In Vitro Effects of Cognitives and Nootropics on Mitochondrial Respiration and Monoamine Oxidase Activity
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články
Grantová podpora
15-28967A
AZV, Ministry of Health, Czech Republic
15-28616A
AZV, Ministry of Health, Czech Republic
PubMed
27660276
DOI
10.1007/s12035-016-0121-y
PII: 10.1007/s12035-016-0121-y
Knihovny.cz E-zdroje
- Klíčová slova
- Cognitives, Mitochondrial respiration, Monoamine oxidase, Nootropics, Reactive oxygen species,
- MeSH
- Alzheimerova nemoc metabolismus MeSH
- cholinesterasové inhibitory farmakologie MeSH
- donepezil MeSH
- galantamin metabolismus MeSH
- indany farmakologie MeSH
- kognice účinky léků MeSH
- memantin farmakologie MeSH
- mitochondrie účinky léků metabolismus MeSH
- monoaminoxidasa účinky léků metabolismus MeSH
- mozek účinky léků metabolismus MeSH
- nootropní látky farmakologie MeSH
- piperidiny farmakologie MeSH
- prasata MeSH
- rivastigmin farmakologie MeSH
- spotřeba kyslíku účinky léků MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- cholinesterasové inhibitory MeSH
- donepezil MeSH
- galantamin MeSH
- indany MeSH
- memantin MeSH
- monoaminoxidasa MeSH
- nootropní látky MeSH
- piperidiny MeSH
- rivastigmin MeSH
Impairment of mitochondrial metabolism, particularly the electron transport chain (ETC), as well as increased oxidative stress might play a significant role in pathogenesis of Alzheimer's disease (AD). Some effects of drugs used for symptomatic AD treatment may be related to their direct action on mitochondrial function. In vitro effects of pharmacologically different cognitives (galantamine, donepezil, rivastigmine, 7-MEOTA, memantine) and nootropic drugs (latrepirdine, piracetam) were investigated on selected mitochondrial parameters: activities of ETC complexes I, II + III, and IV, citrate synthase, monoamine oxidase (MAO), oxygen consumption rate, and hydrogen peroxide production of pig brain mitochondria. Complex I activity was decreased by galantamine, donepezil, and memantine; complex II + III activity was increased by galantamine. None of the tested drugs caused significant changes in the rate of mitochondrial oxygen consumption, even at high concentrations. Except galantamine, all tested drugs were selective MAO-A inhibitors. Latrepirdine, donepezil, and 7-MEOTA were found to be the most potent MAO-A inhibitors. Succinate-induced mitochondrial hydrogen peroxide production was not significantly affected by the drugs tested. The direct effect of cognitives and nootropics used in the treatment of AD on mitochondrial respiration is relatively small. The safest drugs in terms of disturbing mitochondrial function appear to be piracetam and rivastigmine. The MAO-A inhibition by cognitives and nootropics may also participate in mitochondrial neuroprotection. The results support the future research aimed at measuring the effects of currently used drugs or newly synthesized drugs on mitochondrial functioning in order to understand their mechanism of action.
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Br J Pharmacol. 2006 Jan;147(2):199-208 PubMed
Br J Pharmacol. 2010 May;160(2):246-57 PubMed
Eur J Med Chem. 2013 Apr;62:745-53 PubMed
Acta Pharmacol Sin. 2012 Sep;33(9):1170-5 PubMed
Neurochem Int. 2010 Feb;56(3):394-403 PubMed
Transl Psychiatry. 2013 Oct 22;3:e317 PubMed
Eur J Med Chem. 2014 Jun 10;80:543-61 PubMed
Curr Drug Targets. 2012 Jul;13(8):1089-106 PubMed
Antioxid Redox Signal. 2012 Jun 15;16(12):1421-33 PubMed
Toxicol Lett. 2012 Sep 18;213(3):345-52 PubMed
Toxicol Lett. 2011 Mar 5;201(2):176-80 PubMed
Neuro Endocrinol Lett. 2010;31(5):645-56 PubMed
Mol Neurobiol. 2015 Oct;52(2):970-8 PubMed
Neuropharmacology. 2015 Aug;95:29-36 PubMed
Naunyn Schmiedebergs Arch Pharmacol. 2010 Jun;381(6):563-72 PubMed
J Alzheimers Dis. 2004 Dec;6(6 Suppl):S61-74 PubMed
Curr Opin Investig Drugs. 2010 Jan;11(1):80-91 PubMed
Cytometry A. 2004 Dec;62(2):89-96 PubMed
Biochem Pharmacol. 2008 Feb 15;75(4):956-64 PubMed
J Neurochem. 2002 Mar;80(5):780-7 PubMed
Neuro Endocrinol Lett. 2011;32(3):259-63 PubMed
Biol Psychiatry. 2003 Nov 15;54(10):1049-59 PubMed
J Pharmacol Exp Ther. 2005 Dec;315 (3):1346-53 PubMed
J Neurol Sci. 2003 Jan 15;206(1):23-6 PubMed
Biochem Soc Trans. 2013 Oct;41(5):1331-4 PubMed
Bioorg Med Chem Lett. 2010 Oct 15;20(20):6093-5 PubMed
Biochem Soc Trans. 2008 Oct;36(Pt 5):976-80 PubMed
Methods Mol Biol. 2012;810:25-58 PubMed
Farmakol Toksikol. 1988 May-Jun;51(3):16-8 PubMed
Curr Alzheimer Res. 2013 Oct;10(8):893-906 PubMed
Clin Chim Acta. 1994 Jul;228(1):35-51 PubMed
Neuro Endocrinol Lett. 2010;31(3):336-42 PubMed
Biull Eksp Biol Med. 1986 Jun;101(6):700-2 PubMed
J Biol Chem. 1951 Nov;193(1):265-75 PubMed
Biochim Biophys Acta. 2013 Oct;1830(10):4537-42 PubMed
Biochem Pharmacol. 1976 May 15;25(10):1133-8 PubMed
Expert Opin Drug Saf. 2014 Jun;13(6):759-74 PubMed
Molecules. 2010 Dec 02;15(12):8804-12 PubMed
Methods Enzymol. 1996;264:484-509 PubMed
J Biol Chem. 2008 Aug 1;283(31):21649-54 PubMed
Eur J Med Chem. 2016 Oct 4;121:774-84 PubMed
Psychol Neuropsychiatr Vieil. 2010 Jun;8(2):123-31 PubMed
Jpn J Pharmacol. 1999 Sep;81(1):115-21 PubMed
Assessment of the Effects of Drugs on Mitochondrial Respiration
