Lipofuscin products, lipid peroxides and aluminum accumulation in red blood cells of hemodialyzed patients.

This study examines whether there is a relationship between aluminum overload and the accumulation of lipofuscin products (aging pigments) and lipid peroxides in red blood cells (RBC) of hemodialyzed patients. Lipid peroxides levels were assessed by the thiobarbituric acid reactivity; lipofuscin products were assessed by determining fluorescence in the lipid extracts at excitation 360 nm and emission 440 nm. Aluminum was measured by atomic absorption spectrophotometry. Controls were age-matched normal volunteers. Data show that there was a significant increase in the lipid peroxides and lipofuscin products in hemodialyzed patients compared with controls even after normalization with hemoglobin or phospholipids in RBC. Further, the increase in the lipid peroxides and lipofuscin products significantly correlated with the levels of aluminum accumulation in RBC of hemodialyzed patients. This study suggests that aluminum overload has a role in increased membrane peroxidation, which in turn can cause reduced RBC life span and contribute to anemia in chronic renal failure patients.

The effect of glycemic control on plasma prealbumin levels in type-1 diabetic children.

Plasma prealbumin levels have been used as a sensitive biochemical index in the assessment of nutritional status. The present study was undertaken to determine if diabetic children with uncontrolled diabetes are at greater nutritional risk than those with controlled glycemia. Plasma prealbumin was determined using a radial immunoassay in 42 diabetics and 20 age-matched normal volunteers. Results (mean +/- SE) show that prealbumin levels are significantly (p < 0.02) lower in diabetics (21.5 +/- 1.0) than in normals (25.8 +/- 1.3). Compared with normals, prealbumin levels in controlled diabetics are similar; whereas uncontrolled diabetics have significantly lower (p < 0.05) prealbumin levels. Prealbumin levels were 20.4 +/- 1.7 in uncontrolled diabetics (GHb > 9.00), 21.8 +/- 2.3 in intermediately controlled diabetics (GHb 7.0-9.0), and 22.2 +/- 1.5 in controlled diabetics (GHb < 7.0). The data suggest that diabetics in good control are nutritionally similar to the normal population and that patients in poor control have significantly lower prealbumin than the normal population indicating that metabolic derangement may result in malnutrition.

The effect of glycemic control and duration of diabetes on cholesterol and phospholipid classes in erythrocytes of type I diabetes.

Abnormalities in the lipid composition of erythrocytes can alter blood rheology and viscosity. These alterations have been implicated in the pathogenesis of microvascular disease in diabetic patients. The present study was undertaken to examine whether or not long-term glycemic control or duration of diabetes has any role in the altered membrane cholesterol and phospholipid composition of erythrocytes in type I diabetes. Long-term glycemic control was assessed by measuring glycosylated hemoglobin (GHb) from diabetic patients and age-matched normal volunteers. There was no significant correlation between GHb or duration of diabetes with total cholesterol, phospholipid, and cholesterol to phospholipid molar ratios in erythrocytes of these patients. Among phospholipid classes, GHb showed a significantly negative relationship with sphingomyelin (SM) (r = .55, P less than .01) levels, but was not related to phosphatidylcholine (PC) and phosphatidylethanolamine (PE) levels of erythrocytes. Duration of diabetes had no effect on SM, PC, or PE levels of erythrocytes.

Reduced vitamin E and increased lipofuscin products in erythrocytes of diabetic rats.

Vitamin E deficiency in erythrocytes causes decreased cell survival, hypercoagulability, and increased adhesiveness to the endothelium. Similar abnormalities are found in erythrocytes of the diabetic population. This study examines the effect of diabetes on vitamin E and lipofuscin products (aging pigments) in erythrocytes of streptozocin-induced diabetic rats. Controls were injected with buffer alone, and a subgroup consisting of insulin-treated diabetic rats were injected daily with insulin for 2 mo. Mean +/- SD vitamin E levels were 23.2 +/- 4.9, 19.4 +/- 3.2, and 25.9 +/- 2.5 nmol/mumol phospholipid. Lipid fluorescence values (relative values/phospholipid) were 11.1 +/- 1.9, 14.1 +/- 2.6, and 11.9 +/- 1.8 (excitation/emission 360/440 nm) in control, diabetic, and insulin-treated diabetic rats, respectively. Differences in vitamin E and lipofuscin products were significant between all control and diabetic groups and diabetic and insulin-treated diabetic groups. Reduction in vitamin E and increases in lipofuscin products in diabetic rats were significant even when values were expressed per micromole Hb or per 100 ml erythrocytes. This study demonstrates that hyperglycemia significantly reduces vitamin E and increases lipofuscin products in erythrocytes of diabetic rats. These effects were prevented with insulin treatment.

