Biomedical subjects

C Rice-Evans

Publications and source records attributed to C Rice-Evans.

104 records · Page 6Linked to original sources

PubMed1987

Modulation of iron-mediated oxidant damage in erythrocytes by cellular energy levels.

In this work we have investigated the effects of iron-induced oxidative stress on erythrocytes and their membranes, the importance of haemoglobin oxidation and of the maintenance of the metabolic properties of the cells. The results show that by maintaining the energy requirements of the erythrocyte, methaemoglobin production is minimised under conditions of iron-stress. However, in this situation, the membranes of the erythrocytes become more susceptible to the oxidative damage and increased lipid peroxidation ensues.

Energy Metabolism↗

PubMed1986

Sickle cell membranes and oxidative damage.

Sickle erythrocytes and their membranes are susceptible to endogenous free-radical-mediated oxidative damage which correlates with the proportion of irreversibly sickled cells. The suppression of incubation-induced oxidative stress by antioxidants, free radical scavengers and an iron chelator suggest that oxidation products of membrane-bound haemoglobin contribute towards the pathology of the disease.

Anemia, Sickle Cell↗

PubMed1986

Susceptibility of tamarin (Saguinus labiatus) red blood cell membrane lipids to oxidative stress: implications for wasting marmoset syndrome.

Captive Callitrichids frequently suffer a fatal wasting disease, wasting marmoset syndrome (WMS), of unexplained cause. This paper describes studies on the erythrocytes from animals in a breeding colony of tamarins (Saguinus labiatus), in which deaths from anaemia and wasting were occurring, to seek evidence for biochemical changes which could lead to oxidative damage and premature cell lysis. In only one animal of 33 studied did the red blood cell lipids show an increased susceptibility to oxidative damage. This animal, with some degree of certainty, could be diagnosed as having WMS. It was concluded that evidence for a primary deficiency of antioxidants as a cause of unexplained deaths, or WMS, in the colony could not at present be substantiated.

Animals↗

PubMed1985

t-butyl hydroperoxide-induced perturbations of human erythrocytes as a model for oxidant stress.

Erythrocytes were incubated with t-butyl hydroperoxide in the presence and absence of hemoglobin as a model system for oxidative stress and the alterations in the structure and integrity of the membranes were investigated. The results showed that in the presence of hemoglobin a significant modification in the membrane surface charge was induced but no such alteration was observed in peroxidized hemoglobin-free membranes. As increased hemoglobin oxidation occurred in the erythrocytes, membrane lipid peroxidation diminished, suggesting a protective role for methemoglobin in t-butyl hydroperoxide-induced lipid peroxidation. Electrophoresis on polyacrylamide gels showed modification of the cytoplasmic protein region but no high molecular weight aggregates formed at the concentrations of the hydroperoxide used in this work. The results suggest that the t-butyl hydroperoxide/normal erythrocyte system seems to be an instructive model for membrane perturbations characteristic of oxidative disorders.

Erythrocyte Membrane↗

PubMed1985

Oxidative effects of iron on erythrocytes.

In this work we have investigated the effects of iron-induced free radical formation in normal human erythrocytes in vitro, as a model system for studying iron damage, and in erythrocytes from patients with beta-thalassaemia major. The resulting oxidative effects were measured in terms of methaemoglobin formation and reduced glutathione loss. The effects of desferrioxamine, an iron-chelating agent, were also investigated. The results show that the increased methaemoglobin formation after iron-induced oxidative stress is consistent with a decline in the intracellular glutathione levels and that this process is inhibited by desferrioxamine. Similar treatment of red cell haemolysates produces less methaemoglobin. This suggests that, on exposure of intact erythrocytes to iron-induced free radical effects, the red cell membrane exacerbates the breakdown of the antioxidant defences of the cell and the oxidation of haemoglobin.

Ascorbic Acid↗

PubMed1982