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Biomedical subjects

O Eriksson

Publications and source records attributed to O Eriksson.

At least 109 records · Page 6Linked to original sources
PubMed1992

Inhibition of lipid peroxidation in isolated rat liver mitochondria by the general anaesthetic propofol.

The effect of the general anaesthetic propofol (2,6-diisopropylphenol) on lipid peroxidation in rat liver mitochondria was assessed with the thiobarbituric acid (TBA) assay. Propofol was shown to inhibit the accumulation of TBA-reactive compounds after initiation of radical production by the addition of the ADP-Fe2+ complex. Analysis of kinetics showed that propofol caused a concentration-dependent delay as well as a decrease in the rate of the peroxidation process. 1H-NMR spectra of mitochondrial lipid extracts indicated that 95% of the added propofol remained intact after 30 min incubation under conditions of low oxidative stress. The ESR spectrum of propofol incubated in the presence of EDTA-Fe2+ and H2O2 as initiators of radical production showed a radical that was most likely a decomposition product of the primary phenoxy radical of propofol. It is concluded that (a) propofol acts as a chain reaction-breaking antioxidant by forming a stable radical and (b) propofol does not seem to be metabolized in mitochondria in vitro.

Adenosine Diphosphate↗
PubMed1992

The role of endotoxins in induced ruminal acidosis in calves.

Experimentally induced ruminal acidosis was carried out in 4 calves to investigate the possibility of resorption of endotoxins from Gram negative bacteria originating from the gastro-intestinal tract. The ruminal acidosis was induced by overfeeding of oats and the effect was evaluated by clinical and blood biochemical changes. Blood samples were collected every 2 h for 60 h before and after experimental feeding. The animals showed signs of ruminal acidosis and also the clinical and blood biochemical changes were similar to those seen after experimental endotoxaemia. However, although being less dramatic the changes in many relevant parameters such as an increase in prostaglandin F metabolite levels, body temperature, endotoxins and a decrease in iron indicate that an endotoxaemic state had occurred. The results of the present study show that ruminal acidosis/stasis is linked to resorption of endotoxins from the gastro-intestinal tract causing endotoxaemia/endotoxicosis.

Acidosis↗
PubMed1991

Effects of the membrane potential upon the Ca(2+)- and cumene hydroperoxide-induced permeabilization of the inner mitochondrial membrane.

A protonophore-induced delta psi decrease in a 180-140 mV range causes an increase in the lag-period of Ca(2+)-induced mitochondrial permeabilization but has little effect on the cumene hydroperoxide-induced permeability transition of mitochondria. Suppression of the non-specific permeability induction seems to be mediated by an increase in [ADP] in the mitochondrial matrix. A further decrease in delta psi leads to additional suppression of the non-specific permeability as a result of a partial ruthenium red-sensitive efflux of the previously accumulated Ca2+. On the other hand, complete dissipation of delta psi causes immediate induction of the non-specific permeability. It is concluded that only complete dissipation of delta psi caused by H+ leakages may act as a trigger for non-specific permeability induction.

Animals↗
PubMed1991

1H-NMR studies of lipid extracts of rat liver mitochondria.

Lipid extracts of rat liver mitochondria were studied by 1H-NMR at 200 MHz. Each spectrum, obtained in 6 min with routine acquisition parameters, allowed the estimation of the phosphatidylcholine/phosphatidylethanolamine ratio, the cholesterol/total lipid molar ratio, the average fatty acid length, the unsaturation ratio and the oxidation state of the ubiquinone/ubiquinol couple. 1H-NMR spectroscopy was also used to analyze structural changes of the lipids following peroxidation. In model liposomes subjected to enzymatic peroxidation the appearance of hydroperoxides and conjugated double bonds were detected, whereas in mitochondria no such changes were seen even after a period of relatively high oxidative stress. This suggests that the systems for protection against oxidative damage in mitochondria are able to keep the amount of peroxidation products below the detection limit of the technique.

Animals↗