期刊
MOLECULAR NUTRITION & FOOD RESEARCH
卷 52, 期 3, 页码 379-385出版社
WILEY-V C H VERLAG GMBH
DOI: 10.1002/mnfr.200600190
关键词
advanced glycation end products; advanced lipid end products; cytotoxicity; lipid peroxidation; reactive oxygen species
Carbonyls generated by autoxidation of carbohydrates or lipid peroxidation have been implicated in advanced glycation end product (AGE) formation in tissues adversely affected by diabetes complications. Tissue AGE and associated pathology have been decreased by vitamin B-1/B-6 in trials involving diabetic animal models. To understand the molecular cytoprotective mechanisms involved, the effects of B-1/B-6 vitamers against cytotoxicity induced by AGE/advanced lipid end product (ALE) carbonyl precursors (glyoxal/acrolein) have been compared to cytotoxicity induced by oxidative stress (hydroperoxide) or mitochondrial toxins (cyanide/copper). Thiamin was found to be best at preventing cell death induced by carbonyl stress and mitochondrial toxins but not oxidative stress cell death suggesting that thiamin pyrophosphate restored pyruvate and a-ketoglutarate dehydrogenases inhibited by rnitochondrial toxicity. However, B-6 vitamers were most effective at preventing oxidative stress or lipid peroxidation cytotoxicity suggesting that pyridoxal or pyridoxal phosphate were antioxidants and/or Fe/Cu chelators. A therapeutic vitamin cocktail could provide maximal prevention against carbonyl stress toxicity associated with diabetic complications.
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