phosphocreatine and Alcoholic-Intoxication

Creatine kinase reaction rates were measured by the magnetisation transfer technique in brains of healthy adult and aged rats and in rats with chronic cerebral ischemia and chronic ethanol intoxication. These measurements indicated that the rate constant of the creatine kinase reaction is significantly reduced in the case of severe chronic cerebral ischemia in aged rats. In the adult rats, during chronic ethanol intoxication after 3 weeks of administration of 3 ml of 30% ethanol once a day via a gastric tube, a significant decrease in the pseudo first-order rate constant k(for) of the creatine kinase reaction was also found. In contrast, mild chronic cerebral ischemia in adult rats produced an increase in the reaction rate 4 weeks after occlusion. At the same time, corresponding conventional phosphorus magnetic resonance spectra showed negligible changes in signal intensities.

Topics: Adenosine Triphosphate; Aging; Alcoholic Intoxication; Alcoholism; Animals; Brain; Brain Ischemia; Chronic Disease; Creatine Kinase; Phosphocreatine; Rats; Rats, Wistar

In this work, 31P phosphorus NMR (31P NMR) studies of the brain have been conducted in rats acutely and chronically intoxicated with ethanol. In both groups, changes in levels of high-energy phosphates were observed: increase of phosphocreatinine (PCr)/beta AaTP and PCr/inorganic phosphate (Pi) in acute and long-term ethanol exposure, and decrease of Pi/beta ATP after acute ethanol administration. These changes in high-energy phosphates, indicative of a reduction of adenosine triphosphate (ATP) and PCr consumption (PCr+ ADP+ H+ ATP+ Cr; ATP ADP+ Pi), suggest a reduction of cerebral metabolism both in acute and chronic ethanol exposure. In addition, in the group of rats chronically intoxicated with ethanol, there were variations in phosphodiester peak intensities (decrease of phosphomonoester (PME)/phosphodiester (PDE), increase of PDE/beta ATP), suggesting increased breakdown of membrane phospholipids. These changes could provide a metabolic explanation for the development of cerebral atrophy in chronic alcoholism.

Topics: Adenosine Triphosphate; Alcoholic Intoxication; Alcoholism; Animals; Brain; Ethanol; Magnetic Resonance Spectroscopy; Male; Phosphates; Phosphocreatine; Phospholipids; Rats; Rats, Wistar

Topics: Adult; Alcoholic Intoxication; Alcoholism; Aspartate Aminotransferases; Chronic Disease; Creatine Kinase; Humans; Male; Middle Aged; Phosphocreatine