|Budget Amount *help
¥2,000,000 (Direct Cost : ¥2,000,000)
Fiscal Year 1996 : ¥800,000 (Direct Cost : ¥800,000)
Fiscal Year 1995 : ¥1,200,000 (Direct Cost : ¥1,200,000)
Drinking tests were carried out using healthy volunteers, which had been detertmined the DNA types (ALDH2 and CYP2E1), after alcohol withdrawal for 2 weeks and after successive drinking for 2 weeks (50g/day) before the test. Under starved conditions, the subjects took alcohol (0.4g/Kg body weight), and after 0,1,2,3 and 5 hours, blood samples were obtained, and the concentrations of ethanol, glucose, pyruvate and lactate were determined. In the experiment after alcohol withdrawal for 2 weeks, the blood glucose levels of all subjects were decreased at one hour after alcohol ingestion. The decrease of blood glucose level was partially suppressed after successive drinking. The following mechanisms were thought as the reason. Cytochrome p-450 2E1 was induced by successive drinking, and the induction prevented partially the increase of NADH/NAD ratio, and suppressed the inhibition of gluconeogenesis. Then, we examined the possibility that increased O2 consumption by activation of MEOS and decreased blood flow by secretion of noradrenaline under stress meight cause liver injury, inducing hypoxia in the liver. Rats were given ethanol instead of water at least for 2 weeks, then, 2 ml of 20% ethanol was given through stomch tubing, and stress was given by immersing the rats body in water or by simply fixing in a cage. After giving the above stress, blood samples were collected and GOT,GPT,gammaGTP,LDH and CPK activities were measured. In the rats which were given ethanol instead of water, stress by fixing in cages increased gammaGTP activity. Above results strongly suggest that alcoholic liver injury is induced when a person who ingests alcohol for long period takes alcohol under stress.