Ingrid U. Schraufstatter

TL;DR: Both the estimated rates of ADP phosphorylation by glycolysis and mitochondria and the estimated rate of ATP hydrolysis by ongoing metabolism were utilized to model the approximate decline in intracellular ATP expected at 15-min exposure to various H2O2 concentrations.

TL;DR: Results suggest that DNA damage induced within seconds after addition of oxidant may lead to stimulation of poly-ADP-ribose polymerase, and a consequent fall in NAD sufficient to interfere with ATP synthesis.

TL;DR: In the current studies, inhibition of poly(ADP-ribose) polymerase by 3-aminobenzamide, nicotinamide, or theophylline in cells exposed to lethal concentrations of H2O2 prevented the sequence of events that eventually led to cell lysis--i.e., the decrease in NAD, followed by depletion of ATP, influx of extracellular Ca2+, actin polymerization and, finally, cell death.

TL;DR: Examination of leukocytic oxidant species that induce oxidant damage of DNA in whole cells indicated that H2O2 formed hydroxyl radical intracellularly, which appeared to be the most likely free radical responsible for DNA damage.

TL;DR: Results indicate that IL-8 activates both the CXCR1 and the CxCR2 on microvascular endothelial cells, using different signal transduction cascades, which may contribute to the increased vascular permeability observed in acute inflammation and during the angiogenic response.