Influence of hypoxia on mitochondrial function and energy status in CCl4-induced cirrhotic rat liver.
The influence of hypoxia on hepatic mitochondrial function and energy status was studied in normal and carbon tetrachloride (CCl4)-induced cirrhotic rats. Under hypoxemia of 50 mm Hg-PaO2, hepatic energy status was suppressed both in normal and cirrhotic rats. After the reversal of hypoxia, it was completely restored in normal rats concomitant with a rapid elevation of hepatic mitochondrial redox state (overshoot phenomenon) and increase in the mitochondrial oxidative phosphorylative activity. By contrast, in cirrhotic rats, such an enhancement of mitochondrial function was not observed. It was clarified that cirrhotic liver mitochondrial function was not observed. It was clarified that cirrhotic liver mitochondria have little capacity to respond to the hypoxic stress. A lower resistance to hypoxic episode in cirrhotics might be attributable to the absence of mitochondrial enhancement which is a compensatory mechanism for the deranged energy metabolism of the liver.
Wakashiro
S
S
Dept. II of Surgery, Kyoto University Faculty of Medicine, Japan.
Shimahara
Y
Y
Ikai
I
I
Tokunaga
Y
Y
Ozaki
N
N
Tanaka
A
A
Morimoto
T
T
Ozawa
K
K
D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000503:physiopathology*; D004734:Energy Metabolism; D000860:Hypoxia / Q000503:physiopathology*; D007773:Lactates / Q000378:metabolism; D008106:Liver Cirrhosis, Experimental / Q000503:physiopathology*; D008297:Male; D008930:Mitochondria, Liver / Q000503:physiopathology*; D010084:Oxidation-Reduction; D010085:Oxidative Phosphorylation; D010100:Oxygen / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains
D007773:Lactates; D010100:Oxygen