Effect of cadmium uptake and heat stress on root ultrastructure, membrane damage and antioxidative response in rice seedlings

摘要

Excess cadmium (Cd~(2+)) in the soil environment is taken up by plants and can cause phytotoxicity. Elevated temperatures also lead to deleterious effects on plants. Plants are very often exposed to a combination of stresses rather than a single stress. The effect of Cd~(2+) and heat stress (HS) on the growth, root ultrastructure, lipid peroxidation (MDA), hydrogen peroxide accumulation and the activities of antioxidant enzymes peroxidase (POD), catalase (CAT) and ascor-bate peroxidase (APX) of riceroots from sensitive cv. DR-92 and tolerant cv. Bh-1 were investigated at 10 and 20 day of growth under controlled conditions. At day 10 under all Cd~(2+) treatments, the Cd~(2+) content between the two rice cultivars were almost similar. Application of500 mu M Cd~(2+) significantly increased metal concentrations at day 20 in the roots of rice seedlings resulting in a maximum accumulation of 44.25 mu g Cd~(2+) g~(-1) dry wt in cv. DR-92 and 30 mu g Cd~(2+) g~(-1) dry wt in cv. Bh-1 with a -25 % declinein Relative Growth Index (RGI) in cv. DR-92. TEM studies revealed slight disorganization with cell wall ingrowths in root tissues from cv. DR-92 grown in 100 mu M Cd~(2+) + HS. Uptake and accumulation of Cd~(2+) increased upon heat treatment in parenchyma, vacuoles and vascular cylinder of root tissues. Peroxidase primarily located in cell walls, the intensity being higher in sensitive cv. DR-92. Under Cd~(2+) stress alone, plants of sensitive cv. DR-92 significantly increased the H_2O_2 and MDA levelstogether with increased activities of the enzymes POD, CAT and APX at day 10 but remained almost stable at day 20. A strong increase in MDA levels was noted at day 20 in tolerant cv. Bh-1. Cd~(2+) + HS treatments in tolerant cv.Bh-1 led to a decreased H_2O_2 and MDA levels and decreased activities of the enzymes POD, CAT and APX. Results suggest stimulation of root antioxidant system under combination of two stresses and that heat stress seem to have a direct protective role by mitigating the effect ofmild Cd~(2+) toxicity largely by enhanced Cd~(2+)-MT formation contributing thereby towards the management of Cd~(2+) toxicity at cellular level that confers Cd~(2+) tolerance to rice cv. Bh-1.