Comments for:
Abstract
Cell death by apoptosis or necrosis is often important in the etiology and treatment of disease. Since mitochondria play important roles in cell death pathways, these organelles are potentially prime targets for therapeutic intervention. Here we discuss the mechanisms through which mitochondria participate in the cell death process and also survey some of the pharmacological approaches that target mitochondria in various ways.
Authors
Lisa Bouchier-Hayes, Lydia Lartigue, Donald D. Newmeyer
Mitochondria and apoptosis
Submitter: Heikki Savolainen | heikki.savolainen@stm.fi
Dept. of Occup.Safety & Hlth., Tampere, Finland
Published October 5, 2005
This timely and thought-provoking review opens up new vistas for clinicians and research people. It is also very pertinent to occupational toxicology. As an example, I would like to cite the fact that toxic metabolites from alkoxyethyl ethers, the corresponding alkokyacetic acids, inhibit the succinate dehydrogenase at complex II in mitochondria (1). The enzyme links the tricarboxylic acid cycle to the respiratory chain. The inhibition activates the caspase pathway (2), and it seems that the accumulating succinate also inhibits HIF-alpha proline hydroxylation resulting in the activation of hypoxia responsive elements. Thus, the mitochondrial effects are also critical to modern toxicology.
1. Liesivuori et al. Arch Toxicol 73: 229 (1999) 2. Dathe et al. Hautarzt 56: 768 (2005)
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