D B Hinshaw

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: H2O2 injury produced a marked increase in F actin with an associated rearrangement of the microfilaments and simultaneous changes in the plasma membrane prior to cell death in the P388D1 cell line.

TL;DR: H2O2 exposure induces a dose‐dependent disturbance of intracellular calcium homeostatis and the rise in [Ca+++]i is mediated by exposure to H2 O2 in the early phase of the injury, and is not dependent on the continuing presence of the oxidant.