Acute CCl-induced intoxication reduces complex I, but not complex II-based mitochondrial bioenergetics - protective role of succinate.

The main therapeutic strategy for the treatment of patients with toxic liver failure is the elimination of the toxic agent in combination with the targeted mitigation of pathological processes that have been initiated due to the toxicant. In the current research we evaluated the strategy of metabolic supplementation to improve mitochondrial bioenergetics during acute liver intoxication. In our study, we have shown that acute CCl-induced intoxication negatively affects Complex I (in the presence of glutamate-malate as energy substrates) based respiration, generation of mitochondrial membrane potential (ΔΨ), mitochondrial NAD(P)H pool and NADH redox index, mitochondrial calcium retention capacity (CRC) and structure and functions of the liver.

Possibilities of chromoesophagoscopy for diagnosis of Barrett's esophagus.

When the distal esophagus is covered with columnar gastric mucosa up to 2 cm from the esophagogastric junction it is considered normal. If the distal esophagus is covered with columnar epithelium more than 2 cm from the esophagogastric junction, it is called Barrett's esophagus. We have developed a new chromoesophagoscopic method to improve diagnostic testing for Barrett's esophagus.