"Remarkably, apoptosis proceeded normally under conditions of iron
deprivation"

Hydrogen peroxide inhibits caspase-dependent apoptosis by inactivating
procaspase-9 in an iron -dependent manner. Nov 15, 2007
Alexandra Barbouti,Christos Amorgianiotis,Evangelos
Kolettas,Panagiotis Kanavaros,Dimitrios Galaris
Apoptosis represents a physiological form of cell death, the
perturbation of which may contribute to the development of several
diseases connected with accumulation of unwanted cells or excessive
cell loss. We have previously shown that the continuous presence of
low concentrations of H(2)O(2) (generated by the action of glucose
oxidase) was able to inhibit caspase-mediated apoptosis in Jurkat
cells. The main purpose of the present study was to elucidate the
exact molecular mechanism(s) underlying this inhibitory action of
H(2)O(2). The results presented show that events like outer
mitochondrial membrane permeabilization, release of cytochrome c from
mitochondria, oligomerization of Apaf-1, and recruitment of
procaspase-9 to apoptosomes were taking place normally, but further
advancement toward activation of the execution caspases was
interrupted when H(2)O(2) was present during the apoptotic process.
From the results presented in this work, it emerges that the
inhibition of procaspase-9 autoactivation was probably due to the
reversible oxidation of sensitive cysteine residues in this molecule.
Remarkably, caspase-9 activation and the ensuing caspase cascade
proceeded normally in the presence of H(2)O(2) under conditions of
iron deprivation, indicating that the inhibition of procaspase-9
activation was an iron -dependent process. Collectively, these results
highlighted the potential role of available intracellular iron ions in
signaling mechanisms related to apoptotic cell death.

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http://en.wikipedia.org/wiki/Apoptosis

Processes of disposal of cellular debris whose results do not damage
the organism differentiate apoptosis from necrosis.

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