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2012 | 12 | 4 | 247-254
Article title

Ocena wpływu amisulprydu na grupy tiolowe osocza w modelu in vitro

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Title variants
EN
The assessment of amisulpride effects in vitro on plasma thiol groups
Languages of publication
EN
Abstracts
EN
Clinical studies indicate that amisulpride – the second generation antipsychotic – does not cause any increase in plasma lipid peroxidation. We do not know in what way this medicinal drug affects the activity of the key enzymes of antioxidative protection and low-molecular antioxidants, including the plasma thiol groups. The study was aimed at establishing the effects of amisulpride, in doses recommended for treatment of acute episode of schizophrenia, on free thiols in human plasma under in vitro conditions and lipid peroxidation measured by the level of TBARS. Material and methods: Blood for the study was collected from 10 healthy male volunteers (aged 24-26 years) for ACD solution. Active substance of amisulpride was dissolved in 0.01% dimethyl sulfoxide to the final concentrations (278 ng/ml and 578 ng/ml) and incubated with plasma for 24 hours at 37°C. Control samples were performed for each experiment. The free thiols level was measured using the Ellman method, whereas the levels of thiobarbituricacid-reactive substances by spectrophotometric method (acc. to Rice-Evans, 1991). The results were analysed using the paired Student t-test (StatSoft Inc., Statistica v. 6.0). Results: Amisulpride after 24 hours’ incubation with plasma, as compared to control samples (without drug), caused an increase in the level of free thiols in plasma – statistically significant for concentration 578 ng/ml (p<0.03). At this concentration after 24 hours’ incubation with plasma the drug caused also a significant decrease in lipid peroxidation (p<0.003). Conclusions: Amisulpride in concentration 578 ng/ml, corresponding to doses used for treatment of acute episode of schizophrenia, induces antioxidative effects, causing a significant decrease in plasma lipid peroxidation and increasing the concentration of free thiols in plasma.
PL
W badaniach klinicznych wykazano, że amisulpryd – lek przeciwpsychotyczny drugiej generacji – nie powoduje wzrostu peroksydacji lipidów osocza. Nie wiadomo, w jaki sposób lek ten wpływa na aktywność kluczowych enzymów obrony antyoksydacyjnej oraz niskocząsteczkowe antyoksydanty, w tym grupy tiolowe osocza. Celem badania było ustalenie wpływu amisulprydu w dawkach rekomendowanych do leczenia ostrego epizodu schizofrenii na wolne tiole w ludzkim osoczu w modelu in vitro oraz peroksydację lipidów, mierzoną za pomocą oznaczenia stężenia TBARS. Materiał i metody: Krew do badań pobrano od 10 zdrowych ochotników płci męskiej (w wieku 24-26 lat) na roztwór ACD. Substancję aktywną amisulprydu rozpuszczono w 0,01% dimetylosulfotlenku do stężeń końcowych (278 ng/ml i 578 ng/ml) i inkubowano z osoczem 24 godziny w temperaturze 37°C. Do każdego doświadczenia wykonano próby kontrolne. Oznaczenia poziomu wolnych tioli przeprowadzono metodą Ellmana, a stężenia związków reagujących z kwasem tiobariturowym – metodą spektrofotometryczną (Rice-Evans, 1991). Do analizy wyników zastosowano sparowany test t-Studenta (StatSoft Inc., Statistica v. 6.0). Wyniki: Amisulpryd po 24-godzinnej inkubacji z osoczem w porównaniu z próbami kontrolnymi (bez leku) spowodował wzrost poziomu wolnych tioli w osoczu – istotny statystycznie dla stężenia 578 ng/ml (p<0,03). W stężeniu tym po 24-godzinnej inkubacji z osoczem lek spowodował również istotny spadek peroksydacji lipidów (p<0,003). Wnioski: Amisulpryd w stężeniu 578 ng/ml, odpowiadającym dawkom leku stosowanym w leczeniu ostrego epizodu schizofrenii, wywiera działania antyoksydacyjne, powodując istotny spadek peroksydacji lipidów osocza oraz zwiększając stężenie wolnych tioli w osoczu.
