Adriamycin causes hyperlipemia as a consequence of nephrotoxicity.
Adriamycin induced hyperlipemia: its features and mechanism(s) in rats were investigated. Massive hyperlipemia occurred 14-21 days after a single dose of adriamycin (7.5 mg/kg i.v.). All lipoprotein fractions were affected. Mild but significant changes in tissues were observed (liver and intestine triglycerides and kidney phospholipids were reduced). Lipid synthesis and secretion was decreased, as shown by the Triton WR1339 test 7 days after treatment, but subsequently returned to normal. Mitochondrial oxidation of long-chain fatty acids was markedly reduced in kidney, and a slight reduction was also observed in heart. Lipoprotein lipase activity was reduced in adipose tissue. These results suggest that adriamycin hyperlipemia is due to reduced lipid storage and utilization. Carnitine did not counteract hyperlipemia and proteinuria after adriamycin. Analogies to hyperlipemia following puromycin aminonucleoside-induced nephrotoxicity are discussed.
D000818:Animals; D004317:Doxorubicin / Q000633:toxicity*; D005227:Fatty Acids / Q000378:metabolism; D006949:Hyperlipidemias / Q000139:chemically induced*; D007668:Kidney / Q000187:drug effects*; D008071:Lipoprotein Lipase / Q000097:blood; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D010084:Oxidation-Reduction; D051381:Rats
D005227:Fatty Acids; D004317:Doxorubicin; D008071:Lipoprotein Lipase