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Arno G. Siraki
Researcher at University of Alberta
Publications - 65
Citations - 2421
Arno G. Siraki is an academic researcher from University of Alberta. The author has contributed to research in topics: Myeloperoxidase & Radical. The author has an hindex of 21, co-authored 61 publications receiving 2063 citations. Previous affiliations of Arno G. Siraki include Research Triangle Park & National Institutes of Health.
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Journal ArticleDOI
Aldehyde sources, metabolism, molecular toxicity mechanisms, and possible effects on human health.
TL;DR: The human health risks from clinical and animal research studies are reviewed, including aldehydes as haptens in allergenic hypersensitivity diseases, respiratory allergies, and idiosyncratic drug toxicity; the potential carcinogenic risks of the carbonyl body burden.
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Dietary flavonoid iron complexes as cytoprotective superoxide radical scavengers.
TL;DR: It is suggested that the initial step in superoxide radical scavenging (SRS) activity involves a redox-active flavonoid:Fe(3+) complex, which should, therefore, be tested as a therapy for the treatment of ischemia/reperfusion injury.
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Molecular cytotoxic mechanisms of anticancer hydroxychalcones.
Omid Sabzevari,Omid Sabzevari,Giuseppe Galati,Majid Y. Moridani,Arno G. Siraki,Peter J. O'Brien +5 more
TL;DR: The highest pKa chalcones were the most effective at collapsing the mitochondrial membrane potential which suggests that the cytotoxic activity of hydroxychalcones are likely because of their ability to uncouple mitochondria.
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A conceptual framework for predicting the toxicity of reactive chemicals: modeling soft electrophilicity.
Terry W Schultz,R E Carlson,Mark T. D. Cronin,Joop L. M. Hermens,R Johnson,Peter J. O'Brien,David W. Roberts,Arno G. Siraki,Kendall B. Wallace,Gilman D. Veith +9 more
TL;DR: Empirical measures of the chemical reactivity of xenobiotics with a model nucleophile are used to simulate the relative rates at which a reactive chemical is likely to bind irreversibly to cellular targets.
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Endogenous and endobiotic induced reactive oxygen species formation by isolated hepatocytes.
TL;DR: Endogenous ROS formation was markedly increased in catalase-inhibited or GSH-depleted hepatocytes, and was inhibited by ROS scavengers or desferoxamine, which suggests endogenous ROS formation can largely be attributed to oxygen reduction by reduced mitochondrial electron transport components and reduced cytochrome P450 isozymes.