Glyceraldehyde and glyceraldehyde-derived advanced glycation end-products have negative effect on chicken myoblasts

Abstract

Advanced glycation end-products (AGEs) are formed through glycation between reducing sugars or their metabolites, including glyceraldehyde (GA). AGEs are associated with various chronic diseases in humans. Among them, GA-derived AGEs (GA-AGEs) exhibit strong toxicity in several cell types and are considered toxic AGEs. However, the effects of GA and GA-AGEs have not been examined in birds. The present study investigated whether GA and GA-AGEs negatively affect chicken embryo myoblasts. Myoblasts exposed to GA became sparse and small and exhibited a significant reduction in intracellular nicotinamide adenine dinucleotide (NADH) levels. Since the GA-induced decrease in NADH level was attenuated by aminoguanidine, which inhibits glycation and the production of AGEs, the effect would be attributed to the GA-AGEs, at least in part. Indeed, GA-AGEs itself also significantly decreased the intracellular NADH level. On the other hand, GA and GA-AGEs did not induce cell death such as apoptosis, and the production of reactive oxygen species in chicken myoblasts. Furthermore, neither GA nor GA-AGEs reduced the ratio of ATP levels to the total amount of ATP and ADP. In addition, GA did not affect mitochondrial membrane potential, whereas GA-AGEs decreased it. These results demonstrated that GA- and GA-AGEs decreased the intracellular NADH levels in chicken myoblasts, and the effect would not be due to cell death but the decrease in cell number.