Death mechanisms caused by carotenoid biosynthesis inhibitors in green and in undeveloped plant tissues

Abstract

This study was carried out to investigate the difference in physiological processes leading to two different responses of albinism and necrosis to the phytoene desaturase inhibitor fluridone, which is dependent on the developmental state of tissue at the time of fluridone treatment. A soil-drench of fluridone solution at the 40% growth of the 3rd leaf of maize ( Zea mays L.) caused the leaf to grow into a white/green mixed leaf; completely white in the basal part (W), pale green in the middle part (PG), and green in apical part of the leaf blade (G). In the PG and G, the effective quantum yield of electron transport through photosystem II (Yield) was significantly inhibited, Fv/Fm was decreased but Fo increased, hydrogen peroxide was more accumulated than untreated control, and cellular leakage was faster and more pronounced than in the white tissue (W). In the W, however, all of Fo, Fm, and Yield values were near zero due to loss of chlorophyll. Moreover, there was a relatively low content of hydrogen peroxide, slower cellular leakage and longer survival of tissue in the W. On the other hand, the level of antioxidants such as carotenoids, tocopherols, and ascorbic acid was lower in the W than untreated control. However, the specific activities of antioxidant enzymes were elevated in the W; 3.47 times in superoxide dismutase (SOD), 3.21 times in peroxidase (POD), 1.59 times in catalase and 1.21 times in glutathione reductase. In particular, SOD and POD activities had a tendency to be increased during senescence. In the kinetics experiment carried out during a senescence of the 2nd white leaf, increase of wilting and browning began to occur prior to any significant change in MDA-equivalents, and high reduction of carbohydrate contents occurred prior to increase of wilting and necrosis. Carbohydrate supplement significantly delayed the death of white leaves. Taken together, the above results indicated that in the developed tissue, whose greening has already taken place at the time of herbicide treatment, its death was related to the cell destruction by excessive oxidative stress induced through photosynthetic electron transport blockade. Conversely, in the developing or undifferentiated tissue at the time of herbicide treatment, that eventually grown into a white tissue, its death seemed to be more dependent on a loss of photosystem function followed by carbohydrate deficiency.