H
Henry Jay Forman
Researcher at University of Southern California
Publications - 314
Citations - 27464
Henry Jay Forman is an academic researcher from University of Southern California. The author has contributed to research in topics: Glutathione & Oxidative stress. The author has an hindex of 73, co-authored 307 publications receiving 24061 citations. Previous affiliations of Henry Jay Forman include University of Alabama at Birmingham & University of Kansas.
Papers
More filters
Journal ArticleDOI
Hydroperoxide-induced Increases in Intracellular Calcium Due to Annexin VI Translocation and Inactivation of Plasma Membrane Ca2+-ATPase
TL;DR: Results suggest that exposure to oxidative stress results in early alterations to the plasma membrane and concomitant release of Ca2+ into the cytosol, and suggests a mechanism for participation of annexin VI translocation that may underlie the alterations in macrophage function by oxidative stress.
Journal ArticleDOI
A critical review of assays for hazardous components of air pollution.
TL;DR: There is low consistency across chemical and cell-based assays for oxidative and inflammatory activity in AAP components, and crosstalk in detoxification pathways mediated by AHR, NF-κB, and Nrf2 is suggested.
Journal ArticleDOI
Increased gamma-glutamylcysteine synthetase and gamma-glutamyl transpeptidase activities enhance resistance of rat lung epithelial L2 cells to quinone toxicity.
TL;DR: The results suggest that elevation of GCS and GGT activities participated in acquired resistance to quinone toxicity.
Journal ArticleDOI
Induction of p21 Mediated by Reactive Oxygen Species Formed during the Metabolism of Aziridinylbenzoquinones by HCT116 Cells
TL;DR: It is suggested that p21 induction is mediated by an increase in the cellular steady-state concentration of oxygen radicals and that the greater effectiveness in p 21 induction by DZQ may be related to its efficient metabolism by NAD(P)H:quinone oxidoreductase activity in HCT116 cells.
Journal Article
Mechanism for the potentiation of oxygen toxicity by disulfiram.
TL;DR: The contrast between the inhibition by disulfiram of lung superoxide dismutase activity in vivo and its lack of effect in vitro suggests metabolism of disulfIRam to diethyldithiocarbamate and subsequent inhibition of superoxide Dismutase.