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      Within-plant isoprene oxidation confirmed by direct emissions of oxidation products methyl vinyl ketone and methacrolein

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          PLANT MITOCHONDRIA AND OXIDATIVE STRESS: Electron Transport, NADPH Turnover, and Metabolism of Reactive Oxygen Species.

          The production of reactive oxygen species (ROS), such as O2- and H2O2, is an unavoidable consequence of aerobic metabolism. In plant cells the mitochondrial electron transport chain (ETC) is a major site of ROS production. In addition to complexes I-IV, the plant mitochondrial ETC contains a non-proton-pumping alternative oxidase as well as two rotenone-insensitive, non-proton-pumping NAD(P)H dehydrogenases on each side of the inner membrane: NDex on the outer surface and NDin on the inner surface. Because of their dependence on Ca2+, the two NDex may be active only when the plant cell is stressed. Complex I is the main enzyme oxidizing NADH under normal conditions and is also a major site of ROS production, together with complex III. The alternative oxidase and possibly NDin(NADH) function to limit mitochondrial ROS production by keeping the ETC relatively oxidized. Several enzymes are found in the matrix that, together with small antioxidants such as glutathione, help remove ROS. The antioxidants are kept in a reduced state by matrix NADPH produced by NADP-isocitrate dehydrogenase and non-proton-pumping transhydrogenase activities. When these defenses are overwhelmed, as occurs during both biotic and abiotic stress, the mitochondria are damaged by oxidative stress.
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            Abiotic stresses and induced BVOCs.

            Plants produce a wide spectrum of biogenic volatile organic compounds (BVOCs) in various tissues above and below ground to communicate with other plants and organisms. However, BVOCs also have various functions in biotic and abiotic stresses. For example abiotic stresses enhance BVOCs emission rates and patterns, altering the communication with other organisms and the photochemical cycles. Recent new insights on biosynthesis and eco-physiological control of constitutive or induced BVOCs have led to formulation of hypotheses on their functions which are presented in this review. Specifically, oxidative and thermal stresses are relieved in the presence of volatile terpenes. Terpenes, C6 compounds, and methyl salicylate are thought to promote direct and indirect defence by modulating the signalling that biochemically activate defence pathways. Copyright 2010 Elsevier Ltd. All rights reserved.
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              Isoprene produced by leaves protects the photosynthetic apparatus against ozone damage, quenches ozone products, and reduces lipid peroxidation of cellular membranes.

              Many plants invest carbon to form isoprene. The role of isoprene in plants is unclear, but many experiments showed that isoprene may have a role in protecting plants from thermal damage. A more general antioxidant action has been recently hypothesized on the basis of the protection offered by exogenous isoprene in nonemitting plants exposed to acute ozone doses. We inhibited the synthesis of endogenous isoprene by feeding fosmidomycin and observed that Phragmites australis leaves became more sensitive to ozone than those leaves forming isoprene. Photosynthesis, stomatal conductance, and fluorescence parameters were significantly affected by ozone only in leaves on which isoprene was not formed. The protective effect of isoprene was more evident when the leaves were exposed for a long time (8 h) to relatively low (100 nL L(-1)) ozone levels than when the exposure was short and acute (3 h at 300 nL L(-1)). Isoprene quenched the amount of H(2)O(2) formed in leaves and reduced lipid peroxidation of cellular membranes caused by ozone. These results indicate that isoprene may exert its protective action at the membrane level, although a similar effect could be obtained if isoprene reacted with ozone before forming active oxygen species. Irrespective of the mechanism, our results suggest that endogenous isoprene has an important antioxidant role in plants.
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                Author and article information

                Journal
                Global Change Biology
                Glob Change Biol
                Wiley-Blackwell
                13541013
                March 2012
                March 2012
                : 18
                : 3
                : 973-984
                Article
                10.1111/j.1365-2486.2011.02610.x
                696580a6-1de5-4ab8-8306-56fb4208c1cb
                © 2012

                http://doi.wiley.com/10.1002/tdm_license_1.1

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