Lipid peroxidation paraquat toxicity

However, the superoxide dismutase may be overwhelmed by the amount of superoxide being produced after a toxic dose of paraquat. The superoxide may then cause lipid peroxidation via the production of hydroxyl radicals. These may be produced from hydrogen peroxide in the presence of transition metal ions (see chap. 6). 

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. 

Modulation of paraquat toxicity with the mixed-valence complex of penicillamine also involves the prevention of lipid peroxidation [637, 638]. Chloro-plast fragments of flax cotyledons had fatty acids that were closer to non-treat-ed control levels than paraquat-treated plants. Decreases in chlorophyll, carotenes and xanthophyll produced by paraquat were also prevented by treatment with the mixed-valence complex. These protective effects of this... 

Lipid peroxidation leads to cellular destruction and death. Herbicides that divert photosynthetic electron transport, such as the bipyridyls paraquat and diquat, yield the superoxide anion. Superoxide levels produced overtax the normal defense mechanisms. More toxic species such as hydroxyl free radicals are also probably produced which instigate lipid peroxidation and lead to cellular disorganization and death. 

The lipid peroxide stimulation mechanism of paraquat acute toxicity has been questioned by Shu et al. (1979), who have shown that it is possible by pre-treatment with N,ivr-diphenyl-p-phenylene-diamine, an antioxidant, to prevent the paraquat stimulation of lipid peroxidation without protecting the animals against its lethal effects. 

In contrast to the S plants, practically no lipid degradation and FA peroxidation was observed in the R biotype treated with paraquat, which may indicate that the toxic effects of oxygen radicals did not develop following paraquat treatment in this biotype. The data on the lipid and FA composition also indicate that the high constitutive level of superoxide dismu-tase, ascorbat peroxidase and glutation reductase proposed by Shaaltiel and Gressel (1986), can protect the R plant from damage of paraquat. 

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