Paraquat, a quarternary nitrogen herbicide, is a highly toxic compound for humans and animals and many cases of
acute poisoning and death have been reported over the past few decades. The mechanisms of paraquat toxicity involve:
the generation of the superoxide anion, which can lead to the formation of more toxic reactive oxygen species, such as
hydrogen peroxide and hydroxyl radical; and the oxidation of the cellular NADPH, the major source of reducing
equivalents for the intracellular reduction of paraquat, which results in the disruption of important NADPH-requiring
biochemical processes. The major cause of death in paraquat poisoning is respiratory failure due to an oxidative insult
to the alveolar epithelium with subsequent obliterating fibrosis. Management of paraquat poisoning has remained
mostly supportive and has been directed towards the modification of the toxicokinetics of the poison. Currently, there
are no true pharmacological antagonists for paraquat and there are no chelating agents capable of binding the poison in
the blood or other tissues. Recognizing the fact that paraquat induces its toxic effects via oxidative stress-mediated
mechanisms, innovations in the management of paraquat poisoning are directed towards the use of antioxidants. In
this review, the status of antioxidants in ameliorating or treating the toxic effects produced by paraquat is
presented. # 2002 Elsevier Science Ireland Ltd. All rights reserved.
Paraquat, a quarternary nitrogen herbicide, is a highly toxic compound for humans and animals and many cases of
acute poisoning and death have been reported over the past few decades. The mechanisms of paraquat toxicity involve:
the generation of the superoxide anion, which can lead to the formation of more toxic reactive oxygen species, such as
hydrogen peroxide and hydroxyl radical; and the oxidation of the cellular NADPH, the major source of reducing
equivalents for the intracellular reduction of paraquat, which results in the disruption of important NADPH-requiring
biochemical processes. The major cause of death in paraquat poisoning is respiratory failure due to an oxidative insult
to the alveolar epithelium with subsequent obliterating fibrosis. Management of paraquat poisoning has remained
mostly supportive and has been directed towards the modification of the toxicokinetics of the poison. Currently, there
are no true pharmacological antagonists for paraquat and there are no chelating agents capable of binding the poison in
the blood or other tissues. Recognizing the fact that paraquat induces its toxic effects via oxidative stress-mediated
mechanisms, innovations in the management of paraquat poisoning are directed towards the use of antioxidants. In
this review, the status of antioxidants in ameliorating or treating the toxic effects produced by paraquat is
presented. # 2002 Elsevier Science Ireland Ltd. All rights reserved.
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