Parma Nand Sharma

Nitric oxide (NO) has been reported to alleviate Fe-deficiency effects, possibly by enhancing the functional Fe status of plants. This study examines changes in tissue Fe status and oxidative metabolism in Fe-deficient maize (Zea mays L.) plants enriched with NO using sodium nitroprusside (SNP) as a source. Measurements included changes in concentrations of H₂O₂, non-protein thiols, levels of lipid peroxidation and activities of superoxide dismutase (SOD) and of the Fe-requiring antioxidant haem enzymes catalase, peroxidase and ascorbate peroxidases. Internal NO in Fe-deficient maize plants was manipulated with SNP and the NO scavenger, methylene blue (MB). A key control was treatment with sodium ferrocyanide (SF), a non-NO-supplying analogue of SNP. SNP but not SF caused re-greening of leaves in Fe-deficient maize plants over 10–20 days, increased in vivo NO content, raised chlorophyll and carotenoid concentrations, promoted growth in dry weight, increased the activities of H₂O₂-scavenging haem enzymes and enhanced lipid peroxidation, while decreasing SOD activity and H₂O₂ concentrations. The NO scavenger, MB, blocked the effects of the SNP. Although SNP and SF each donated Fe and increased active Fe, only SNP increased leaf chlorophyll. NO plays a role in Fe nutrition, independently of its effect on total or active Fe status. The most probable mechanism of NO involvement is to increase the intracellular availability of Fe by means of modulating redox. This is likely to be achieved by enhancing the chemical reduction of foliar Fe(III) to Fe(II).

The aim of the study was to induce B deficiency symptoms and to relate the generation of reactive oxygen species (ROS) and altered cellular redox environment with the effects of B deficiency in mulberry (Morus alba L.) cv. Kanva-2 plants. Study was undertaken on antioxidant responses, malondialdehyde (MDA) content as an indicator of oxidative damage and ratio of dehydroascorbate (DHA) to ascorbic acid (AsA) as an index of cellular redox environment in B-deficient (0.0 μM) and B-supraoptimal (33 μM) mulberry plants. B deficiency symptoms appeared as upward cupping of the young emerging leaves. Later on, B-deficient plants developed lenticels like cracks on major vein, petiole and stem. B-deficient leaves had higher water potential (Ψ) and relative water content (RWC), contained a lower concentration of B, less chloroplastic pigments and high tissue Fe, Mn and Zn concentrations compared to the controls. Hydrogen peroxide was accumulated in leaves of B-deficient and B-supraoptimal plants. B-supraoptimal plants also showed an increased DHA/AsA ratio. The activities of superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), peroxidase (POD, EC 1.11.1.7) and ascorbate peroxidase (APX, EC 1.11.1.11) were increased in B-deficient leaves. The activities of SOD and POD were decreased in B-supraoptimal plants. The results suggest that B deficiency aggravates oxidative stress through enhanced generation of ROS in mulberry plants.

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 CdSO₄. 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 H₂O₂ 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 NiSO₄ (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 H₂O₂ 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.

In this study, we examined the modulation of Cu toxicity-induced oxidative stress by excess supply of iron in Zea mays L. plants. Plants receiving excess of Cu (100 μM) showed decreased water potential and simultaneously showed wilting in the leaves. Later, the young leaves exhibited chlorosis and necrotic scorching of lamina. Excess of Cu suppressed growth, decreased concentration of chloroplastic pigments and fresh and dry weight of plants. The activities of peroxidase (EC 1.11.1.7; POD), ascorbate peroxidase (EC 1.11.1.11; APX) and superoxide dismutase (EC 1.15.1.1; SOD) were increased in plants supplied excess of Cu. However, activity of catalase (EC 1.11.1.6; CAT), was depressed in these plants. In gel activities of isoforms of POD, APX and SOD also revealed upregulation of these enzymes. Excess (500 μM)-Fe-supplemented Cu-stressed plants, however, looked better in their phenotypic appearance, had increased concentration of chloroplastic pigments, dry weight, and improved leaf tissue water status in comparison to the plants supplied excess of Cu. Moreover, activities of antioxidant enzymes including CAT were further enhanced and thiobarbituric acid reactive substance (TBARS) and H₂O₂ concentrations decreased in excess-Fe-supplemented Cu-stressed plants. In situ accumulation of H₂O₂, contrary to that of O₂ ^·− radical, increased in both leaf and roots of excess-Cu-stressed plants, but Cu-excess plants supplied with excess-Fe showed reduced accumulation H₂O₂ and little higher of O₂ ^·− in comparison to excess-Cu plants. It is, therefore, concluded that excess-Cu (100 μM) induces oxidative stress by increasing production of H₂O₂ despite of increased antioxidant protection and that the excess-Cu-induced oxidative damage is minimized by excess supply of Fe.

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.

The aim of the study was to implicate the generation of reactive oxygen species (ROS) and altered cellular redox environment with the effects of Cu-deficiency or Cu-excess in mulberry (Morus alba L.) cv. Kanva 2 plants. A study of antioxidative responses, indicators of oxidative damage and cellular redox environment in Cu-deficient or Cu-excess mulberry plants was undertaken. While the young leaves of plants supplied with nil Cu showed chlorosis and necrotic scorching of laminae, the older and middle leaves of plants supplied with nil or 0.1 μM Cu showed purplish-brown pigmented interveinal areas that later turned necrotic along the apices and margins of leaves. The Cu-excess plants showed accelerated senescence of the older leaves. The Cu-deficient plants showed accumulation of hydrogen peroxide and superoxide anion radical. The accumulation of hydrogen peroxide was strikingly intense in the middle portion of trichomes on Cu-deficient leaves. Though the concentration of total ascorbate increased with the increasing supply of Cu, the ratio of the redox couple (DHA/ascorbic acid) increased in Cu-deficient or Cu-excess plants. The activities of superoxide dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6), peroxidase (EC 1.11.1.7), ascorbate peroxidase (EC 1.11.1.11) and glutathione reductase (EC 1.6.4.2) increased in both Cu-deficient and Cu-excess plants. The results suggest that deficiency of Cu aggravates oxidative stress through enhanced generation of ROS and disturbed redox couple. Excess of Cu damaged roots, accelerated the rate of senescence in the older leaves, induced antioxidant responses and disturbed the cellular redox environment in the young leaves of mulberry plants.