Mechanism of mitochondrial ROS production, cell signalling for cell death and proliferation, side effects associated to mutagensis and transformation
| Author: | M. Giorgio |
|---|---|
| Submitted: | Thursday 10th of February 2011 09:34:27 AM |
| Submitted by: | egf |
| Language: | English |
| Content type: | Learning resource |
| Educational levels: | expert, qc3 |
Contents
Topics
- Genetics + genomics
- Molecular genetics
- Molecular genetics > Studies of DNA
- Molecular genetics > Studies of DNA > Mitochondrial DNA
- Molecular genetics > Studies of RNA
- Molecular genetics > Studies of RNA > Studies of coding RNA
- Molecular genetics > Studies of RNA > Studies of coding RNA > Studies of protein
- Clinical/medical genetics
- Clinical/medical genetics > Disease related (typology of disorder)
- Clinical/medical genetics > Disease related (typology of disorder) > Cancer genetics
- Clinical/medical genetics > Patient related
- Clinical/medical genetics > Patient related > Patient/family related
- Clinical/medical genetics > Patient related > Patient/family related > Patient management
- Clinical/medical genetics > Patient related > Patient/family related > Patient management > Diagnosis of patient disease
- Clinical/medical genetics > Patient related > Patient/family related > Patient management > Diagnosis of patient disease > Laboratory investigation
- Clinical/medical genetics > Patient related > Patient/family related > Patient management > Diagnosis of patient disease > Laboratory investigation > Biochemical (clinical investigation)
Abstract
Reactive oxygen species (ROS), as generated by mitochondria during respiration, induce oxidative stress, which accumulates over life and is considered the proximal mechanism of aging and a major determinant of degenerative disease, including cancer, and lifespan (the free radical or mitochondrial theory of aging). Recent data showed that specific ROS molecule, H2O2 in particular, is directly implicated in the physiological regulation of different signal transduction pathways, including the insulin/IGF1 pathway. Indeed mitochondrial ROS production has been found to contribute to the regulation of several cellular processes in a specific manner. A role for ROS as signaling molecules is further supported by recent findings that the generation of H2O2 by mitochondria is not just the by-product of respiration, but can also be the result of specific enzymatic systems, such as p66Shc. P66Shc functions as an inducible redox enzyme, which is activated by stress and generates H2O2 to trigger apoptosis, to regulate signal transduction and transcription. Regardless of the purpose p66Shc utilizes to shift the intracellular redox balance towards oxidation, it appears that mitochondrial ROS formation ability evolved to set intracellular ROS levels. Therefore one could hypothesize that the mitochondrial-mediated oxidative stress may have a critical oncogenic role when tumor suppressor mechanisms defect rather than acting as primary mutagens.Download
Original version - English
Citation
M. Giorgio. Mechanism of mitochondrial ROS production, cell signalling for cell death and proliferation, side effects associated to mutagensis and transformation . EUROGENE portal. February 2011. online: http://eurogene.open.ac.uk/content/mechanism-mitochondrial-ros-production-cell-signalling-cell-death-and-proliferation-side-eff
Keywords
adenomatous polyposis coli, adenosine triphosphate, apoptosis, cell, coupling, deletion, deoxyribonucleic acid, enzyme, expression, fitness, isolated, linkage disequilibrium, metabolism, mitochondria, mutation rate, oncogene, protein, recombinant, survival, syndromeTerms of use
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