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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.

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.