Nitric oxide alleviates heat stress-induced oxidative damage in Pleurotus eryngii var. tuoliensis
文献类型: 外文期刊
第一作者: Kong, Weiwei
作者: Kong, Weiwei;Huang, Chenyang;Chen, Qiang;Zou, Yajie;Zhang, Jinxia
作者机构:
关键词: Heat stress;Nitrate reductase;Nitric oxide;Nitric oxide synthase;Pleurotus eryngii var. tuoliensis
期刊名称:FUNGAL GENETICS AND BIOLOGY ( 影响因子:3.495; 五年影响因子:3.831 )
ISSN: 1087-1845
年卷期: 2012 年 49 卷 1 期
页码:
收录情况: SCI
摘要: High temperature is one of the major impediments limiting the growth and development of most edible fungi. While many efforts have been made in agricultural practice, the mechanism for resistance to high temperature remains elusive. Nitric oxide (NO) is considered as a signaling molecule involved in regulation of diverse physiological processes and stress responses in animals and plants. However, the role of NO in regulating fungal, particularly edible fungi, response to abiotic stresses, is unknown. The present study demonstrated that NO could effectively alleviate oxidative damage induced by heat stress in mycelia of Pleurotus etyngii var. tuoliensis. Heat stress induced increased thiobarbituric acid reactive substance (TBARS) content in mycelia, and the NO donor sodium nitroprusside (SNP) dramatically decreased TBARS content under high temperature. Moreover, the specific NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-1-oxyl-3-oxide (cPTIO), could arrest the SNP action under the stress. Heat stress induced an increase in endogenous NO production in mycelial cells. However, the effect was significantly blocked by the NO synthase (NOS) inhibitor L-N-G-nitroarginine methyl ester (L-NAME). In contrast, nitrate reductase (NR) activities were not obviously altered during heat stress. The NR suppressor tungstate had no effect on intracellular NO abundance under heat stress. These results suggest that NO can effectively protect mycelia of edible fungi from heat stress-induced oxidative damage and the NOS-dependent NO production may participate in the response to heat stress. (C) 2011 Elsevier Inc. All rights reserved.
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