- MeSH
- biologie buňky trendy MeSH
- biologie dějiny trendy MeSH
- buněčná membrána fyziologie genetika metabolismus MeSH
- buněčné jádro fyziologie genetika MeSH
- buněčné struktury fyziologie metabolismus MeSH
- centrozom fyziologie MeSH
- chloroplasty genetika metabolismus MeSH
- Golgiho aparát fyziologie MeSH
- lékařská genetika metody trendy MeSH
- mitochondrie genetika metabolismus MeSH
- peroxizomy fyziologie MeSH
The recent knowledge on mitochondria as the substantial source of reactive oxygen species, namely superoxide and hydrogen peroxide efflux from mitochondria, is reviewed, as well as nitric oxide and subsequent peroxynitrite generation in mitochondria and their effects. The reactive oxygen species formation in extramitochondrial locations, in peroxisomes, by cytochrome P450, and NADPH oxidase reaction, is also briefly discussed. Conditions are pointed out under which mitochondria represent the major ROS source for the cell: higher percentage of non-phosphorylating and coupled mitochondria, in vivo oxygen levels leading to increased intensity of the reverse electron transport in the respiratory chain, and nitric oxide effects on the redox state of cytochromes. We formulate hypotheses on the crucial role of ROS generated in mitochondria for the whole cell and organism, in concert with extramitochondrial ROS and antioxidant defense. We hypothesize that a sudden decline of mitochondrial ROS production converts cells or their microenvironment into a "ROS sink" represented by the instantly released excessive capacity of ROS-detoxification mechanisms. A partial but immediate decline of mitochondrial ROS production may be triggered by activation of mitochondrial uncoupling, specifically by activation of recruited or constitutively present uncoupling proteins such as UCP2, which may counterbalance the mild oxidative stress.
- MeSH
- antioxidancia farmakologie MeSH
- biologické modely MeSH
- financování organizované MeSH
- homeostáza MeSH
- hypoxie metabolismus MeSH
- lidé MeSH
- mitochondrie fyziologie účinky léků MeSH
- oxidace-redukce účinky léků MeSH
- oxidativní fosforylace MeSH
- peroxidace lipidů genetika MeSH
- peroxizomy fyziologie MeSH
- reaktivní formy dusíku metabolismus MeSH
- reaktivní formy kyslíku metabolismus MeSH
- respirační komplex I metabolismus MeSH
- respirační komplex III metabolismus MeSH
- rozpřahující látky farmakologie MeSH
- superoxidy metabolismus MeSH
- systém (enzymů) cytochromů P-450 metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH