original articles (in vitro, experimental and human studies) which examined the effect of external zinc on AGE formation, AGE ‐induced apoptosis, or oxidative stress in mammals were included. To review the effect of zinc on AGE generation, the search keywords were as follows: “zinc” in title and “ AGE s” or “methylglyoxal” or “pentosidine” or “carboxymethyllysine” or “glucosylation” or “carbonyl stress” or “ AGE s‐induced apoptosis or oxidative stress or inflammation” in title/abstract. In total, 90 titles and abstracts were identified. Fifty‐two studies were screened after duplicates were removed. Six articles were chosen for review following analysis of both titles and summaries. Finally, based on intensive critical appraisal, 5 articles were included in the study. The evidence presented indicates that zinc has anti‐glycation, anti‐oxidative and anti‐apoptotic effects. Zinc insufficiency may stimulate AGE s formation. Whereas, zinc supplementation could inhibit formation of AGE s, AGE ‐induced cell apoptosis and oxidative stress status, and protein carbonyl formation possibly through various signalling pathways.