Oxidative metabolism studies on thermal regulation‐Protective mechanism against free radical in zebrafish brain

Abstract

Exposure of ectothermic vertebrates to fluctuated temperatures accelerates mitochondrial respiration and has been shown to increase the formation of mitochondrial reactive oxygen species (ROS), such as O2−, H2O2, and O2−·. Excess ROS production by intensively respiring mitochondria is held responsible for cellular damage. The present study was to test whether a protective oxidative‐stress pathway would be initiated in fish central nervous system upon cold stress.Effects of acute cold exposure (from 28 °C to 18 °C) on brain oxidative stress parameters were investigated in zebrafish (Danio rerio). Concentrations of cellular protein carbonyl groups (biomarkers of oxidative stress) were significantly increased after 1‐hour cold exposure. Increased levels of anti‐oxidative stress parameters, catalase (CAT) and superoxide dismutase (SOD) were observed at 1‐ and 6‐hour cold exposure, respectively. In spite of maintained anti‐oxidant capacity, the increment status of cellular oxidized protein accumulation was still observed. A neuronal defense pathway against ROS, peroxisome proliferator‐activated receptor (PPAR), acts with genes encoding uncoupling proteins (UCPs) was further monitored. Real‐time PCR analysis indicated that ppar‐1αb increased was transcriptionally regulated the expression of zucp2 and zucp2l. Mitochondrial biogenesis activation, mild uncoupling, and reduction of free radicals may result intracellular pO2 levels drop. Moreover, these protective mechanisms in fish brain have been found to cause hypoxia‐induced factor (HIF) stabilization that facilitates an increase in energy supply.