Effects of acute and chronic hypoxia on mitochondrial ros production and respiration in brook trout (Salvelinus fontinalis)

Abstract

Molecular oxygen is vital for all aerobic life. Environmental hypoxia is increasing due to natural and anthropogenic factors causing aquatic environments to vary substantially in the amount of dissolved oxygen. This decrease in oxygen is only projected to become more severe and persist for longer periods of time leading to major oxygen-limiting challenges for aerobic aquatic organisms. Low-environmental oxygen has direct effect on mitochondrial function and is known to trigger reactive oxygen species (ROS) production. There are few studies which examine the effects of prolonged hypoxia exposure in fish, but they suggest hypoxia duration may influence mitochondrial physiology. To understand the long-term exposure effects of hypoxia on mitochondrial physiology, brook trout (Salvelinus fontinalis), a hypoxia sensitive species, were exposed to acute (24 hour) and chronic (7 days) hypoxia. Following exposure, we isolated mitochondria to examine oxygen consumption and ROS production rates in nonphosphorylating and phosphorylating respiration states. We found no changes in mitochondrial respiration in either phosphorylating or non-phosphorylating states across any exposure groups. However, we found an increase in the rate of ROS production following acute hypoxia but not after exposure to chronic hypoxia. The results suggest that this severity/duration of hypoxia in combination with starvation brook trout appear to be able to acclimate to longer periods of hypoxia where they can limit mitochondrial ROS production and maintain respiration.