Abstract

Cold hardiness is a key determinant of the distribution and abundance of ectothermic animals, and thermal acclimation can strongly influence stress tolerance phenotypes. However, the effect of cold acclimation on oxidative stress and antioxidant defenses is still not well understood. Here, we investigated the effects of long-term cold exposure (30 days at 4°C in darkness versus 30 days at 20°C in natural light) on the redox state and antioxidant defenses of the high-altitude frog, Nanorana pleskei, indigenous to the Tibetan plateau. We found that cold acclimation, under conditions mimicking winter, led to a significant increase in the ratio of oxidized glutathione (GSSG) to its reduced form (GSH) in liver and skeletal muscle tissues, suggesting that cold exposure induced oxidative stress in this species. Furthermore, malondialdehyde (MDA) contents were significantly augmented in heart, liver and muscle, indicating cold-related oxidative damage in these tissues. In the brain, GST activity, total antioxidant capacity (T-AOC), and vitamin C content showed a significant reduction after cold acclimation. In liver, an apparent decrease was also observed in the activities of SOD and GST, as well as T-AOC, whereas CAT and GPX activities showed a prominent increase in cold-acclimated groups. In kidney, there was a significant decrease in most antioxidant enzyme activities except for SOD and GST activity. In skeletal muscle, the activity of SOD, CAT, GR as well as T-AOC significantly decreased but GPX activity showed a significant increase in cold-acclimated frogs. These findings indicate that, in general, cold acclimation induces a suppression of the antioxidant defense system. Overall, our present study systematically describes the responses of antioxidant defenses to long-term cold acclimation and these findings contribute to extending the current understanding of the mechanisms of cold tolerance in high-altitude frogs.

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