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Effect of chromium (both CrIII and CrVI) were studied on the oxidative damages and the induction of antioxidant defence in turnip. For this purpose turnip (Brassica rapa L.) plants were grown in refined sand under three different sources of chromium, i.e., chromium sulphate (CrIII), potassium chromate (CrVI) and potassium dichromate (CrVI) supplied at 250 µM concentrations for 4, 24 and 168 h (7 days) after 50 days of growth in normal nutrition. The extent of oxidative damage was most in dichromate as it caused a maximum increase in lipid peroxidation and H2O2 concentration in leaves of turnip plants. The growth and biomass of plants decreased, while the levels of chloroplastic pigment and iron increased in plants supplied CrVI (both potassium chromate and potassium dichromate). Exposure of plants to Cr led to increase in Cr concentration, more in the roots than in shoots. Excess supply of Cr (chromium sulphate, potassium chromate and potassium dichromate), though inhibited peroxidase activity (at 4 and 168 h exposure), stimulated catalase, ascorbate peroxidase and superoxide dismutase activities. Localization of different isoforms of APX and SOD on native gels revealed activation of certain isoform in the Cr-treated plants.

The aim of the study was to induce S deficiency symptoms and to relate the generation of reactive oxygen species (ROS) and altered cellular redox environment with the effects of S deficiency in mulberry (Morus alba L.) cv. Kanva-2 plants. A study of 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 S-deficient mulberry plants was undertaken. The S deficiency effects appeared as paling of the youngest emerging leaves. Soon, the leaves, as they expanded, became devoid of the green pigment and turned completely yellow. These leaves showed upward curling of the leaf margins and prominent wrinkles in the lamina tissues. Sulphur-deficient plants showed improved leaf water status, as indicated by increases in the degree of succulence (DS), specific water content (SWC), relative water content (RWC) and water potential (Ψ) of leaves, contained less tissue S concentration, less chloroplastic pigments, decreased tissue Fe and Cu and had improved tissue Mn concentrations. Increased hydrogen peroxide concentration under deficiency of S did not induce oxidative damage as indicated by decreased MDA concentration. The S-deficient plants exhibited significant decreases in the concentrations of DHA and total ascorbate. The ratio DHA/AsA decreased in these plants. While the activity of catalase (EC 1.11.1.6) decreased in S-deficient plants, activities of peroxidase (EC 1.11.1.7), superoxide dismutase (EC 1.15.1.1), and ascorbate peroxidase (EC 1.11.1.11) were increased. The results suggest that deficiency of S induced oxidative stress, however, because of low tissue Fe and Cu and enhanced antioxidant enzymes activities other than catalase, provided ample protection against oxidative challenge to the S-deficient 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 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.

The aim of the study was to implicate induction of oxidative stress and antioxidative responses with the effects of Mg deficiency in mulberry plants. Mulberry (Morus alba L.) cv. Kanva-2 plants grown in hydroponics were subjected to deficiency of Mg. Mg-deficient plants developed visible symptoms—deep interveinal chlorotic mottling and necrosis in the older and middle leaves. The decreases in the dry matter yield of plants and concentrations of sugars and starch in the leaves of Mg-deficient plants are suggestive of decreased photosynthetic activity. Mg-deficiency decreased concentrations of photosynthetic pigments, and increased concentrations of H2O2 and ascorbate and activities of antioxidative enzymes—peroxidase (POD), ascorbate peroxidase (APX) and superoxide dismutase (SOD). The results suggest induction of oxidative stress by enhancing generation of ROS and inducing alterations in redox status, accompanied by activation of antioxidant machinery including induction of some new SOD isoforms in Mg-deficient mulberry plants. Despite significant increase in H2O2, lipid peroxidation was decreased in Mg-deficient plants.

