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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.

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Objectives: It is unknown when inosine was first employed as a renoprotective agent in the context of kidney transplantation procedures. However, there is no clinical evidence to support a protective role of inosine. The aim of this study was to investigate the effect of inosine on graft recovery.

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