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Light-induced modulation of the mitochondrial respiratory chain activity: possibilities and limitations
M. Lunova, B. Smolková, M. Uzhytchak, KŽ. Janoušková, M. Jirsa, D. Egorova, A. Kulikov, Š. Kubinová, A. Dejneka, O. Lunov,
Language English Country Switzerland
Document type Journal Article
Grant support
SOLID21 - CZ.02.1.01/0.0/0.0/16_019/0000760
Ministerstvo Školství, Mládeže a Tělovýchovy (CZ)
NLK
PubMed Central
from 1997
ProQuest Central
from 1997-01-01 to 1 year ago
Medline Complete (EBSCOhost)
from 2000-01-01 to 1 year ago
Health & Medicine (ProQuest)
from 1997-01-01 to 1 year ago
- MeSH
- Apoptosis radiation effects MeSH
- Hep G2 Cells MeSH
- Phototherapy * MeSH
- Low-Level Light Therapy * MeSH
- Humans MeSH
- Membrane Potential, Mitochondrial genetics radiation effects MeSH
- Mitochondrial Membranes metabolism radiation effects MeSH
- Mitochondria genetics radiation effects MeSH
- Oxidation-Reduction radiation effects MeSH
- Reactive Oxygen Species metabolism MeSH
- Gene Expression Regulation radiation effects MeSH
- Electron Transport Complex IV genetics MeSH
- Electron Transport genetics radiation effects MeSH
- Cell Survival genetics radiation effects MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
Biological effects of high fluence low-power (HFLP) lasers have been reported for some time, yet the molecular mechanisms procuring cellular responses remain obscure. A better understanding of the effects of HFLP lasers on living cells will be instrumental for the development of new experimental and therapeutic strategies. Therefore, we investigated sub-cellular mechanisms involved in the laser interaction with human hepatic cell lines. We show that mitochondria serve as sub-cellular "sensor" and "effector" of laser light non-specific interactions with cells. We demonstrated that despite blue and red laser irradiation results in similar apoptotic death, cellular signaling and kinetic of biochemical responses are distinct. Based on our data, we concluded that blue laser irradiation inhibited cytochrome c oxidase activity in electron transport chain of mitochondria. Contrary, red laser triggered cytochrome c oxidase excessive activation. Moreover, we showed that Bcl-2 protein inhibited laser-induced toxicity by stabilizing mitochondria membrane potential. Thus, cells that either overexpress or have elevated levels of Bcl-2 are protected from laser-induced cytotoxicity. Our findings reveal the mechanism how HFLP laser irradiation interfere with cell homeostasis and underscore that such laser irradiation permits remote control of mitochondrial function in the absence of chemical or biological agents.
Institute for Clinical and Experimental Medicine 14021 Prague Czech Republic
Institute of Physics Czech Academy of Sciences 18221 Prague Czech Republic
References provided by Crossref.org
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