Oxidative stress in response to cold acclimation in threespine sticklebacks (Gasterosteus aculeatus)


Meeting Abstract

P3.57  Wednesday, Jan. 6  Oxidative stress in response to cold acclimation in threespine sticklebacks (Gasterosteus aculeatus) KAMMER, A.R.*; O’BRIEN, K.M.; University of Alaska Fairbanks; University of Alaska Fairbanks arkammer@alaska.edu

We sought to quantify levels of oxidative stress during cold acclimation and to determine if increases in reactive oxygen species (ROS) might be responsible for stimulating cold-induced mitochondrial biogenesis in threespine sticklebacks. Fishes were held at 20°C for 12 wk and then acclimated to 8°C for 9 wk or held at 20°C for an additional 9 wk. Animals were harvested on the first four days of cold acclimation and at wk 1, 4 and 9. Levels of protein carbonyls were quantified by HPLC as an indirect measure of ROS production. The activity of superoxide dismutase (SOD) was measured at 14°C and at the acclimation temperature of 20ºC or 8ºC. All measurements were made in liver, glycolytic skeletal muscle, and oxidative pectoral adductor muscle. Protein carbonylation levels significantly increased in liver tissue after animals were maintained for 1 wk at 8°C but did not change in either oxidative or glycolytic muscles. When measured at a common temperature, SOD activity significantly increased in all tissues by day 2 of cold acclimation. When measured at the acclimation temperature, SOD activity in oxidative muscle was significantly greater in animals held at 8°C for 9 wk compared to those held at 20°C for 9 wk but remained unchanged in liver and glycolytic muscle. High levels of SOD in oxidative muscle may protect cells against cold-induced oxidative damage, thereby preventing an increase in protein carbonylation. The increase in protein carbonylation in liver tissue corresponds with an increase in the expression of some transcription factors (PGC-1α and TFAM) that may play a role in cold acclimation. However, the lack of increase in ROS in oxidative and glycolytic muscles suggests that they do not play a role in inducing mitochondrial biogenesis in these tissues.

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