Discipline
Year
Volume
12
Issue
4
Pages
247-254
Physical description
References
  • 1. Arvindakshan M., Sitasawad S., Debsikdar V. i wsp.: Essential polyunsaturated fatty acid and lipid peroxide levels in nevermedicated and medicated schizophrenia patients. Biol. Psychiatry 2003; 53: 56-64.
  • 2. Dietrich-Muszalska A., Kontek B.: Lipid peroxidation in patients with schizophrenia. Psychiatry Clin. Neurosci. 2010; 64: 469-475.
  • 3. Dietrich-Muszalska A., Olas B.: Isoprostanes as indicators of oxidative stress in schizophrenia. World J. Biol. Psychiatry 2009; 10: 27-33.
  • 4. Dietrich-Muszalska A., Olas B., Rabe-Jablonska J.: Oxidative stress in blood platelets from schizophrenic patients. Platelets 2005; 16: 386-391.
  • 5. Khan M.M., Evans D.R., Gunna V. i wsp.: Reduced erythrocyte membrane essential fatty acids and increased lipid peroxides in schizophrenia at the never-medicated first-episode of psychosis and after years of treatment with antipsychotics. Schizophr. Res. 2002; 58: 1-10.
  • 6. Mahadik S.P., Mukherjee S., Correnti E.E., Scheffer R.: Elevated levels of lipid peroxidation products in plasma of drug-naive patients at the onset of psychosis. Schizophr. Res. 1995; 15: 66.
  • 7. Yao J.K., Reddy R.D., van Kammen D.P.: Oxidative damage and schizophrenia: an overview of the evidence and its therapeutic implications. CNS Drugs 2001; 15: 287-310.
  • 8. Petronijević N.D., Mićić D.V., Duricić B. i wsp.: Substrate kinetics of erythrocyte membrane Na,K-ATPase and lipid peroxides in schizophrenia. Prog. Neuropsychopharmacol. Biol. Psychiatry 2003; 27: 431-440.
  • 9. Dietrich-Muszalska A., Kontek B., Rabe-Jabłońska J.: Quetiapine, olanzapine and haloperidol affect human plasma lipid peroxidation in vitro. Neuropsychobiology 2011; 63: 197-201.
  • 10. Dietrich-Muszalska A., Kopka J., Kontek B., Kwiatkowska A.: Wpływ stężeń terapeutycznych zyprazydonu na poziom wolnych tioli i związków reagujących z kwasem tiobarbiturowym w osoczu – badania in vitro. Psychiatr. Psychol. Klin. 2012; 12: 237-246.
  • 11. Parikh V., Khan M.M., Mahadik S.P.: Differential effects of antipsychotics on expression of antioxidant enzymes and membrane lipid peroxidation in rat brain. J. Psychiatr. Res. 2003; 37: 43-51.
  • 12. Dakhale G., Khanzode S., Khanzode S. i wsp.: Oxidative damage and schizophrenia: the potential benefit by atypical antipsychotics. Neuropsychobiology 2004; 49: 205-209.
  • 13. Kropp S., Kern V., Lange K. i wsp.: Oxidative stress during treatment with first- and second-generation antipsychotics. J. Neuropsychiatry Clin. Neurosci. 2005; 17: 227-231.
  • 14. Pillai A., Parikh V., Terry A.V. Jr, Mahadik S.P.: Long-term antipsychotic treatments and crossover studies in rats: differential effects of typical and atypical agents on the expression of antioxidant enzymes and membrane lipid peroxidation in rat brain. J. Psychiatr. Res. 2007; 41: 372-386.
  • 15. Bai O., Wei Z., Lu W. i wsp.: Protective effects of atypical antipsychotic drugs on PC12 cells after serum withdrawal. J. Neurosci. Res. 2002; 69: 278-283.
  • 16. Dietrich-Muszalska A., Olas B.: Inhibitory effects of polyphenol compounds on lipid peroxidation caused by antipsychotics (haloperidol and amisulpride) in human plasma in vitro. World J. Biol. Psychiatry 2010; 11: 276-281.
  • 17. Do K.Q., Trabesinger A.H., Kirsten-Krüger M. i wsp.: Schizophrenia: glutathione deficit in cerebrospinal fluid and prefrontal cortex in vivo. Eur. J. Neurosci. 2000; 12: 3721-3728.
