[Influence of prodigiozan-dependent comuton on the resistance of liver mitochondria against damage by protonofor].

An effector of tissue stress of hepatocytes, prodigiozan-dependent comuton (PDC), provokes deenergiezation of liver mitochondria, preloaded by Ca2+ ions. In this case a decrease of membrane potential (MP) and Ca2+ efflux by cyclosporine A sensitive mechanism of megapore is observed. If megapore is blocked by cyclosporin A, protonofor FCCP provoked decrease of MP and Ca2+ efflux by cyclosporin A-insensitive mechanism.

[Intraorganic and intratissue mechanisms of protective action of activated Kupffer cells on hepatocytes].

Endotoxine activated Kupfer cells release into the intercellular space several mediators which act directly on hepatocytes as well as via stellet cells. In both cases Kupfer cells downregulate hepatocytes as a part of paracrine system. However, downregulated part of liver parenchyma might be extended by several mechanisms.

[Mechanisms of protective influence of endotoxin-activated Kupffer cells on hepatocytes].

Various aspects of protective and damaging influences of endotoxin-activated Kupffer cells on hepatocytes are discussed. Requests for protective subcellular mechanism activated by Kupffer cells mediators were formulated. Two possible mechanisms of activated Kupffer cells protective influence on hepatocytes which satisfy these requests are considered.

[Mechanisms of hypermetabolic states].

Current concepts of mechanisms of hypermetabolic states in the body and its selected organs are discussed. Special attention is given to hepatic processes and changes of energy metabolism in hypermetabolic hepatocytes. It is shown that hypermetabolic cells have properties characteristic of the metabolism stimulation phase in cells showing a non-specific reaction to an injury.