Induction of heat resistance in wheat seedlings by exogenous calcium, hydrogen peroxide, and nitric oxide donor: functional interaction of signal mediators

Abstract

Functional interactions of calcium ions, hydrogen peroxide, and nitric oxide as signal mediators in root cells of wheat (Triticum aestivum L.) seedlings upon induction of their heat resistance was studied with use of inhibitor-based analysis. Treatment of the seedlings with hydrogen peroxide or a combination of calcium chloride with ionophore A23187 significantly increased their content of nitric oxide, which peaked 0.5–1 h after the start of the treatment. CaCl2 or exogenous NO donor (sodium nitroprusside, SNP) transitorily increased the hydrogen peroxide level in the roots. Seedlings pretreatments with calcium chelator (EGTA), blocker of Ca2+ channels (LaCl3), inhibitor of phospholipase C (neomycin), or antagonist of cyclic adenosine-5'-diphosphatribose formation (nicotinamide) more or less prevented the rise in the nitric oxide content in roots caused by exogenous H2O2; the SNP-induced rise in hydrogen peroxide was also damped down. However, the seedlings pretreatment with antioxidants ionol or dimethylthiourea did not hinder the increase in the NO level, which was caused by exogenous Ca2+. The inhibitors of NO synthase (NG-nitro-L-arginine methyl ester, L-NAME) or nitrate reductase (sodium tungstate) did not interfere in the accumulation of H2O2 in root tissues stimulated by exogenous calcium. Calcium antagonists diminished the seedlings heat resistance increased by hydrogen peroxide or SNP. Antioxidants and inhibitors of NO synthase or nitrate reductase weakened the calcium-stimulated enhancement in the seedlings heat resistance. It was concluded that calcium may activate NO- and H2O2-generating enzymatic systems as well as participate in the transduction of signals of these mediators into genetic apparatus and in the formation of physiological reactions underlying the enhanced heat resistance.