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

Molecules

Piotr Tomaszewski¹  Grazyna Kubiak-Tomaszewska¹  Jan Pachecka¹  Marcin Balcerzak¹  Bozena Haznar¹  Cezary Pszenny¹  Marek Krawczyk¹  Pawel Paczkowski¹ 

[1] ¹Department of Biochemistry and Clinical Chemistry, Medical University of Warsaw, 1 Banacha St, 02-097 Warsaw, Poland ²Department of General Surgery and Liver Diseases, Medical University of Warsaw, 1A Banacha St, 02-097 Warsaw, Poland ³Central Hospital of Ministry for Home Affairs and Administration, 137 Woloska St, Warsaw, Poland

关键词: mitochondrial redox potential;    arterial ketone body ratio;    total ketone body concentration;    liver metastatic cancer;    circulatory insufficiency;   

DOI  :  10.3390/80100146

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
This is an open access article distributed under the Creative Commons Attribution License (CC BY) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.