Hepatic Mitochondrial Redox Potential in Patients with Liver Metastatic Cancers and Circulatory Insufficiency

• Main Authors: Marek Jarecki, Pawel Paczkowski, Marek Krawczyk, Cezary Pszenny, Bozena Haznar, Marcin Balcerzak, Jan Pachecka, Grazyna Kubiak-Tomaszewska, Piotr Tomaszewski
• Format: Article
• Language: English
• Published: MDPI AG 2003-01-01
• Series: Molecules
• Subjects: mitochondrial redox potential; arterial ketone body ratio; total ketone body concentration; liver metastatic cancer; circulatory insufficiency
• Online Access: http://www.mdpi.com/1420-3049/8/1/146/

Arterial ketone body ratio (AKBR), which reflects hepatic intramitochodrial redox potential, was measured in 20 patients with Carcinoma hepatis metastaticum and good circulatory condition (group A), and 16 patients with Carcinoma hepatis metastaticum and chronic cardiogenic circulatory insufficiency (group B). Total ketone body concentration (TKB) and arterial oxygen tension (PaO2) was simultaneously determined. We have stated that AKBR values in both groups of patients were decreased below the normal level. AKBR values in group B were significantly lower than in group A. At the same time TKB values in both groups were statistically equal and significantly increased above the normal level. The levels of arterial oxygen tension (PaO2) in group A were physiologically high, whereas in group B were significantly decreased. Furthermore arterial oxygen tension of patients in group B correlated with AKBR values significantly. In group A we found statistically significant negative correlation between TKB and AKBR values. Our study indicate that the main mechanism which may explain the decrease of intrahepatic mitochondrial redox potential in patients with liver metastatic cancers and good circulatory condition, is the enhanced beta-oxidation of fatty acids, when the efficiency of NAD+ to NADH reduction in beta-oxidation pathway and tricarboxylic acid cycle is higher than re-oxidation of NADH to NAD+ in the oxidative phosphorylation. In patients with coexisting chronic cardiogenic circulatory insufficiency deprivation of blood oxygen supply initiate the irreversible dysfunction of oxidative phosphorylation.