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Marie A. Amoruso

Researcher at Rutgers University

Publications -  26
Citations -  1011

Marie A. Amoruso is an academic researcher from Rutgers University. The author has contributed to research in topics: Superoxide & Alveolar macrophage. The author has an hindex of 16, co-authored 26 publications receiving 1002 citations. Previous affiliations of Marie A. Amoruso include University of Medicine and Dentistry of New Jersey & New York University.

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Protease inhibitors antagonize the activation of polymorphonuclear leukocyte oxygen consumption.

TL;DR: The results indicate that proteolysis may be involved in activating the burst of oxygen consumption following stimulation of phagocytic cells, and this effect was observed with a variety of stimuli used to activate O 2 − • production in human polymorphonuclear leukocytes.
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Stimulation of human polymorphonuclear leukocyte superoxide anion radical production by tumor promoters

TL;DR: The rate of O-2 production was found to correlate with the tumor-promoting activity of the phorbol esters as opposed to their inflammatory activity, suggesting a possible role for O-.2 and other reactive oxygen species in tumor promotion.
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Retinoid inhibition of superoxide anion radical production by human polymorphonuclear leukocytes stimulated with tumor promoters.

TL;DR: All-trans retinol, retinyl acetate and retinoic acid were found to be effective inhibitors of O 2 − • polymorphonuclear leukocytes stimulated with the tumor promoter phorbol myristate acetate.
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Decrease in mouse lung and liver glutathione peroxidase activity and potentiation of the lethal effects of ozone and paraquat by the superoxide dismutase inhibitor diethyldithio-carbamate

TL;DR: The potentiation of the lethal effects of exogenous agents by diethyldithiocarbamate does not necessarily indicate a role for superoxide anion radical in the toxicity of these agents, and could be prevented by the addition of superoxide dismutase or by anaerobic conditions.
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Degradation of soluble collagen by ozone or hydroxyl radicals

TL;DR: An alternative mechanism by which oxygen‐derived free radicals participate in the destruction of extracellular matrix observed during acute lung injury by oxidant gas is suggested, in addition to the commonly accepted proteinase‐antiproteinase theory of lung injury.