Parma Nand Sharma

Modulation of oxidative stress responsive enzymes by excess cobalt

Abstract 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.

Zinc requirement for stomatal opening in cauliflower

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.

Zinc deficiency and pollen fertility in maize (Zea mays)

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.

Development and enzymatic changes during pollen development in boron deficient maize plants

Abstract 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.

Early Signs of Oxidative Stress in Wheat Plants Subjected to Zinc Deficiency

Abstract 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, particularly that of cyanide-sensitive superoxide dismutase. Restoration of Zn supply significantly increased activities of cyanide-sensitive and total superoxide dismutase and ascorbate peroxidase, and concentration of H2O2, and decreased malondialdehyde significantly within 24 h. Induction of anti-oxidative responses to Zn deficiency occurred rapidly and before symptoms of severe Zn deficiency. There was a depression of anti-oxidative responses as Zn deficiency become more severe, suggesting a break down of these defense systems at the onset of visible effects of Zn deficiency

Sodium nitroprusside-mediated alleviation of iron deficiency and modulation of antioxidant responses in maize plants

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.

Manganese deficiency in maize affects pollen viability

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.

Mineral nutrient deficiencies affect plant water relations

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.

Morphology and oxidative physiology of boron-deficient mulberry plants

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 microM) and B-supraoptimal (33 microM) 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 (Psi) 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.

Oxidative stress and antioxidant responses of mulberry (Morus alba) plants subjected to deficiency and excess of manganese

The aim of the study was to relate the effects of deficiency and excess of Mn with the generation of reactive oxygen species (ROS) and altered cellular redox environment in mulberry (Morus alba L.) cv. Kanva-2 plants. Mn deficiency symptom appeared as mild interveinal chlorosis in middle leaves. Mn-excess did not produce any specific symptom. Leaf water potential (Ψ) was increased in Mn-deficient and Mn-excess mulberry plants. Mn-deficient leaves contained less Mn, less chloroplastic pigments and high tissue Fe, Zn and Cu concentrations. Starch content was increased with increasing Mn supply. While reducing sugar content increased in Mn-deficient and Mn-excess plants as well, non-reducing sugars remained unaffected in Mn-deficient plants and decreased in Mn-excess plants. Moreover, study of antioxidative responses, oxidative stress (H2O2 and lipid peroxidation) and cellular redox environment [dehydroascorbate (DHA)/ascorbic acid (AsA) ratio] in Mn-stressed mulberry plants was also undertaken. Both hydrogen peroxide and lipid peroxidation were enhanced in the leaves of Mn-deficient plants. Increased H2O2 concentration in Mn-excess leaves did not induce oxidative damage as indicated by no change in lipid peroxidation. The ratio of the redox couple (DHA/AsA) was increased both in Mn-deficient or Mn-excess plants. The activities of superoxide dismutase (EC 1.15.1.1) and catalase (EC 1.11.1.6) increased in Mn-deficient plants. The activity of ascorbate peroxidase (EC 1.11.1.11) increased with increasing Mn supply. The results suggest that deficiency or excess of Mn induces oxidative stress through enhanced ROS generation and disturbed redox couple in mulberry plants.