| Research Abstract |
Versatile capacity of land plants to tolerate ever-fluctuating environmental conditions, e. g. light, temperature, water supply, gases and nutrients, is the prerequisite for the immotile life of them. It has been shown recently that various environmental stresses induce oxidative damage in plants. Indeed, in vivo electron spin resonance spectrometry (ESR) revealed that the oxidation level of leaf cells is raised by drought, UV, strong light, herbicides and other environmental stresses at early stages of these stresses (Heber et al. 1996). In this study, aiming at describing how and what factors determine the fate of environmentally stressed cells, biochemical events at early stages of water stress in plants were investigated.
The following results were obtained: (1) Water-stress made by a high osmoticum on lettuce roots induced higher production of monodehydroascorbate (MDA) radicals in the leaves, even prior to any visible changes of leaves. (2) Chloroplastic (Cp) CuZn-superoxide dismu
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tase (SOD) in leaves was inactivated specifically by a weak osmotic stress that did not induce leaf wilting. (3) A stronger osmotic stress leading to irreversible leaf wilting resulted in the inactivation of catalase in addition to Cp-SOD, while ascorbate peroxidase (APX) and the reaction center of photosystem II were kept intact. (4) The oxidative stress-inducing agent methylviologen inactivated Cp-APX in spinach very quickly and specifically. Resulting loss of H2O2-scavenging capacity of chloroplasts lead to inactivation other H_2O_2-sensitive enzymes in cells. Thus, development of oxidative damages of leaves by MV is ascribed to the inactivation of Cp-APX.
These results revealed the antioxidant enzymes as sensitive targets of environmental stresses, as well as the importance of their primarily defensive roles. The target enzymes were specific to specific types of environmental stress. This finding will not only lead to strategic designing of molecular breeding of stress-tolerant crops, but also pose new questions how and for what such specific inactivation of the defense enzymes is regulated. Less
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