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PubMed2004

[Methods of monitoring oxidation-reduction balance and its potential role in diagnostics].

Results of the latest investigations confirm that the injury of redox homeostasis of human organism can be the starting point of many diseases. The pathogenesis of these diseases, including atherosclerosis, diabetes mellitus, chronic liver diseases, renal failure, rheumatoid arthritis and neurodegenerative diseases could be cleared up more deeply by the investigation of parameters of oxidative stress and by the observation of their changes in connection with the different organ and tissue damages. It is well known, that individuals with lowered antioxidant defences may be at greater risk of developing diseases induced by free radicals. The goal of the authors is to direct attention to the possible role of some redox parameters in detecting of general health status of the human body and in the risk assessment of the different diseases. These measurements can perhaps help the clinician in determining optimal treatment and monitoring its effectiveness.

Antioxidants↗
PubMed1989

Measurement of tissue oxidation-reduction state with carbon-13 nuclear magnetic resonance spectroscopy.

The oxidation state of tissues influences their response to cancer therapy. We have devised a novel approach to the measurement of thiol redox which is based on the relative nuclear magnetic resonance signal intensity from carbon-13 adjacent to sulfur in metabolites of the redox-sensitive phosphorothioate drug, S-2-(3-methylaminopropylamino)ethylphosphorothioic acid (WR3689). Incubation of WR3689 metabolites under oxidizing conditions results in quantifiable changes in the 13C nuclear magnetic resonance spectrum stoichiometrically related to the degree of oxidation in mouse liver homogenate in vitro. Drug oxidation is competitive with the oxidation of tissue-derived thiol groups under these conditions. Noninvasive measurement of redox state may assist in designing more effective strategies for altering normal and malignant tissue response to cancer therapy.

Amifostine↗
PubMed1982

Multiphasic oxidation-reduction of cytochrome b in the succinate-cytochrome c reductase.

The triphasic course previously reported for the reduction of cytochrome b in the succinate-cytochrome c reductase by either succinate or duroquinol has been shown to be dependent on the redox state of the enzyme preparation. Prior reduction with increasing concentrations of ascorbate leads to partial reduction of cytochrome c1, and a gradual decrease in the magnitude of the oxidation phase of cytochrome b. At an ascorbate concentration sufficient to reduce cytochrome c1 almost completely, the reduction of cytochrome b by either succinate or duroquinol becomes monophasic. Owing to the presence of a trace amount of cytochrome oxidase in the reductase preparation employed, the addition of cytochrome c makes electron flow from substrate to oxygen possible. Under such circumstances, the addition of a limited amount of either succinate or duroquinol leads to a multiphasic reduction and oxidation of cytochrome b. After the initial three phases as described previously, cytochrome b becomes oxidized before cytochrome c1 when the limited amount of added substrate is being used up. However, at the end of the reaction when cytochrome c1 is being rapidly oxidized, cytochrome b becomes again reduced. The above observations support a cyclic scheme of electron flow in which the reduction of cytochrome b proceeds by two different routes and its oxidation controlled by the redox state of a component of the respiratory chain.

Animals↗