Reduced Vitamin E and Increased Lipofuscin Products in Erythrocytes of Diabetic Rats

Abstract

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.

Vitamin E supplementation restores glutathione and malondialdehyde to normal concentrations in erythrocytes of type 1 diabetic children.

“…Vitamin E as ␣-tocopherol was measured by HPLC (23). Freshly obtained erythrocytes were stored in 2% pyrogallol in ethanol at Ϫ70°C.…”

“…Freshly obtained erythrocytes were stored in 2% pyrogallol in ethanol at Ϫ70°C. All samples were analyzed within 1 month of storage using a reverse-phase C-18 column (Waters, Milford, MA), a 95% methanol solvent system, and a uv/vis detector set at 292 nm (23). Lipid peroxidation was determined by measuring malondialdehyde, which is an end product of lipid peroxidation.…”

“…Many investigators have reported lower concentrations of glutathione in the erythrocytes, aorta, and lenses of diabetic patients compared with healthy subjects (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19), except for some studies that reported similar glutathione concentrations (20). In addition, an increase in malondialdehyde concentration has been reported in erythrocytes and other tissues of diabetic animals and patients (21)(22)(23)(24)(25)(26)(27)(28).…”

Oxidative stress status in patients with diabetes mellitus: relationship to diet

“…Hyperglycaemia results in glucose auto-oxidation, nonenzymatic glycation and monocyte dysfunction, which lead to increased production of free radicals (Hiramatsu & Arimori, 1988;Hunt et al, 1990;Mullarkey et al, 1990;Brownlee, 1994). This is further aggravated by the decreased levels of antioxidants (Murakami et al, 1989;Jain et al, 1991;Sinclair et al, 1991) and leads to oxidative damage, illustrated by the high levels of lipid and DNA peroxidation products found in these patients (Griesmacher et al, 1995;Dandona et al, 1996). All these diabetes-related abnormalities can intensify the endothelial dysfunction, oxidation of LDL and foam cell formation, which ultimately lead to the formation of the atheroma plaque (Ross, 1993).…”

Oxidative stress in adipose tissue as a primary link in pathogenesis of insulin resistance

“…Оба типа сахарного диабета связаны со снижением содержания в клетке антиоксидантов, прежде всего, восстановленного глутатиона (GSH) и витаминов С и Е [37,51]. Гликирование белков при гипергликемии затрагивает и антиоксидантные ферменты, что вызывает подавление их ферментативной активности, способствует окислительному стрессу и прогрессированию уже сформировавшегося диабета.…”