Paraquat: model for oxidant-initiated toxicity
Paraquat, a quaternary ammonium bipyridyl herbicide, produces degenerative lesions in the lung after systemic administration to man and animals. The pulmonary toxicity of paraquat resembles in several ways the toxicity of several other lung toxins, including oxygen, nitrofurantoin and bleomycin. Although a definitive mechanism of toxicity of parquat has not been delineated, a cyclic single electron reduction/oxidation of the parent molecule is a critical mechanistic event. The redox cycling of paraquat has two potentially important consequences relevant to the development of toxicity: generation of activated oxygen (e.g., superoxide anion, hydrogen perioxide, hydroxyl radical) which is highly reactive to cellular macromolecules; and/or oxidation of reducing equivalents (e.g., NADPH, reduced glutathione) necessary for normal cell function. Paraquat-induced pulmonary toxicity, therefore, is a potentially useful model for evaluation of oxidant mechanisms of toxicity. Furthermore, characterization of the consequences of intracellular redox cycling of xenobiotics will no doubt provide basic information regarding the role of this phenomena in the development of chemical toxicity. 105 references, 2 figures.
- Research Organization:
- Chemical Industry Institute of Toxicology, Research Triangle Park, NC
- OSTI ID:
- 5564144
- Journal Information:
- Environ. Health Perspect.; (United States), Vol. 55
- Country of Publication:
- United States
- Language:
- English
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Related Subjects
HERBICIDES
TOXICITY
LUNGS
PATHOLOGICAL CHANGES
OXYGEN COMPOUNDS
ANIMALS
BIOLOGICAL MODELS
HYDROGEN PEROXIDE
HYDROXYL RADICALS
REDOX REACTIONS
REVIEWS
SUPEROXIDE RADICALS
BODY
CHEMICAL REACTIONS
DOCUMENT TYPES
HYDROGEN COMPOUNDS
ORGANS
PEROXIDES
PESTICIDES
RADICALS
RESPIRATORY SYSTEM
560305* - Chemicals Metabolism & Toxicology- Vertebrates- (-1987)