ABSTRACT
The effect of ethanol on the kinetics of folic acid urinary excretion was studied in five chronic alcoholic patients who were maintained in a folate replete state. For 17 days, 95% ethanol was administered orally at 2-h intervals (X9). The folate pool(s) were labeled with the tritium labeled pteroyl glutamic acid at the start of the period of ethanol ingestion and at the start of a control abstinent period. The 24-h urine volume did not change with consumption of ethanol. Total urinary folate excretion was significantly greater by 20 to 40% in four of five patients during the ethanol administration period (p less than 0.05). The fall-off in urinary radioactivity corrected for total folate excretion (dpm/microgram Lactobacillus casei folate) was resolved into a biexponential decay with two distinct slopes. Ethanol caused the slope of the second component to flatten significantly with mean t1/2 of 63.7 days on ethanol versus 9.6 days off (p less than 0.05). These kinetic results are consistent with the known interference by ethanol of folate utilization in a functional tissue pool.
Subject(s)
Alcoholism/urine , Folic Acid/urine , Adult , Humans , Kinetics , Lacticaseibacillus casei/metabolism , Male , Middle AgedABSTRACT
The higher incidence of blue-yellow color blindness (tritanopia) found among alcoholics could be due to genetic or acquired factors. The acute administration of ethanol to alcoholics and normal subjects transiently resulted in poorer color discrimination in all spectra but with significantly more errors in the blue-yellow versus the red-green color range (p < 0.005, p < 0.01). Thus, ethanol appears to act as a toxin to inner retinal layers, which could account for the higher incidence of tritanopia found among alcoholics.
