Mechanism of manganese toxictty and tolerance of plants VII. effect of light intensity on manganese‐induced chlorosis

Horiguchi, T.

doi:10.1080/01904168809363799

Cited by 34 publications

(17 citation statements)

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“…Although previous studies have suggested that low illumination delayed (McCool, 1935;Sirkar and Amin, 1974;Horiguchi, 1988;Nable et al, 1988) or even increased (Wissemeier and Horst, 1992) the symptoms of Mn toxicity, only one study focused specifically on the effect of light intensity on chlorophyll content of Mnstressed plants, and to our knowledge no previous reports have addressed the combined effect of light intensity and Mn toxicity on leaf antioxidants. Horiguchi (1988) grew common bean and maize under four different light regimes (100%, 80%, 40%, and 5% of the total radiation) and several Mn levels. Leaf chlorophyll content for all three light levels were compared in plants grown at 32 ppm Mn and control plants (0.32 ppm Mn).…”

Section: Discussionmentioning

confidence: 78%

“…The effect of light intensity on Mn-toxicity symptoms was first reported in 1935, when McCool (1935) found that plants grown in low light displayed fewer symptoms of Mn toxicity than those grown in high light. Subsequent reports with different crops found a similar effect of low light (Sirkar and Amin, 1974;Elamin and Wilcox, 1986;Horiguchi, 1988;Nable et al, 1988). Wissemeier and Horst (1992) reported that symptoms of Mn toxicity (localized brown spots and callose formation) in mature leaves of cowpea were enhanced under low-light conditions, but did not rule out that chlorosis in immature leaves might be enhanced under highlight conditions.…”

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confidence: 94%

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Light and Excess Manganese

1998

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The effect of light intensity on antioxidants, antioxidant enzymes, and chlorophyll content was studied in common bean (Phaseolus vulgaris L.) exposed to excess Mn. Leaves of bean genotypes contrasting in Mn tolerance were exposed to two different light intensities and to excess Mn; light was controlled by shading a leaflet with filter paper. After 5 d of Mn treatment ascorbate was depleted by 45% in leaves of the Mn-sensitive genotype ZPV-292 and by 20% in the Mn-tolerant genotype CALIMA. Nonprotein sulfhydryl groups and glutathione reductase were not affected by Mn or light treatment. Ten days of Mn-toxicity stress increased leaf ascorbate peroxidase activity of cv ZPV-292 by 78% in low light and by 235% in high light, and superoxide dismutase activity followed a similar trend. Increases of ascorbate peroxidase and superoxide dismutase activity observed in cv CALIMA were lower than those observed in the susceptible cv ZPV-292. The cv CALIMA had less ascorbate oxidation under excess Mn-toxicity stress. Depletion of ascorbate occurred before the onset of chlorosis in Mn-stressed plants, especially in cv ZPV-292. Lipid peroxidation was not detected in floating leaf discs of mature leaves exposed to excess Mn. Our results suggest that Mn toxicity may be mediated by oxidative stress, and that the tolerant genotype may maintain higher ascorbate levels under stress than the sensitive genotype.

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Section: Discussionmentioning

confidence: 78%

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confidence: 94%

Light and Excess Manganese

1998

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“…Chlorosis of young leaves induced by excess Mn is enhanced at higher light intensities in tobacco and cucumber Horiguchi, 1988). Since Mn toxicity has been shown to reduce the affinity of rubisco for CO 2 , in chlorotic leaves, high light intensities may lead to enhanced production of toxic O~.…”

Section: Discussionmentioning

confidence: 94%

Effect of light intensity on manganese toxicity symptoms and callose formation in cowpea (Vigna unguiculata (L.) Walp.)

1992

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In cowpea typical Mn toxicity symptoms are brown speckles on mature leaves representing depositions mainly in the cell walls and formation of non-constitutive callose. The histochemical characterization of the brown speckles indicates the presence of oxidized Mn. However, the reducing agent hydroxylamine hydrochloride only slightly while thioglycolic acid almost completely decolorized the speckles. Brown boron-deficient roots treated with hydroxylamine hydrochloride and thioglycolic acid showed the same pattern of decoloration suggesting that the brown color of the Mn toxicity symptoms derives mainly from oxidized phenolics. To evaluate the effect of light on the formation of brown speckles by high Mn concentrations and non-constitutive callose in leaves, three approaches were used: (i) comparison of shaded and unshaded plants at different Mn supplies via the roots, (ii) local application of Mn to leaves in the light and in the dark, (iii) local application of Mn to leaves in the dark with subsequent light and dark treatments. Shading of whole plants (i) aggravated formation of both brown speckles and caliose at similar Mn concentrations in the leaves. When the Mn application and the light treatments were locally confined (ii, iii), light had no effect on formation of either brown speckles or callose. The present results are in contradiction to the available reports in the literature showing aggravation of Mn toxicity by high light intensities.

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“…However, the decreased value of TF under increasing levels of Mn showed that plants stored higher amounts of the metal in their roots. The lowering of Mn transport in J. effusus suggests a reduction in the mobility of Mn from roots that contributes to the metal stress tolerance [29,44] or avoiding metal stress [45]. Different factors like decrease in pH, reduction of MnO 2 and Mn complex formation affect the Mn availability.…”

Section: Discussionmentioning

confidence: 99%