Gen. Pharmac. Vol. 24, No. 6, pp. 1411-1413,1993 0306-3623/93$6.00 + 0.00 Printed in Great Britain Pergamon Press Ltd THE EFFECTS OF TAURINE ON PERFUSED HEART MUSCLE MALONDIALDEHYDE LEVELS BIRSENKAPLAN,I AYSEL ARICIOGLU, 2 DENIZERBAS, I SEMRA ERBAS 3 and NURTEN TURKOZKAN 2 IDepartment of Physiology, Medical Faculty, Gazi University, 06510 lksevler, Ankara, Turkey [Tel. 90-4-212 81 28; Fax 90-4-213 43 38] 2Department of Biochemistry, Medical Faculty, Gazi University, 06510 lksevler, Ankara, Turkey 3Department of Statistics, Art and Science, Faculty, Gazi University, 06330 Besevler, Ankara, Turkey (Received 23 March 1993) Abstract--l. Taurine is found as a free amino acid in plasma and many tissues such as heart, muscle, brain and blood. Its exact role is not fully defined but it appears to have an important effect on the function of the heart. 2. The purpose of this study was to investigate the effects of taurine (10-3 M and 10 -2 M) on malondialdehyde levels in perfused heart muscle. 3. In this study we found that administrated taurine before anoxia and repeffusion increased the malondialdehyde levels but administrated taurine after anoxia decreased the malondialdehyde levels in perfused heart muscle compared to the taurine administrated group before anoxia. 4. Anoxia did not change the perfused heart muscle malondialdehyde levels. INTRODUCTION Pion et al. demonstrated a cardiomyopathy that could be associated with taurine deficiency (Pion et al., 1987). It is found as a free amino acid in plasma and many tissues such as heart, muscle, brain and blood (Huxtable, 1989). In the heart taurine is the most abundant free amino acid, making up as much as 60% of the total free amino acids. Taurine is synthesized by the heart but the major determinant of myocardial taurine is uptake from the plasma. Ischemia or hypoxia decreases heart taurine. In humans it was shown that addition of dietary taurine resulted in symptomatic improvement in patients with congestive heart failure (Tenaglia and Cody, 1988). Taurine protects against ischemic damage in myocardial cells. It has been suggested that the ability of taurine to protect membrane lipids from peroxi- dation may be one of the intraeellular roles of this amino acid (Hochachka, 1986; Tseng et al., 1990). Ischemic injury may be exacerbated by readmission of oxygen into the myocardium probably due to the formation of free radicals and their interaction with membrane lipids (Subramanian et al., 1987). We wanted to test the myocardial damage during anoxia and exacerbation during reperfusion using the isolated perfused guinea pig heart by measuring malondialdehyde (MDA) levels as an index of lipid peroxidation of heart muscle damage. Since oxygen free radicals or lipid peroxides are short lived and difficult to measure directly MDA a *To whom all correspondence should be addressed. more stable and longer lived degradative product of lipid peroxides was assayed as reflecting lipid peroxi- dation levels. MATERIALS AND METHODS Guinea pigs weighing between 250-300 g were used and anesthesized with sodium pentothal (Abbott 0.03 mg kg-i i.p.). The chests were opened and the hearts were excised, placed in buffer and mounted on a perfusion apparatus within 60 sec. The rate of peristaltic pump was adjusted to 7 ml min- i Each heart was initially perfused through aorta in a non-recirculating retrograde fashion for 60 rain. The perfusion medium was Krebs-Henseleit bicarbonate buffer (NaCI, ll8mM; KC1, 4.7mM; CaCI,, 3.0mM; MgSO4, 1.2mM; KH2PO4, 1.2 mM; EDTA, 0.5 raM; and Nail2 CO2, 25 raM; pH 7.4) 10 -3 M and 10-2M taurine (from Sigma Chemical Co., St. Louis, MO, USA) was added into the perfusion solution. Experimental design: Hearts were divided into seven groups. All perfusion were gassed with 95% 02-5% CO2. Group 1: HeaRs were perfused only with Krebs-Henseieit for 80 min and used as controls (n = 6). Group 2: Hearts were peffused with 10 -3M taurine+Krebs-Henseleit and after then established the anoxic perfusion (without oxygen) through 20min (n =6). Group 3: Hearts were perfused with 10 -2M taurine + Krebs-Henseleit and after then established the anoxic perfusion (without oxygen) through 20 min (n = 6). Group 4:10 -2 M taurine was added into the perfusion solution for 20 rain after 60 min normally perfused hearts (n = 6). Group 5: Hearts were perfused in anoxic position (without oxygen) through 20 rain and then 10 -2 M taurine was added to the perfusion solution (n = 6). Group 6: After normal peffusion hearts were peffused without oxygen for 20 min and after this period hearts were perfused with oxygeneted Krebs-Henseleit (n ffi 6). Group 7: After normal perfusion hearts were perfused with Krebs--Henseleitwithout oxygen for 20 rain (n = 6). 1411