Exploring pathways of NO and H2S signaling in metabolic depression: The case of anoxic turtles

In contrast to most vertebrates, freshwater turtles of the genera Trachemys and Chrysemys survive total oxygen deprivation for long periods of time. This remarkable tolerance makes them ideal August Krogh's model animals to study adaptions to survive oxygen deprivation. The gasotransmitters nitric oxide (NO) and hydrogen sulfide (H2S) and their metabolic derivatives are central in regulating the physiological responses to oxygen deprivation. Here, we explore the role of these signaling molecules in the anoxia tolerance of the freshwater turtle, including metabolic suppression and protection against oxidative damage with oxygen deprivation. We describe the interaction of NO and H2S with protein thiols and specifically how this regulates the function of central metabolic enzymes. These interactions contribute both to metabolic suppression and to prevent oxidative damage with oxygen deprivation. Furthermore, NO and H2S interact with ferrous and ferric heme iron, respectively, which affects the activity of central heme proteins. In turtles, these interactions contribute to regulate oxygen consumption in the mitochondria, as well as vascular tone and blood flow during oxygen deprivation. The versatile biological effects of NO and H2S underscore the importance of these volatile signaling molecules in the remarkable tolerance of freshwater turtles to oxygen deprivation.

Automated summary

Freshwater turtles of the genera Trachemys and Chrysemys can survive total oxygen deprivation for long periods of time, with the gasotransmitters nitric oxide (NO) and hydrogen sulfide (H2S) playing central roles in regulating their physiological responses. These signaling molecules interact with protein thiols to modulate metabolic suppression and protect against oxidative damage, highlighting their importance in the remarkable tolerance of freshwater turtles to oxygen deprivation.