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The aim of this study was to induce symptoms of zinc deficiency and Zn excess and to relate the generation of reactive oxygen species (ROS) and the altered cellular redox environment to the effects of Zn stress in mulberry (Morus alba L.) cv. Kanva-2 plants. The antioxidative responses of Zn-stressed mulberry plants were studied by determining malondialdehyde content (MDA, a measure of lipid peroxidation) as indicator of oxidative damage and the ratio of dehydroascorbate (DHA) to ascorbic acid (AsA) as an index of the cellular redox state. The Zn-deficiency effects appeared as faint paling and upward cupping of the young emerging leaves. The paling intensified with time, and affected leaves finally developed necrotic spots. At advanced stage of Zn deficiency, newly emerged leaves were spindle-shaped, pale, and small in size. Apart from their stunted appearance, the plants supplied excess Zn did not show any specific visible symptom. Leaf water status of mulberry plant was affected in Zn-stressed plants. Deficient leaves had decreased water potential (Ψ) and specific water content (SWC), contained less tissue Zn, less chloroplastic pigments, and high tissue Fe and Mn concentrations. However, excess supply of Zn was found to increase Ψ and decrease tissue Fe. Both hydrogen peroxide and MDA accumulated in leaves of Zn-stressed plants. While the concentration of DHA did not vary in Zn-deficient leaves, it was increased in leaves of plants supplied excess Zn. The ratio of the redox couple (DHA to AsA) was increased both in Zn-deficient or Zn-excess plants. The activities of superoxide dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6), peroxidase (EC 1.11.1.7), and ascorbate peroxidase (EC 1.11.1.11) increased in Zn-stressed plants. The results suggest that deficiency or excess of Zn aggravates oxidative stress through enhanced generation of ROS and a disturbed redox homeostasis in mulberry plants.

Maize (Zea mays L. cv. 777) plants grown in hydroponic culture were treated with 50 μM CdSO 4 . Growth and metabolic parameters indicative of oxidative stress and antioxidant responses were studied in leaves of plants treated with Cd. Apart from increasing lipid peroxidation and H 2 O 2 accumulation, supply of Cd suppressed growth, fresh and dry mass of plants and decreased the concentrations of chloroplastic pigments. The activities of catalase (CAT; EC 1.11.1.6), peroxidase (POD; EC 1.11.1.7), ascorbate peroxidase (APX; EC 1.11.1.11) and superoxide dismutase (SOD; EC 1.15.1.1) were increased in plants supplied 50 μM Cd. Localization of activities of isoforms of these enzymes (POD, APX and SOD) on native gels also revealed increase in the intensities of pre-existing bands. Stimulated activities of CAT, POD, APX and SOD in maize plants supplied excess Cd do not appear to have relieved plants from excessive generation of reactive oxygen species (ROS). It is, therefore, concluded that supply of 50 μM Cd induces oxidative stress by increasing production of ROS despite increased antioxidant protection in maize plants.

Maize (Zea mays L. cv. 777) plants grown in hydroponic culture were treated with 100 μM NiSO 4 (moderate nickel (Ni) excess). In addition to growth parameters, metabolic parameters representative of antioxidant responses in leaves were assessed 24 h and 3, 7, and 14 d after initiating the Ni treatment. Extent of oxidative damage was measured as accumulation of malondialdehyde and hydrogen peroxide in leaves 7 and 14 d after treatment initiation. Apart from increasing membrane-lipid peroxidation and H 2 O 2 accumulation, excess supply of Ni suppressed plant growth and dry mass of shoots but increased dry mass of roots and decreased the concentrations of chloroplastic pigments. Excess supply of Ni, though inhibited the catalase (EC 1.11.1.6) activity, increased peroxidase (EC 1.11.1.7), ascorbate peroxidase (EC 1.11.1.11), and superoxide dismutase (EC 1.15.1.1) activities. Localization of isoforms of these enzymes (peroxidase, ascorbate peroxidase, and superoxide dismutase) on native gels also revealed increases in the intensities of pre-existing bands. Enhanced activities of peroxidase, ascorbate peroxidase, and superoxide dismutase, however, did not appear to be sufficient to ameliorate the effects of excessively generated reactive oxygen species due to excess supply of Ni.

The aim of this study was to associate the generation of reactive oxygen species (ROS) with induced antioxidant responses and disturbed cellular redox environment in the nitrogen-(N), phosphorus-(P), or potassium-(K) deficient mulberry (Morus alba L. var. Kanva-2) plants. The indicators of oxidative stress and cellular redox environment and antioxidant defense-related parameters were analyzed. Deficiency of N, P or K suppressed growth, accelerated senescence, and decreased concentrations of chloroplastic pigments and glutathione. Lipid peroxidation and activities of superoxide dismutase, ascorbate peroxidase and glutathione reductase were also increased in these N, P, or K deprived plants. Concentration of hydrogen peroxide increased in plants deficient in N or P. Deficiency of N or P particularly altered the cellular redox environment as indicated by changes in the redox couples, namely ascorbic acid/total ascorbate decreased in P-, glutathione sulfydryl/total glutathione decreased in N-, and increased in P-deficient plants. Activity staining of native gels for superoxide dismutase revealed increased activity as indicated by increased intensity of bands, and induction of few new isoforms in P- and K-deficient plants. Differences in the patterns of superoxide dismutase isoforms and redox status (ascorbic acid/total ascorbate and glutathione sulfydryl/total glutathione) indicate that N-, P-, or K-deficiency altered antioxidant responses to varying extents in mulberry plants.