抄録
Glycative stress has drawn attention in recent years as a factor that significantly affects tissues and organs of the human body and is directly related to health maintenance and aging-related diseases. Glycative stress refers to the excessive formations of carbohydrate-derived aldehydes or fatty-acid-derived aldehydes in the body. These aldehydes impact diverse substances such as proteins, lipids, and bases in cells, and subcellular organelles. Proteins in the body are modified by non-enzymatic procedure and abnormal proteins, i.e., carbonylated proteins, advanced glycation end-products (AGEs), are formed and stored intra- and extra-cellularly. AGEs induce endoplasmic reticulum stress, causing the deterioration of cellular functions Although glyceraldehyde-3-phosphate dehydrogenase (GAPDH), glyoxalase, and aldehyde dehydrogenase (ALDH) are prepared for protection in the body as a defensive measure against aldehydes, a co-enzyme, nicotinamide adenine dinucleotide (NAD) is consumed to a large extent through metabolic process. As a result, a tricarboxylic acid cycle (TCA cycle) in mitochondria, where NAD is needed, is unable to function smoothly. Fumaric acid is elevated and important proteins such as GAPDH and adiponectin undergo succinylation, which causes the deterioration of functional proteins. The present study reviewed the involvement of glycative stress in the insulin secretion of pancreatic β cell and Alzheimer's dementia (AD). For AD protectiom, it is important to inhibit peroxidation of lipids which exist abundantly in the brain and inhibit glycative modification of amyloid β (Aβ) and tau proteins. We hope that further extensive research on anti-glycation will be undertaken, and deeper understanding and increased participation will be encouraged. Studies on glycative stress are necessary to lead to a social implementation as a practical science.
