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Herbicides toxic oxygen species

Although the results of these extensive experiments are not easily interpreted, the hypotheses were made (a) that PChlide is the most important and ubiquitous photodynamic species caused to accumulate by ALA-based treatments, (b) that MV PChlide is a more effective photodynamic pigment than DV PChlide in DDV/LDV and DMV/LDV species, and (c) that both DDV/LDV and DMV/LDV species are highly susceptible to a mixture of Mg-PPIX and Mg-PPIXME (14) The results are difficult to interpret because equimolar levels of different porphyrins were not produced and the combinations of porphyrins produced by different modulators varied with species. Potential differences in tolerance to toxic oxygen species between species were not considered. Others have attempted to explain differential sensitivity to porphyrin-generating herbicides between species (15) and between herbicide-sensitive biotypes within species (16) by differences in ability to detoxify toxic oxygen species. As with other herbicides, penetration of the leaf cuticle by ALA and/or DP can also play a role in differences in efficacy of this herbicide combination (17). [Pg.376]

To date, only six publications (5, 13, 14> IZ-IS) exist on ALA as a herbicide. Another paper has been published on ALA as an Insecticide (2Q). Although most of these are highly substantial papers, several questions remain regarding results of these studies. The actual relative phytotoxicity of various porphyrins Is not clear. The Intracellular s1te(s) of porphyrin accumulation are also not known. Furthermore, the complex Interactions between greening type, tolerance to toxic oxygen species, and capacity to synthesize porphyrins Is poorly understood. [Pg.377]

The other major class of herbicides involved with photosynthesis are compounds that act as divertors of electron flow at photosystem I (PSI). After the initial discovery of diquat and paraquat in the late 1950s, other related compounds have had limited use. One of these, morfamquat, has now been withdrawn. Thirty years later, there are no new chemicals or herbicide families to rival paraquat and diquat at this particular target site. We have, however, an increased understanding of the nature of the damaging radical species that are generated as a result of the action of these compounds. With these herbicides, as also with the electron transport inhibitors, toxic oxygen species have a major role. [Pg.3]

Finally, exogenous application of ascorbate or galactonolactone, a direct precursor of ascorbate in plants, has been reported to antagonize the activity of herbicides generating toxic oxygen species, such as paraquat and... [Pg.183]

In addition lipid peroxidation can result from action of active oxygen species. This leads to destruction of metabolically necessary lipid molecules and damage to the structural integrity of cellular membranes. Damage from oxidative stress can occur with excessive production of active oxygen species, inadequate protection against such species, or both. Examples of toxicity from active oxygen species include the pancreatic beta-cell destruction by alloxan, the neurotoxicity of 6-hydroxydopamine, the cardiotoxicity of the anthracy-cline antibiotics, and the pulmonary toxicity of the herbicide paraquat. [Pg.14]


See other pages where Herbicides toxic oxygen species is mentioned: [Pg.227]    [Pg.324]    [Pg.382]    [Pg.218]    [Pg.175]    [Pg.175]    [Pg.51]    [Pg.83]    [Pg.181]    [Pg.44]    [Pg.248]    [Pg.1170]    [Pg.343]    [Pg.1305]    [Pg.1170]    [Pg.1222]    [Pg.18]    [Pg.192]    [Pg.582]    [Pg.275]    [Pg.322]    [Pg.113]   
See also in sourсe #XX -- [ Pg.175 ]




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