The rates of radical formation from the dipyridylium herbicides paraquat, diquat, and morfamquat in homogenates of rat lung, kidney, and liver: An inhibitory effect of carbon monoxide

Baldwin, Robert C.; Pasi, Aurelio; MacGregor, James T.; Hine, Charles H.

doi:10.1016/0041-008x(75)90220-3

Cited by 94 publications

(21 citation statements)

References 21 publications

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“…These observations again suggested the potential for a two-electron reduction of molecular oxygen catalyzed by paraquat. In similar studies (30), rat lung, kidney and liver homogenates generated paraquat radical in the presence of NADPH. The reaction was not inhibited by carbon monoxide, cyanide or SKF-525A, which was consistent with the hypothesis that the microsomalcatalyzed reduction of paraquat occurred at some site prior to cytochrome P-450.…”

Section: Mechanisms Of Paraquattoxicity Redox Cycling Of Paraquatmentioning

confidence: 89%

Paraquat: model for oxidant-initiated toxicity.

Bus¹,

Gibson²

1984

Environ Health Perspect

507

238

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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 paraquat 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 peroxide, 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.

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Section: Mechanisms Of Paraquattoxicity Redox Cycling Of Paraquatmentioning

confidence: 89%

Paraquat: model for oxidant-initiated toxicity.

Bus¹,

Gibson²

1984

Environ Health Perspect

507

238

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“…PQ is believed to be reduced to the radical cation with subsequent reoxidation to the di-cation by molecular oxygen (1). With each reduction-oxidation cycle, superoxide may be produced (1) by the interaction of the mitochondria and PQ.…”

Section: Discussionmentioning

confidence: 99%

“…However, the dipyridylium dications are thought to be reduced to the radical cations with subsequent reoxidation to the di-cations by molecular oxygen (1). Thus, there is ample evidence that the dipyridylium radical cations are necessary intermediates in the mechanism of toxicity (9,13,15).…”

mentioning

confidence: 99%

The Effect of Paraquat on the Mitochondrial Energy Transfer Reaction

Ogata

Hasegawa

1978

Cell Struct. Funct.

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“…In addition, PQ has emerged as a putative risk factor for Parkinson's disease (Dinis-Oliveira et al, 2006). The primary mechanism of PQ toxicity is based on redox cycling and the generation of reactive oxygen species (ROS) (Baldwin et al, 1975). Therefore, researchers and clinicians have placed great emphasis on the use of antioxidants as a treatment modality for PQ toxicity (Suntres, 2002).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of myotube formation by paraquat in the myoblast cell line C2C12

et al. 2011

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-Paraquat (PQ) is one of the most frequently used pesticides in worldwide. In most countries, PQ is used without restrictions. To investigate the effect of PQ on myogenesis, cultures of C2C12, a useful model to study differentiation of myoblasts into myotubes, were exposed to various concentrations of PQ. Myotube formation did not occur in the presence of 50 μM PQ. Although cell death was not observed at this concentration, growth inhibition was evident in the growth medium. Production of myosin heavy chain, a myogenesis marker protein, decreased dose dependently with the concentration of PQ, which was added to the C2C12 cell culture during differentiation. Inhibition of myogenesis by PQ was not reversed by the addition of ascorbic acid. These results show that PQ is a strong inhibitor of muscle differentiation in vitro.

show abstract

The rates of radical formation from the dipyridylium herbicides paraquat, diquat, and morfamquat in homogenates of rat lung, kidney, and liver: An inhibitory effect of carbon monoxide

Cited by 94 publications

References 21 publications

Paraquat: model for oxidant-initiated toxicity.

Paraquat: model for oxidant-initiated toxicity.

The Effect of Paraquat on the Mitochondrial Energy Transfer Reaction

Inhibition of myotube formation by paraquat in the myoblast cell line C2C12

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