Saldaña-Balmori Y, Zentella de Piña M, Guinzberg R, Rocha-Hernández A, Piña E
Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, D.F., México.
Eur J Pharmacol. 1996 Dec 19;317(2-3):225-9. doi: 10.1016/s0014-2999(96)00733-9.
It has been reported that piroxicam prevents the hepatic increase of triacylglycerides and thiobarbituric acid-reactive substances observed after acute ethanol intoxication in rats and also causes a decrease in blood ethanol concentration. The aim of this study was to assess the effect of piroxicam on these 3 metabolic indicators, using isolated rat hepatocytes incubated with ethanol or lactate, supplemented or not with epinephrine. Epinephrine stimulated the consumption of lactate, but not of ethanol. In the isolated hepatocytes, and in a dose-dependent fashion, piroxicam alone raised the consumption of lactate and ethanol, increased the triacylglyceride pool in cells incubated with lactate or ethanol, and decreased the content of thiobarbituric acid-reactive substances in cells incubated with ethanol, but not with lactate. Epinephrine blocked these actions of piroxicam, except the lowering of the content of thiobarbituric acid-reactive substances. Thus, piroxicam helps to control the oxidative stress produced in isolated hepatocytes by ethanol.
