Energy metabolism changes and oxidative attack after hepatic arterial embolization and chemoembolization in thioacetamide-induced cirrhotic livers.
Hepatic energy metabolism and oxidative attack were studied after transcatheter arterial embolization (TAE) and chemoembolization (TAC) of the left and median lobes of the liver using thioacetamide (TAA)-induced cirrhotic rats. TAE was carried out using gelatin sponge (1.5 mg/cm3) dissolved in saline solution (SS). TAC was performed by adding mitomycin C (MMC) (1.6 mg/kg body weight) to the previous embolic solution. The energy charge (EC) of embolized lobes decreased from 0.86 to 0.78 and 0.74 1 h after TAE and TAC, respectively, but was restored 3 h later. Adenosine 5'-triphosphate (ATP) and total adenine nucleotide content (TAN) of embolized and non-embolized lobes was also temporarily decreased. Total hepatic blood flow (THBF) of embolized and chemoembolized lobes was reduced in almost 50%, and it took 1 week to become normalized. After TAC (3 and 6 h, respectively), total glutathione (TGSH) content was reduced from 7.02 mumol/g of liver to around 4.5 mumol/g, and malondialdehyde (MDA) content increased from 196.94 nmol/g of liver to values above 300 nmol/g. TAE in cirrhotic livers did not induce any changes in these parameters. In conclusion, after TAE and TAC the hepatic energy metabolism is temporarily altered by ischemia. TAC-induced oxidative attack, in addition to ischemia and MMC, could be one of the mechanisms explaining the effectiveness of this therapy.
Hashimoto
L
L
First Department of Surgery, Tohoku University School of Medicine, Sendai City, Japan.
Ouchi
K
K
Suzuki
M
M
Matsuno
S
S
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D004621:Embolization, Therapeutic / Q000009:adverse effects; D004734:Energy Metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006499:Hepatic Artery; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008102:Liver Circulation; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000378:metabolism / Q000628:therapy*; D008297:Male; D016685:Mitomycin; D008937:Mitomycins / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D011919:Rats, Inbred Strains; D013853:Thioacetamide / Q000633:toxicity
D000227:Adenine Nucleotides; D008937:Mitomycins; D013853:Thioacetamide; D016685:Mitomycin; D005979:Glutathione Peroxidase; D005978:Glutathione