  • 18. Dietrich-Muszalska A., Olas B., Głowacki R., Bald E.: Oxidative/ nitrative modifications of plasma proteins and thiols from patients with schizophrenia. Neuropsychobiology 2009; 59: 1-7.
  • 19. Dietrich-Muszalska A., Olas B.: Modifications of blood platelet proteins of patients with schizophrenia. Platelets 2009; 20: 90-96.
  • 20. Sheehan D.V., Lecrubier Y., Sheehan K.H. i wsp.: The Mini- International Neuropsychiatric Interview (M.I.N.I.): the development and validation of a structured diagnostic psychiatric interview for DSM-IV and ICD-10. J. Clin. Psychiatry 1998; 59 supl. 20: 22-33.
  • 21. Rice-Evans C.A., Diplock A.T., Symons M.C.R.: Techniques in Free Radical Research. Vol. 22 serii: Burdon R.H., van Knippenberg P.H. (red.): Laboratory Techniques in Biochemistry and Molecular Biology. Elsevier, Amsterdam 1991: 51-100.
  • 22. Ellman G., Lysko H.: A precise method for the determination of whole blood and plasma sulfhydryl groups. Anal. Biochem. 1979; 93: 98-102.
  • 23. Bradford M.: A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein- dye binding. Anal. Biochem. 1976; 72: 248-254.
  • 24. Huang T.L., Liou C.W., Lin T.K.: Serum thiobarbituric acidreactive substances and free thiol levels in schizophrenia patients: effects of antipsychotic drugs. Psychiatry Res. 2010; 177: 18-21.
  • 25. Medina-Hernández V., Ramos-Loyo J., Luquin S. i wsp.: Increased lipid peroxidation and neuron specific enolase in treatment refractory schizophrenics. J. Psychiatr. Res. 2007; 41: 652-658.
  • 26. Yao J.K., Reddy R., van Kammen D.P.: Reduced level of plasma antioxidant uric acid in schizophrenia. Psychiatry Res. 1998; 80: 29-39.
  • 27. Yao J.K., Reddy R., van Kammen D.P.: Abnormal age-related changes of plasma antioxidant proteins in schizophrenia. Psychiatry Res. 2000; 97: 137-151.
  • 28. Raffa M., Atig F., Mhalla A. i wsp.: Decreased glutathione levels and impaired antioxidant enzyme activities in drug-naive firstepisode schizophrenic patients. BMC Psychiatry 2011; 11: 124.
  • 29. Surapaneni K.M.: Status of lipid peroxidation, glutathione, ascorbic acid, vitamin E and antioxidant enzymes in schizophrenic patients. J. Clin. Diagn. Res. 2007; 1: 39-44.
  • 30. Andreazza A.C., Kauer-Sant’Anna M., Frey B.N. i wsp.: Oxidative stress markers in bipolar disorder: a meta-analysis. J. Affect. Disord. 2008; 111: 135-144.
  • 31. Maes M., Galecki P., Chang Y.S., Berk M.: A review on the oxidative and nitrosative stress (O&NS) pathways in major depression and their possible contribution to the (neuro)degenerative processes in that illness. Prog. Neuropsychopharmacol. Biol. Psychiatry 2011; 35: 676-692.
  • 32. Edwards R., Peet M., Shay J., Horrobin D.: Omega-3 polyunsaturated fatty acid levels in the diet and in red blood cell membranes of depressed patients. J. Affect. Disord. 1998; 48: 149-155.
  • 33. Peet M., Horrobin D.F.: A dose-ranging study of the effects of ethyl-eicosapentaenoate in patients with ongoing depression despite apparently adequate treatment with standard drugs. Arch. Gen. Psychiatry 2002; 59: 913-919.
  • 34. Di Simplicio P., Franconi F., Frosalí S., Di Giuseppe D.: Thiolation and nitrosation of cysteines in biological fluids and cells. Amino Acids 2003; 25: 323-339.
  • 35. Włodek L., Iciek M.: S-tiolacja białek jako mechanizm antyoksydacyjny i regulacyjny. Postępy Biochem. 2003; 49: 77-84.
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article
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bwmeta1.element.psjd-be26d4bd-fe86-49da-aca0-c2b9d725d24e
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