Evaluation of in vitro antioxidant activity of Indian bay leaf, Cinnamomum tamala (Buch. -Ham.) T. Nees & Eberm using rat brain synaptosomes as model system.

The study investigated the perturbation of oxidant-antioxidant balance in brain synaptosomes of diabetic rats and determined the antioxidant and free radical-scavenging property of the Indian bay leaf. Brain synaptosomes were isolated from control and streptozotocin-induced diabetic animals and oxidative stress parameters were assayed. A methanolic extract of bay leaf (BLE) was tested for the polyphenolic content and antioxidant activity by in vitro assays. A significant increase in the levels of lipids and lipid peroxidation products and a decline in antioxidant potential were observed in diabetic rat brain synaptosomes. The total polyphenolic content of BLE was found to be 6.7 mg gallic acid equivalents (GAE)/100g. BLE displayed scavenging activity against superoxide and hydroxyl radicals in a concentration-dependent manner. Further, BLE showed inhibition of Fe(2+)-ascorbate induced lipid peroxidation in both control and diabetic rat brain synaptosomes. Maximum inhibition of lipid peroxidation, radical scavenging action and reducing power of BLE were observed at a concentration of 220 microg GAE. These effects of BLE in vitro were comparable with that of butylated hydroxyl toluene (BHT), a synthetic antioxidant. It can be concluded that synaptosomes from diabetic rats are susceptible to oxidative damage and the positive effects of bay leaf in vitro, could be attributed to the presence of antioxidant phytochemicals.

Sustained leves of ascorbic acid are toxic and immunosuppressive for human T cells

Ascorbate (vitamin C) can protect from oxidative damage to DNA and lipids that may lead to aging, cancer, and other dysfunctions. However, we find that purified human T cells deteriorate if maintained in ascorbate in culture for 18 hrs. or more; viability and Il-2 synthesis are over 90 percent curtailed by scorbate at 50 micrograms/ml. T cell proliferation and adhesion are severely suppressed at 10-25 micrograms/ml. Dihydro-ascorbate was much less toxic or suppressive. The suppressive effect of ascorbate appears irreversible, since removal of ascorbate after 18 hrs. did not restore the mitogenic response. Although moderate dietary levels of ascorbate often reach 250-1000 mg or more daily and appear beneficial, our data caution against sustained megadoses of ascorbate for treatment of patients with AIDS and cancer

Effect of vitamin C deficiency and excess on the liver: a histopathological and biochemical study in guinea pigs fed normal or high cholesterol diet.

When guinea pigs were kept on a restricted vitamin C intake of only 0.5 mg daily, their serum ascorbic acid fell to 0.16 +/- 0.06 mg/d1 in 16 weeks as compared to 0.73 +/- 0.11 in control. This was associated with significant increase in liver cholesterol and triglycerides. When they were simultaneously challenged with a high cholesterol load, this fat accumulation was markedly exaggerated. The weight of the liver now increased by almost two-and-half times. Liver cholesterol rose to 12.90 +/- 2.63 mg/gm as compared to 3.23 +/- 0.56 mg/gm with low vitamin C alone. Histopathology showed marked distension and vacuolation of hepatocytes, focal necrosis and fibroplasia. Administration of excess vitamin C (100 mg daily) significantly countered these changes. The vitamin C-lipid relationship has important clinical bearings and liver could be an important site of vitamin C action.