Publication: Reactive oxygen species and the
mitochondrial signaling pathway of cell death
Authors
Le Bras, M. ; Clément, M.V. ; Pervaiz, S. ; Brenner, C.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Reactive oxygen species (ROS) are produced
as a by-product of cellular metabolic pathways and
function as a critical second messenger in a variety of
intracellular signaling pathways. Thus, a defect or
deficiency in the anti-oxidant defense system on the one
hand and/or the excessive intracellular generation of
ROS on the other renders a cell oxidatively stressed. As
a consequence, direct or indirect involvement of ROS in
numerous diseases has been documented. In most of
these cases, the deleterious effect of ROS is a function of
activation of intracellular cell-death circuitry. To that
end, involvement of ROS at different phases of the
apoptotic pathway, such as induction of mitochondrial
permeability transition and release of mitochondrial
death amplification factors, activation of intracellular
caspases and DNA damage, has been clearly established.
For instance, the ROS-induced alteration of constitutive
mitochondrial proteins, such as the voltage-dependent
anion channel (VDAC) and/or the adenine nucleotide
translocase (ANT) can induce the pro-apoptotic
mitochondrial membrane permabilization. Not only do
these observations provide insight into the intricate
mechanisms underlying a variety of disease states, but
they also present novel opportunities for the design and
development of more effective therapeutic strategies.
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