[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.

[The induction of the beta state of the comuton regulation of mitochondrial oxidative phosphorylation by 2,4-DNP and malonate].

The effect of 2,4-DNP and malonate on tissue-specific uncoupling of oxidative phosphorylation (OP) of rat liver and kidney mitochondria by homologous comutons has been studied. The addition of 2,4-DNP in the presence of comuton induced beta state of comuton regulation. Transfer of liver mitochondria from alpha to beta state also resulted from partial inhibition of succinate dehydrogenase activity of addition of 0.

[The effect of a one-time administration of phenobarbital and carbon tetrachloride on comuton activity in the rat liver].

Infusion of phenobarbital and CCl4 was found to induce comuton control of mitochondrial respiration in a liver of starved rats. Comuton regulation of liver mitochondria respiration can be activated either by increase in liver activity or by damage caused by CCl4. The comuton regulation is directly induced by disturbance of energetic homeostasis of liver cells.

[Effect of ruthenium red on the induction by Ca2+ ions of the beta- and gamma states of comuton regulation of mitochondrial respiration and oxidative phosphorylation].

Preincubation of liver mitochondria (Mch) with Ca2+ ions at inorganic phosphate concentration less than I mM in the presence of liver cell soluble phase (CSP) induced rotenone-independent tissue-specific uncoupling of oxidative phosphorylation (beta state of comuton regulation) and rotenone-stimulated tissue-specific uncoupling (gamma state of comuton regulation). The reduction in K+ ion concentration in the incubation medium entirely inhibited the induction of beta state. Tissue-specific stimulation of the rat liver Mch respiration in substrate-containing medium was increased after rotenone addition.