Statin-induced changes in mitochondrial respiration in blood platelets in rats and human with dyslipidemia
3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are widely used drugs for lowering blood lipid levels and preventing cardiovascular diseases. However, statins can have serious adverse effects, which may be related to development of mitochondrial dysfunctions. The aim o...
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| Published in | Physiological research Vol. 65; no. 5; pp. 777 - 788 |
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| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Czech Republic
Institute of Physiology
01.01.2016
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| Abstract | 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are widely used drugs for lowering blood lipid levels and preventing cardiovascular diseases. However, statins can have serious adverse effects, which may be related to development of mitochondrial dysfunctions. The aim of study was to demonstrate the in vivo effect of high and therapeutic doses of statins on mitochondrial respiration in blood platelets. Model approach was used in the study. Simvastatin was administered to rats at a high dose for 4 weeks. Humans were treated with therapeutic doses of rosuvastatin or atorvastatin for 6 weeks. Platelet mitochondrial respiration was measured using high-resolution respirometry. In rats, a significantly lower physiological respiratory rate was found in intact platelets of simvastatin-treated rats compared to controls. In humans, no significant changes in mitochondrial respiration were detected in intact platelets; however, decreased complex I-linked respiration was observed after statin treatment in permeabilized platelets. We propose that the small in vivo effect of statins on platelet energy metabolism can be attributed to drug effects on complex I of the electron transport system. Both intact and permeabilized platelets can be used as a readily available biological model to study changes in cellular energy metabolism in patients treated with statins. |
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| AbstractList | 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are widely used drugs for lowering blood lipid levels and preventing cardiovascular diseases. However, statins can have serious adverse effects, which may be related to development of mitochondrial dysfunctions. The aim of study was to demonstrate the in vivo effect of high and therapeutic doses of statins on mitochondrial respiration in blood platelets. Model approach was used in the study. Simvastatin was administered to rats at a high dose for 4 weeks. Humans were treated with therapeutic doses of rosuvastatin or atorvastatin for 6 weeks. Platelet mitochondrial respiration was measured using high-resolution respirometry. In rats, a significantly lower physiological respiratory rate was found in intact platelets of simvastatin-treated rats compared to controls. In humans, no significant changes in mitochondrial respiration were detected in intact platelets; however, decreased complex I-linked respiration was observed after statin treatment in permeabilized platelets. We propose that the small in vivo effect of statins on platelet energy metabolism can be attributed to drug effects on complex I of the electron transport system. Both intact and permeabilized platelets can be used as a readily available biological model to study changes in cellular energy metabolism in patients treated with statins. Novel drugs have been developed for the treatment of Alzheimer's disease that act on multiple targets, including cholinesterase activity, monoamine oxidase activity, Aß aggregation, y-secretase activity, serotonin transporter activity, production of reactive oxygen species, calcium channels, mitochondrial permeability transition pores, and interactions of amyloid-ß with mitochondrial enzymes (Xie et al. 2006, Lim et al. 2011, Bolea et al. 2013). Components of signaling pathways, with changes in platelets that are supposed to reflect changes in the brain, include serotonin receptors (Mendelson 2000), neurotransmitter transporters and storage vesicles (Mercado and Kilic 2010, Yubero-Lahoz et al. 2013), mitochondrial monoamine oxidase type B (Youdim 1988), brain derived neurotrophic factor (Pláteník et al. 2014), amyloid-ß (Chen et al. 1995), complexes of the mitochondrial respiratory chain (Bosetti et al. 2002, Cardoso et al. 2004, Valla et al. 2006), and a number of blood-based biomarkers (Casoli et al. 2013, Donovan et al. 2013). |
| Author | Singh, N Nekovářová, T Zlatohlávek, L Vevera, J Valeš, K Raboch, J Hroudová, J Fišar, Z Vrablík, M |
| Author_xml | – sequence: 1 givenname: J surname: Vevera fullname: Vevera, J email: zfisar@lf1.cuni.cz organization: Department of Psychiatry, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, Prague, Czech Republic. zfisar@lf1.cuni.cz – sequence: 2 givenname: Z surname: Fišar fullname: Fišar, Z – sequence: 3 givenname: T surname: Nekovářová fullname: Nekovářová, T – sequence: 4 givenname: M surname: Vrablík fullname: Vrablík, M – sequence: 5 givenname: L surname: Zlatohlávek fullname: Zlatohlávek, L – sequence: 6 givenname: J surname: Hroudová fullname: Hroudová, J – sequence: 7 givenname: N surname: Singh fullname: Singh, N – sequence: 8 givenname: J surname: Raboch fullname: Raboch, J – sequence: 9 givenname: K surname: Valeš fullname: Valeš, K |
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| SubjectTerms | Animals Blood platelets Blood Platelets - drug effects Cardiovascular disease Cell Respiration - drug effects Dyslipidemias - drug therapy Humans Hydroxymethylglutaryl-CoA Reductase Inhibitors - adverse effects Mitochondria - drug effects Mitochondrial DNA Rats Statins |
| Title | Statin-induced changes in mitochondrial respiration in blood platelets in rats and human with dyslipidemia |
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