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Heat stress hardening of oriental armyworms is induced by a transient elevation of reactive oxygen species during sublethal stress
Author(s) -
Matsumura Takashi,
Matsumoto Hitoshi,
Hayakawa Yoichi
Publication year - 2017
Publication title -
archives of insect biochemistry and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.576
H-Index - 66
eISSN - 1520-6327
pISSN - 0739-4462
DOI - 10.1002/arch.21421
Subject(s) - reactive oxygen species , catalase , antioxidant , oxidative stress , superoxide dismutase , biology , sod2 , heat shock protein , biochemistry , gene
Pre‐exposure to mild heat stress enhances the thermotolerance of insects. Stress hardening is a beneficial physiological plasticity, but the mechanism underlying it remains elusive. Here we report that reactive oxygen species (ROS) concentrations were quickly and transiently elevated in the armyworms, Mythimna separata , by exposing them to 40°C, but not other tested temperatures. Larvae exposed to 40°C had subsequently elevated antioxidant activity and the highest survival of all tested heating conditions. The elevation of ROS after lethal heating at 44°C for 1 h was approximately twofold compared to heating at 40°C. Injection of an optimal amount of hydrogen peroxide (H 2 O 2 ) similarly caused sequential elevation of ROS and antioxidant activity in the test larval hemolymph, which led to significantly enhanced survival after lethal heat stress. The H 2 O 2 ‐induced thermotolerance was abolished by coinjection of potent antioxidants such as ascorbic acid or N ‐acetylcysteine. Both preheating at 40°C and H 2 O 2 injection enhanced expression of genes encoding superoxide dismutase 1, catalase, and heat shock protein 70 in the fat body of test larvae, indicating the adequate heat stress induced a transient elevation of ROS, followed by upregulation of antioxidant activity. We infer that thermal stress hardening is induced by a small timely ROS elevation that triggers a reduction–oxidation signaling mechanism.