1986 Volume 46 Issue 3 Pages 333-344
It was investigated whether drug-induced lipidosis and porphyria of liver were caused by alminoprofen in rats, compared with chloroquine diphosphate (chloroquine), 4, 4'-bis (diethylaminoethoxy) α, β-diethyldiphenylethane (DH), carbon tetrachloride (CCl4) and 3, 5-diethoxycarbonyl-1, 4-dihydrocollidine (DDC) . Phospholipids (PL) and total cholesterol (TC) in lysosomal fraction and tissue of liver were increased significantly by chloroquine and DH. CCl4caused the remarkable increase of TC, triglyceride (TG) and non-esterified fatty acid (NEFA) in rat liver tissue. Furthermore, chloroqine, DH and CCl4showed the marked rise of GOT, mitochondria-GOT (m-GOT) and GPT in blood biochemical examinations, and also observed the cloudy swelling, fatty degeneration and necrosis of liver in pathological findings. On the other hand, PL in lysosomal fraction and tissue of liver was increased slightly by alminoprofen, ibuprofen, ketoprofen and flurbiprofen. Ibuprofen caused the slight rise of GOT and m-GOT, however, the significant changes in blood biochemical and pathological findings were not observed by repeated oral administration of alminoprofen. In experimental hepatic porphyria studies, δ-aminolevulinic acid (ALA) in urine and porphyrine (coproporphyrine and protoporphyrine) contents in rat liver were increased markedly by repeated oral administration of phenobarbital or DDC. On the contrary, alminoprofen did not show the significant changes on ALA synthetase and ALA dehydrase activities, ALA and porphobilinogen in urine, and porphyrine contents in liver. These results suggested that lipidosis and porphyria of liver were not induced by alminoprofen.
