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Allison Bloodsworth

Researcher at University of Alabama at Birmingham

Publications -  10
Citations -  1047

Allison Bloodsworth is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Nitric oxide & Lipid peroxidation. The author has an hindex of 8, co-authored 9 publications receiving 1018 citations.

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Nitric oxide inhibition of lipid peroxidation: kinetics of reaction with lipid peroxyl radicals and comparison with alpha-tocopherol.

TL;DR: Kinetic analysis revealed that biological *NO concentrations (up to 2 microM) will significantly influence peroxidation reactions in vivo, and steady state concentrations of 30 nM *NO would effectively compete with endogenous alpha-tocopherol concentrations as a scavenger of LOO* in the lipid phase.
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Nitrolinoleate inhibits superoxide generation, degranulation, and integrin expression by human neutrophils: novel antiinflammatory properties of nitric oxide-derived reactive species in vascular cells.

TL;DR: Nitration of lipids by NO- derived reactive species yields products with antiinflammatory properties, revealing a novel mechanism by which NO-derived nitrated biomolecules can influence the progression of vascular disease.
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Nitric Oxide Regulation of Free Radical– and Enzyme-Mediated Lipid and Lipoprotein Oxidation

TL;DR: The regulation of nonenzymatic and enzymatic lipid oxidation reactions by nitric oxide (NO) is potent and pervasive and reveals novel non-cGMP-dependent reactivities for this free radical inflammatory and signal transduction mediator as mentioned in this paper.
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Nitrolinoleate, a nitric oxide-derived mediator of cell function: synthesis, characterization, and vasomotor activity.

TL;DR: Results reveal that synthetic LNO2, identical to lipid derivatives produced biologically by the reaction of •NO and •NO-derived species with oxidizing unsaturated fatty acids (e.g., linoleate), can transduce vascular signaling actions of•NO.
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Nitrolinoleate inhibits platelet activation by attenuating calcium mobilization and inducing phosphorylation of vasodilator-stimulated phosphoprotein through elevation of cAMP.

TL;DR: The platelet inhibitory actions of LNO2 indicate that nitration reactions that occur following NO generation in an oxidizing environment can alter the activity of lipids and lend insight into mechanisms by which NO-derived species may modulate the progression of vascular injury.