Abstract

Calcium (Ca2+) may be involved in plant tolerance to heat stress by regulating antioxidant metabolism or/and water relations. This study was designed to examine whether external Ca2+ treatment would improve heat tolerance in two C(3), cool-season grass species, tall fescue (Festuca arundinacea L.) and Kentucky bluegrass (Poa pratensis L.), and to determine the physiological mechanisms of Ca2+ effects on grass tolerance to heat stress. Grasses were treated with CaCl(2) (10 mM) or H(2)O by foliar application and then exposed to heat stress (35/30 degrees C) in growth chambers. Some of the Ca2+ -untreated plants were maintained at 20/15 degrees C as the temperature control. Heat stress reduced grass quality, relative water content (RWC), and chlorophyll (Chl) content of leaves in both species, but Ca2+ treatment increased all three factors under heat stress. The Ca2+ concentration in cell saps increased with heat stress and with external Ca2+ treatment in both species. Osmotic potential increased with heat stress, but external Ca2+ treatment had no effect. Osmotic adjustment increased during short-term heat stress, but then decreased with a prolonged period of stress; it was not influenced by Ca2+ treatment. The activity of superoxide dismutase (SOD) in both species increased transiently at 12 d of heat stress and then remained at a level similar to that of the control. External Ca2+ treatment had no effect on SOD activity. The activities of catalase (CAT), ascorbate peroxidase (AP), and glutathione reductase (GR) of both species decreased during heat stress. Plants treated with Ca2+ under heat stress had higher CAT, GR and AP activities than untreated plants. Lesser amounts of malondialdehyde (MDA) accumulated in Ca2+ -treated plants than in untreated plants during extended periods of heat stress. The results suggested that exogenous Ca2+ treatment enhanced heat tolerance in both tall fescue and Kentucky bluegrass. This enhancement was related to the maintenance of antioxidant activities and a decrease in membrane lipid peroxidation, but not to the regulation of osmotic potential and osmotic adjustment.

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