Melatonin prevents lipid peroxidation in human erythrocytes but augments deterioration of deformability after in vitro oxidative stress.

Oxidative stress decreases the deformability of erythrocytes. Anti-oxidant measures may alleviate, pro-oxidative damage may augment this decrease. Melatonin is reported to exert both anti-oxidant and pro-oxidant properties on erythrocytes. The aim of the present study was to evaluate the effects of melatonin on erythrocyte deformability under oxidative stress conditions induced by the combination of hydrogen peroxide (20 mM) and sodium azide (100 microM). Erythrocyte suspensions were incubated for 10 min with melatonin (1-1000 microM) prior to oxidative stress. Erythrocyte deformability was measured by Laser-assisted Optical Rotational Cell Analyzer (LORCA). Lipid peroxidation was determined via malondialdehyde (MDA) measurements by HPLC. Melatonin alone did not change erythrocyte deformability. Oxidative stress alone decreased the deformability of erythrocytes by 25.8 +/- 3.1% (P<0.05). Melatonin pre-treatment augmented the decrease in erythrocyte deformability but prevented lipid peroxidation. Melatonin (1 microM) did not cause any additional effect on erythrocyte deformability. Higher concentrations (10-1000 microM) further decreased deformability (P<0.05). Erythrocytes exposed to oxidative stress had MDA levels of 116.3 +/- 14.3 micromol/g Hb. Melatonin (1 microM) slightly increased MDA levels, but 1000 microM melatonin reduced it by 35% (P<0.05). These findings indicate that melatonin exerts antioxidant effect on lipids. Deterioration of erythrocyte deformability may be due to a separate pro-oxidative action on proteins.

Erythrocyte deformability, plasma viscosity and oxidative status in patients with severe obstructive sleep apnea syndrome.

BACKGROUND AND PURPOSE: In patients with severe obstructive sleep apnea syndrome (OSAS), diurnal changes of plasma viscosity and erythrocyte deformability were measured to elucidate the possible mechanism of cardiovascular diseases in OSAS patients. PATIENTS AND METHODS: Plasma viscosity and erythrocyte deformability was determined in 11 OSAS patients and 11 healthy subjects matched by sex and age. Plasma viscosity was measured by a cone-plate viscometer, and erythrocyte deformability was determined by filtration technique. Whole blood counts were performed and oxidative status of the patients' plasma and erythrocytes were evaluated. RESULTS: OSAS patients had higher plasma viscosity than controls, both in the morning (1.74+/-0.3 vs. 1.36+/-0.2 mPas, P<0.002) and evening (1.55+/-0.2 vs. 1.27+/-0.1 mPas, P<0.002), and morning plasma viscosity was significantly higher than the evening level (P<0.05). Morning plasma viscosity of patients was inversely correlated with their mean nocturnal SaO(2). Morning plasma malonyldialdehyde level was significantly higher in the patients than in the controls (69.7+/-30.5 vs. 45.5+/-11.0 nmol/l, P<0.005). Erythrocyte deformability of the patients was slightly lower. CONCLUSIONS: We have observed that plasma viscosity is high both in the morning and in the evening in severe OSAS patients. This elevation may predispose OSAS patients to myocardial infarction and stroke by increasing blood viscosity. Low nocturnal mean SaO(2) may be responsible for the high plasma viscosity in these patients.

Abietic acid inhibits lipoxygenase activity.

In this study, it was shown that abietic acid, an abietane diterpenoid, inhibited soybean 5-lipoxygenase (linoleate: oxygen oxidoreductase, EC 1.13.11.12) and an IC(50) of 29.5 +/- 1.29 microM was determined. Since the lipoxygenase pathway leads to the biosynthesis of leukotrienes this result supports the view that abietic acid may be used in the treatment of allergic reactions.