In: Anatomy and Physiology
Describe why a blocked cerebral artery causes the ratio of NAD+ to NADH+H+ in neurons remains constant, before and after the stroke.
Aging progression also depends on the NAD + /NADH ratio through the regulation of a number of NAD-linked enzymes.Changes in the NAD level or redox state have been observed in a variety of human diseases, such as diabetes, carcinogenesis, ischemia, and neurodegenerative disorders. Thus, methods for studying this important redox parameter are constantly being developed and improved.
NAD+ is a dinucleotide cofactor with the potential to accept electrons in a variety of cellular reduction-oxidation (redox) reactions. In its reduced form, NADH is a ubiquitous cellular electron donor. NAD+, NADH, and the NAD+/NADH ratio have long been known to control the activity of several oxidoreductase enzymes. More recently, enzymes outside those participating directly in redox control have been identified that sense these dinucleotides, including the sirtuin family of NAD+-dependent protein deacylases. In this review, we highlight examples of non-redox enzymes that are controlled by NAD+, NADH, or NAD+/NADH. In particular, we focus on the sirtuin family and assess the current evidence that the sirtuin enzymes sense these dinucleotides and discuss the biological conditions under which this might occur; we conclude that sirtuins sense NAD+, but neither NADH nor the ratio.