Rats of the third generation fed on a diet with 0.3 energy-% (low-essential fatty acids (EFA) or 3 energy-% (normal-EFA) essential fatty acids were given once-daily intraperitoneal injections of ethanol 3 g/kg or isocaloric glucose for 23 days. At the end of the experiment, organs were removed and their weight and lipid composition were determined. The postmortem accumulation of the prostaglandins PGE2, PGF2 alpha and 6-keto-PGF1 alpha was used to assess prostaglandin (PG) precursor availability in the organs. Ethanol was found to amplify the biochemical indicators of EFA-deficiency. The fatty acids 20:3 n-9 in brain phosphatidylethanolamine and phosphatidylinositol and 22:5 n-6 in brain phosphatidylethanolamine and phosphatidylserine were significantly higher in the ethanol group compared to the control group. In the kidney, the 20:3 n-9/20:4 n-6 ratio in phosphatidylinositol and phosphatidylserine was significantly higher in the ethanol group compared to the control group. The low-EFA animals had a lower output of urinary PGF2 alpha than the normal EFA animals. Chronic ethanol treatment gave a pronounced increase of urinary PGF2 alpha in both groups. Kidney levels of PGs were lower in the low EFA-animals. Chronic ethanol treatment gave a further decrease in kidney PGs. PG levels were the same in brains from low-EFA and normal-EFA animals with no effects of ethanol. The data are consistent with an increased utilization of EFA during chronic ethanol intoxication leading to a depletion of PG precursor stores in some but not all organs.