The effects of vitamin B6 on lens antioxidant system in valproic acid-administered rats

Valproic acid (VPA, 2-propyl pentanoic acid) is a broad-spectrum antiepileptic drug (AED) and is commonly used in the treatment of bipolar disorders and epilepsy. AEDs are known to result in vascular disturbances. Vitamin B6 (Vit B6) is water soluble vitamin essential for normal growth, development, and metabolism. In this study, we aimed to investigate the protective effects of Vit B6 against VPA-induced lens damage in experimental animals. In this study, male 4-month-old, Sprague-Dawley rats were used. The animals were divided into four groups. Group I was intact control animals. Group II rats were administered with Vit B6 (50 mg/kg/day) for 7 days. Group III rats were administered with only VPA (500 mg/kg/day) for 7 days. Group IV was given VPA + Vit B6 (in a same dose and time). Vit B6 was given to rats by gavage and VPA was given by intraperitoneally. On the 8th day of experiment, all of the animals were fasted overnight and then killed under ether anesthesia. Lens tissues were taken from animals, homogenized in 0.9% saline to make up a 10% homogenate. The homogenates was used for glutathione (GSH), lipid peroxidation (LPO), protein levels, and enzyme analysis. In VPA groups, levels of lens GSH and LPO and activities of glutathione-S-transferase, glutathione peroxidase, glutathione reductase, and aldose reductase were increased, while superoxide dismutase activity was decreased. Treatment with Vit B6 reversed these effects. These results demonstrated that administration of Vit B6 is potentially beneficial agent to reduce the lens damage in VPA toxicity, probably by decreasing oxidative stress

Vanadyl sulfate administration protects the streptozotocin-induced oxidative damage to brain tissue in rats

Diabetes mellitus manifests itself in a wide variety of complications and the symptoms of the disease are multifactorial. The present study was carried out to investigate the effects of vanadyl sulfate on biochemical parameters, enzyme activities and brain lipid peroxidation, glutathione and nonenzymatic glycosylation of normal- and streptozotocin-diabetic rats. Streptozotocin (STZ) was administered as a single dose (65 mg/kg) to induce diabetes. A dose of 100 mg/kg vanadyl sulfate was orally administered daily to STZ-diabetic and normal rats, separately until the end of the experiment, at day 60. In STZ-diabetic group, blood glucose, serum sialic and uric acid levels, serum catalase (CAT) and lactate dehydrogenase (LDH) activities, brain lipid peroxidation (LPO) and nonenzymatic glycosylation (NEG) increased, while brain glutathione (GSH) level and body weight decreased. In the diabetic group given vanadyl sulfate, blood glucose, serum sialic and uric acid levels, serum CAT and LDH activities and brain LPO and NEG levels decreased, but brain GSH and body weight increased. The present study showed that vanadyl sulfate exerted antioxidant effects and consequently may prevent brain damage caused by streptozotocin-induced diabetes

The effects of vanadyl sulfate on glutathione, lipid peroxidation and nonenzymatic glycosylation levels in various tissues in experimental diabetes

Background and Aims: Diabetes mellitus is characterized by hyperglycemia which over time leads to serious damage of several body systems. Vanadium ions and their complexes have been demonstrated to have various insulin-mimetic and antidiabetic effects. The object of the present work was to investigate the effect of vanadyl sulfate ( VS) on serum total lipid and protein parameters, glutathione, lipid peroxidation and nonenzymatic glycosylation levels in cardiac, lens, lung and skeletal muscle tissues of STZ diabetic rats