The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Paraquat: model for oxidant-initiated toxicity.
Open accessAbstract
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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Cites
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The catalytic decomposition of hydrogen peroxide by iron salts
Haber, F., & Weiss, J. (1934) · Proceedings of the Royal Society of London. Series A - Mathematical and Physical Sciences · doi:10.1098/rspa.1934.0221 · Cited by 2,571
Superoxide‐dependent production of hydroxyl radical catalyzed by iron—EDTA complex
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Intracellular production of superoxide radical and of hydrogen peroxide by redox active compounds
Hassan, H. M., & Fridovich, I. (1979) · Archives of Biochemistry and Biophysics · doi:10.1016/0003-9861(79)90289-3 · Cited by 596
Bus, J. S., Aust, S. D., & Gibson, J. E. (1974) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(74)80481-x · Cited by 535
Self-citationFarrington, J. A., Ebert, M., Land, E. J., & Fletcher, K. (1973) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/0005-2728(73)90121-7 · Cited by 523
Swelling and Lysis of Rat Liver Mitochondria Induced by Ferrous Ions
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The pathogenesis of bleomycin-induced pulmonary fibrosis in mice.
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Superoxide dismutase and pulmonary oxygen toxicity
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Cited by
Targeting oxidative stress in disease: Promise and limitations of antioxidant therapy
Forman, H. J., & Zhang, H. (2021) · Nature Reviews Drug Discovery · doi:10.1038/s41573-021-00233-1 · Cited by 2,900
Mitochondrial Complex I Deficiency in Parkinson's Disease
Schapira, A. H. V., Cooper, J. M., Dexter, D., Clark, J. B., Jenner, P., & Marsden, C. D. (1990) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1990.tb02325.x · Cited by 2,283
The Role of Oxidative Stress in Parkinson's Disease
Dias, V., Junn, E., & Mouradian, M. M. (2013) · Journal of Parkinson’s Disease · doi:10.3233/jpd-130230 · Cited by 1,845
Chinta, S. J., Woods, G., Demaria, M., Rane, A., Zou, Y., McQuade, A., Rajagopalan, S., Limbad, C., Madden, D. T., Campisi, J., et al. (2018) · Cell Reports · doi:10.1016/j.celrep.2017.12.092 · Cited by 530
“PQ is a free radical generator that causes oxidative stress (Bus and Gibson, 1984), which has been demonstrated to induce cellular senescence in replication-competent cell types (Campisi, 2013).”
BackgroundGharagozloo, P., & Aitken, R. J. (2011) · Human Reproduction · doi:10.1093/humrep/der132 · Cited by 522
Metadata
- Authors
- Bus, J. S., & Gibson, J. E.
- Venue
- Environmental Health Perspectives
- Publisher
- American Chemical Society (ACS)
- Published
- 1984-04
- Volume
- 55
- Pages
- 37-46
- ISSN
- 0091-6765 (ISSN-L)
- 1552-9924
- OpenAlex
- W2005736754
- Cited by
- 593
- References
- 45
- FWCI
- 11.35
- Type
- journal article
- Language
- en
- Open access
- gold
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
