Send to

Choose Destination
See comment in PubMed Commons below
Cell Signal. 1999 Apr;11(4):239-44.

Mechanisms of nitric oxide-dependent apoptosis: involvement of mitochondrial mediators.

Author information

Instituto de Bioquímica, Facultad de Farmacia, Madrid, Spain.


Programmed cell death occurs in several physiopathological situations in multicellular organisms and constitutes a common mechanism of cell replacement, tissue remodelling and removal of altered cells. The effectors that induce apoptosis as well as the signalling pathways involved in the process are the subjects of current work. In addition to receptor-mediated apoptosis, highly reactive molecules, such as NO, influence cell viability either by acting as a protection against apoptogenic stimuli, or by inducing apoptosis when produced at elevated concentrations. The contribution to apoptosis of mediators released by the mitochondria and involved in the activation of caspases focused attention on the functional changes caused by NO in this organelle. NO induces mitochondrial permeability transition and promotes apoptosis in cell-free systems containing mitochondria and nuclei. Moreover, NO-dependent apoptosis can be blocked in most cases through the use of permeability transition or caspase inhibitors. The intracellular pathways activated in response to NO challenge and involved in the regulation of apoptosis are analysed.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center