Studies were made to relate signs of oxidative stress in chlorotic and non-chlorotic leaves of plants receiving deficient supply, either nil (chlorotic leaves) or 10 μM (non-chlorotic leaves) of Fe, with thiobarbituric acid reactive substance (TBARS) and Fe status of leaf tissues. Total Fe concentration in the young leaves of mulberry, maize and cauliflower plants supplied deficient Fe did not show any significant change. Deficient supply of Fe caused decreases in the activities of catalase, peroxidase and ascorbate peroxidase and increases in the activity and number of isoforms of superoxide dismutase (SOD), accumulation of superoxide anion radical (O 2 − ) and concentration of H 2 O 2 in the young leaves of each mulberry, maize or cauliflower plants. While the chlorotic leaves of Fe-starved mulberry, maize and cauliflower plants had significantly lower TBARS compared to green leaves of the controls or non-chlorotic leaves of cauliflower plants supplied low Fe (10 μM). While TBARS concentration in the young leaves of these plants was well correlated with the concentrations of chloroplastic pigments, and activities of catalase and ascorbate peroxidase, its relationship with leaf tissue Fe or H 2 O 2 concentration was rather poor. Progressive increase in the activity and induction of new isoforms of SOD and higher accumulation H 2 O 2 and O 2 − may be considered as signs of oxidative stress, whereas, increased ascorbate content along with lower mole fraction of ascorbic acid/total ascorbate are indicative of disturbed cellular redox environment in Fe-starved plants. It is concluded that chlorotic leaves of Fe-starved plants though have elevated titre of reactive oxygen species they are less susceptible to oxidative damage probably due to lower chloroplastic pigments/or low functional Fe in the tissue.

Anti-oxidative defense systems in wheat plants were studied as a function of zinc deficiency in solution culture under glasshouse conditions. Zinc (Zn) deficiency enhanced cyanide-insensitive superoxide dismutase activity significantly, and decreased the activity of cyanide-sensitive superoxide dismutase before the appearance of visible effects of Zn deficiency. The plants with incipient deficiency of Zn also had significantly higher activities of nonspecific peroxidase, ascorbate peroxidase, and glutathione reductase. There was an increase in the concentrations of malondialdehyde, H2O2, dehydroascorbate, glutathione-sulfhydryl, and glutathione-disulphide, and the ratios carotenoids/chlorophyll, dehydroascorbate/ascorbate, and glutathione-sulfhydryl/glutathione-disulphide. As the effects of Zn deficiency became more severe, there was greater accumulation of malondialdehyde and H2O2, and the activities superoxide dismutase, peroxidase, ascorbate peroxidase, and glutathione reductase declined, part...

Induction of oxidative stress in hydroponically raised maize plants subjected to the deficiency of N, P, K, Ca, Mg or S was investigated by studying the levels of lipid peroxidation, H 2O2, and some important enzymatic antioxidative responses. Nutrient deficiency, irrespective of the element involved, resulted in decrease in dry matter yields of plants, enhanced lipid peroxidation and premature senescence of older parts implying oxidative stress in the plants. Foliar necrosis in Ca and S deficient plants and increased level of H 2O2 under N, S and Ca deficiencies suggest particularly severe oxidative stress in these plants. Activities of superoxide dismutase (SOD) and ascorbate peroxidase were stimulated by the deficiency of each of the macronutrients. Enhanced activity of catalase was observed in plants deficient in P, K and Ca and that of non-specific peroxidase in P and S deficiencies. Deficiency of each of the macronutrients increased the number of SOD isoforms and intensified SOD bands on native gel. © 2003 Elsevier Ireland Ltd. All rights reserved.

Excess concentration of cobalt in the growth medium produced visual symptoms of toxicity that intensified with increasing level and duration of metal supply. The tissue concentration of cobalt increased with increasing level of supply. Decreased concentrations of chlorophylls and carotenoids and an increased carotenoids/chlorophyll ratio along with a marked increase in the activities of anti-oxidative enzymes, viz. superoxide dismutase (SOD), ascorbate peroxidase (APOD) and nonspecific peroxidase (POD) suggest strong induction of oxidative stress due to excess cobalt in the growth medium. Decrease in the activity of catalase (CAT)—an iron enzyme, may suggest interference of excess cobalt in iron metabolism of plants, particularly above a 50 μM supply. Decrease in hydrogen peroxide with an increase in cobalt supply has been attributed to increased activities of POD and APOD. Increase in dry matter yield of plants supplied 50 μM cobalt and the decrease in lipid peroxidation with increasing cobalt supply in the range 50–200 μM is suggested as a result from depletion of functional iron as phosphate and/or in ferritin. Appearance of the metal specific toxicity is the likely result of damages predominantly due to enhanced reactive oxygen species (ROS) generation at higher, 300–400 μM, cobalt supplies.

