D-Amphetamine-Induced Hydrogen Peroxide Production in Skeletal Muscle is Modulated by Monoamine Oxidase Inhibition

Abstract

The aim of this paper was to study the influence of d-amphetamine administration as a sympathomimetic drug on the synthesis of hydrogen peroxide (H₂O₂) in mouse soleus muscle and to investigate the modulating effects of pargyline, an inhibitor of monoamine oxidase (MAO) in this context. Charles River mice were assigned to four groups: Control, d-amphetamine treated, pargyline treated, and amphetamine + pargyline treated. Their soleus muscles were removed 0, 15, 30, 60, and 120 min after treatment. The amount of hydrogen peroxide formation within the muscles was estimated using an indirect method. The control data showed a continuous production of hydrogen peroxidase. Pargyline administration lead to an initial increase of H₂O₂ production that later faded below control levels. Administration of amphetamine finally stimulated H₂O₂ production much above control levels. When combining amphetamine and pargyline treatment, H₂O₂ production was accelerated in the initial phase but dropped to control levels at 30 min. It is concluded that in skeletal muscle MAO is an important source of hydrogen peroxide production triggered by amphetamine administration and that this tissue plays a hitherto not described role in oxidizing circulating biogenic monoamines.

Key words

D-amphetamine - pargyline - hydrogen peroxide - MAO - skeletal muscle

References

• 1 Aebi H. Catalase in vitro.  Meth Enzymol. 1984;  105 121-126
• 2 Arida R M, Naffah-Mazzacoratti M G, Soares J, Cavalheiro E A. Monoamine responses to acute and chronic aerobic exercise in normotensive and hypertensive subjects.  Rev Paul Med. 1998;  116 1618-1624
• 3 Biegon A, Segal M, Samuel D. Sex differences in behavioural and thermal responses to pargyline and typtophan.  Psychopharmacology. 1979;  61 77-80
• 4 Branden C VD, Kerckaert I, Roels F. Peroxisomal β-oxidation from endogenous substrates. Demonstration through H₂O₂ production in the unanaesthetized mouse.  Biochem J. 1984;  218 697-702
• 5 Brown M D, Dengel D R, Hogikyan R V, Supiano M A. Sympathetic activity and the heterogeneous blood pressure response to exercise training in hypertensives.  J Appl Physiol. 2002;  92 1434-1442
• 6 Carvalho F, Remiao F, Soares M E, Catarino R, Queiroz G, Bastos M L. d-Amphetamine induced hepatotoxicity - a possible contribution of catecholamines and hyperthermia for this effect studied in isolated rat hepatocytes.  Arch Toxicol. 1997;  71 429-436
• 7 Carvalho F, Fernandes E, Remiao F, Bastos M L. Effect of d-amphetamine repeated administration on rat antioxidant defenses.  Arch Toxicol. 1999;  73 83-89
• 8 Carvalho F, Duarte J A, Neuparth M J, Carmo H, Fernandes E, Remiao F, Bastos M L. Hydrogen peroxide production in mouse tissues after acute d-amphetamine administration. Influence of monoamine oxidase inhibition.  Arch Toxicol. 2001;  75 465-469
• 9 Cohen G, Somerson N L. Catalase-aminotriazole method for measuring secretion of hydrogen peroxide by microorganisms.  J Bacteriol. 1969;  98 543-546
• 10 Duarte J A, Carvalho F, Natsis K, Remiao F, Bastos M L, Soares J M, Appell H J. Structural alterations of skeletal muscle induced by chronic administration of d-amphetamine and food restriction.  Basic Appl Myol. 1999;  9 65-69
• 11 Foley R J, Kapatkin K, Verani R, Weinman E J. Amphetamine induced acute renal failure.  South Med J. 1984;  77 258-260
• 12 George A J. Central nervous system stimulants.  Baillieres Best Pract Res Clin Endocrinol Metab. 2000;  14 79-88
• 13 Halliwell B. How to characterize a biological antioxidant.  Free Rad Res Comm. 1990;  9 1-32
• 14 Himms-Hagen J. Cellular thermogenesis.  Annu Rev Physiol. 1976;  38 315-351
• 15 Hoffman B B, Lefkowitz R J. Catecholamines, sympathomimetic drugs, and adrenergic receptor antagonists. Hardman JG, Limbird LE, Molinoff PB, Ruddon RW, Gilman AG Goodman & Gilman's The Pharmacological Basis of Therapeutics. New York; McGraw-Hill 1996: 199-248
• 16 Huang N K, Wan F J, Tseng C J, Tung C S. Amphetamine induces hydroxyl radical formation in the striatum of rats.  Life Sci. 1997;  61 2219-2229
• 17 Ide T, Tsutsui H, Kinugawa S, Utsumi H, Kang D, Hattori N, Uchida K, Arimura K, Egashira K, Takeshita A A. Mitochondrial electron transport complex I is a potential source of oxygen free radicals in the failing myocardium.  Circ Res. 1999;  85 357-363
• 18 Kita T, Takahashi M, Kubo K, Wagner G C, Nakashima T. Hydroxyl radical formation following methamphetamine administration to rats.  Pharmacol Toxicol. 1999;  85 133-137
• 19 Makisumi T, Yoshida K, Watanabe T, Tan N, Murakami N, Morimoto A. Sympatho-adrenal involvement in methamphetamine-induced hyperthermia through skeletal muscle hypermetabolism.  Eur J Pharmacol. 1998;  363 107-112
• 20 Masuoka N, Wakimoto M, Ubuka T, Nakano T. Spectrophotometric determination of hydrogen peroxide: Catalase activity and rates of hydrogen peroxide removal by erythrocytes.  Clin Chim Acta. 1996;  254 101-112
• 21 Ohta Y, Yamasaki T, Niwa T, Niimi K, Majima Y, Ishiguro I. Role of catalase in retinal antioxidant defence system: Its comparative study among rabbits, guinea pigs, and rats.  Ophthalmic Res. 1996;  28 336-342
• 22 Premereur N, Branden C V, Roels F. Cytochrome P-450-dependent H₂O₂ production demonstrated in vivo. Influence of phenobarbital and allylisopropylacetamide.  FEBS. 1986;  199 19-22
• 23 Radi R. Biological antioxidant systems.  Toxicol Ind Health. 1993;  9 53-62
• 24 Richards J R, Johnson E B, Stark R W, Derlet R W. Methamphetamine abuse and rhabdomyolysis in the ED - a 5-year study.  Am J Emerg Med. 1999;  17 681-685
• 25 Richards J R. Rhabdomyolysis and drugs of abuse.  J Emerg Med. 2000;  19 51-56
• 26 Sinet P M, Heikkila R E, Cohen G. Hydrogen peroxide production by rat brain in vivo.  J Neurochem. 1980;  34 1421-1328
• 27 Spitzmaul G F, Esandi M C, Bouzat C. Amphetamine acts as a channel blocker of the acetylcholine receptor.  Neuroreport. 1999;  10 2175-2181
• 28 Taylor W M, Reinhart P H, Bygrave F L. Stimulation by α-adrenergic agonists of Ca2 + fluxes, mitochondrial oxidation and gluconeogenesis in perfused rat liver.  Biochem J. 1983;  212 555-565
• 29 Thompson J A, Hess M L. The oxygen free radical system: a fundamental mechanism in the production of myocardial necrosis.  Progr Cardiovasc Dis. 1986;  28 449-462