Elevated lipid peroxidation levels in red blood cells of streptozotocin-treated diabetic rats.

This study was performed to determine whether or not hyperglycemia in diabetes results in elevated levels of lipid peroxidation products in red blood cells (RBC). Diabetes was induced in rats by treatment with streptozotocin. The level of lipid peroxidation products was examined in fresh RBC by measuring their thiobarbituric acid (TBA) reactivity after 2 and 4 months of induction of diabetes. Hyperglycemia was assessed by measuring the level of glycosylated hemoglobin and blood glucose. Results show that lipid peroxidation levels were significantly higher (50% to 84%) in RBC of diabetic rats than in controls. The increase in the level of lipid peroxidation was blocked in diabetic rats in which hyperglycemia was controlled by insulin treatment. Among phospholipid classes, relative percentage of sphingomyelin (SM) was significantly reduced in RBC at both 2 and 4 months of diabetes; whereas phosphatidylethanolamine (PE) levels were higher in RBC at 4 months of diabetes only. The level of phosphatidylcholine (PC) did not differ significantly between RBC of control and diabetic rats. This study suggests a significantly altered lipid composition and an accumulation of lipid peroxidation products in RBC of streptozotocin-treated diabetic rats.

The effect of malonyldialdehyde on viscosity of normal and sickle red blood cells.

This study has examined the effect of MDA, an end product of lipid peroxidation, on the viscosity of AA and SS RBC suspensions. MDA accumulation in RBC was accomplished in vitro in human RBC by treating them with exogenous standard MDA. MDA accumulation assessed by the thiobarbituric acid reactivity of in vitro MDA-treated RBC was comparable to that of the RBC in vivo in hemolytic anemias. There was a significant increase in the viscosity of both AA and SS RBC suspensions after in vitro treatment with MDA. The increase in viscosity or RBC was significantly positively correlated with the extent of MDA accumulation.

Low plasma prealbumin and carotenoid levels in sickle cell disease patients.

This study was undertaken to discover whether reduced levels of micronutrients in patients with sickle cell disease are due to the generalized undernutrition. Protein undernutrition was determined by measuring plasma levels of prealbumin. One micronutrient, carotene, was also simultaneously assayed in the plasma. Eighteen sickle cell disease patients were enrolled at random. Controls were 19 normal volunteers and seven family members of the patients. The patients showed significantly reduced levels of prealbumin and carotenoids compared with either normals or family members. Levels of carotenoids did not significantly correlate with level of prealbumin, which suggests that the undernutrition was not the only factor contributing to lower levels of carotenoids in these patients.

Erythrocyte membrane lipid peroxidation and glycosylated hemoglobin in diabetes.

Erythrocytes of diabetic patients have abnormal membrane properties. We examined in vivo membrane lipid peroxidation in erythrocytes of diabetic subjects and its possible relationship with hyperglycemia. Lipid peroxidation was assessed in fresh, untreated erythrocytes by quantitating thiobarbituric acid reactivity and an adduct of phospholipids and malonyldialdehyde (MDA), an end product of lipid peroxidation, with thin-layer chromatography of lipid extract of diabetic erythrocytes. There was a significantly increased membrane lipid peroxidation in diabetic erythrocytes compared with nondiabetic erythrocytes. The degree of membrane lipid peroxidative damage in erythrocytes was significantly correlated with the level of glycosylated hemoglobin, an index of mean glucose level for the preceding 3-4 mo. This suggests that peroxidation of membrane lipids and accumulation of MDA occurs in erythrocytes of diabetic patients.

The accumulation of malonyldialdehyde, an end product of membrane lipid peroxidation, can cause potassium leak in normal and sickle red blood cells.

This study has examined the effect of malonyldialdehyde (MDA), an end product of lipid peroxidation, on the K+ leak in normal (AA) and sickle (SS) red blood cells (RBCs). In vitro MDA accumulation in human RBCs was accomplished by treating them with exogenous standard MDA. MDA accumulation assessed by the thiobarbituric acid reactivity of in vitro MDA-treated RBCs was comparable to the RBCs in hemolytic anemias. There was a significant K+ leak in AA RBCs after in vitro treatment with MDA. The effect of MDA on the K+ leak was greater in SS RBCs. The increase in cellular K+ leak was significantly positively correlated with the extent of MDA accumulation as assessed by thiobarbituric acid reactivity.