The nitric oxide donor sodium nitroprusside (SNP) promotes regreening of Fe-deficient maize plants. The effect is not the outcome of increased tissue Fe but of NO-modulation of oxidative changes that may favour conversions of internal Fe to more readily available ferrous iron., Background and aims 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. Methodology 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. Principal results 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. Conclusions 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).

Maize (Zea mays L. cv. G2) was grown with 0.55 mg L−1 (sufficient), or 0.0055 mg L−1 (deficient) manganese in sand. Manganese-deficient plants developed visible deficiency symptoms and showed poor tasseling and delayed anther development. Compared to Mn-sufficient plants, Mn-deficient plants produced fewer and smaller pollen grains with reduced cytoplasmic contents. Manganese deficiency reduced in vitro germination of pollen grains significantly. Ovule fertility was not significantly affected by Mn. But in Mn-deficient plants seed-setting and development was reduced significantly.

Zinc deficiency decreased pollen viability in maize (Zea mays L. cv. G2) grown in sand culture. On restoring normal zinc supply to zinc-deficient plants before the pollen mother cell stage of anther development, the vegetative yield of plants and pollen fertility could be recovered to a large extent, but the recovery treatment was not effective when given after the release of microspores from the tetrads. If zinc deficiency was induced prior to microsporogenesis it did not significantly affect vegetative yield and ovule fertility, but decreased the fertility of pollen grains, even of those which visibly appeared normal. If the deficiency was induced after the release of microspores from the tetrads, not only vegetative yield and ovule fertility but pollen fertility also remained unaffected.

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 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 microM 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.

Zn deficiency induced increases in epicuticular wax deposits, lamina thickness, degree of succulence, water saturation deficit, diffusive resistance, and proline accumulation and decreases in carbonic anhydrase activity, water potential, stomatal aperture, and transpiration in the leaves of cauliflower (Brassica oleracea L. var botrytis cv Pusa) plants. Restoration of Zn supply to the deficient plants increased stomatal aperture, transpiration, and carbonic anhydrase activity significantly within 2 h. However, leaf water potential in the Zn-deficient plants did not recover within 24 h after resupply of Zn. The guard cells in epidermal peels from the Zn-deficient leaves had less K+ than those from the controls. Stomatal aperture in the epidermal peels from Zn-deficient leaves was 64% less than in the controls when the epidermal strips were floated on 125 mM KCl. Supplementing the ambient medium 25 mM KCl with ZnCl2 enhanced stomatal aperture in both control and Zn-deficient peels, and the effect was significant in the latter. The observations indicate involvement of Zn in stomatal opening, possibly as a constituent of carbonic anhydrase needed for maintaining adequate [HCO3-] in the guard cells, and also as a factor affecting K+ uptake by the guard cells.

Maize (Zea mays L.) plants subjected to severe deficiency of boron (0.0026 ppm B) failed to produce tassels with functional flowers. In plants subjected to moderate deficiency of boron (0.013 ppm B), emergence of tassels and anthesis was suppressed and delayed. In a large percentage of boron deficient plants the stamens lacked sporogenous tissue and appeared as staminodes or floral appendages that either lacked or had branched vascular supply. The apparently normal stamens of these plants also failed to dehisce and showed a marked decrease in pollen producing capacity, pollen size and pollen germination. Even in plants that were only marginally deficient in boron (0.066 ppm B), without any foliar symptoms of boron deficiency, pollen grains showed poor germination and changes in enzyme activities. Pollen grains of such plants had low activities of catalase, acid phosphatase, starch phosphorylase and invertase and high activities of ribonuclease and amylase.

Sand culture studies using cauliflower as the test plant revealed changes in water relations of plants subjected to deficiencies of Fe, Cu, Zn and B. While deficiencies of Zn and B caused a decrease in water potential, transpiration rate and water loss, deficiencies of Fe and Cu caused an increase in each of these. Observed changes in water relations have been examined in terms of changes in leaf morphology and metabolism.