Here we report that coffee showed a strong antibacterial action on Escherichia coli (E. coli) and Helicobacter pylon(H. pylon). This action against H. pylon suggests that coffee may have action as a useful natural inhibitor of gastritis and gastric ulcers.
The present investigation was undertaken to study the effect of pretreatment with the methanolic extract of Asteracantha longifolia(AL) seeds on liver antioxidant defense system during acetaminophen-induced liver damage in rats. Acetaminopheninduced liver injury was manifested by a significant increase in the levels of lipid peroxides with a concomitant decrease in the levels of enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase) and non-enzymic antioxidants (reduced glutathione, vitamin C and vitamin E). Pretreatment with AL extract reversed these alterations to near normal. Results of the study confirm that pretreatment with AL seed extract is very effective in reducing acetaminophen-induced oxidative stress suggesting its antioxidant property.
Vitamin E is a potent antioxidant and has an ability to modulate host immune functions. This manuscript consists of six parts:(1) vitamin E deficiency and immunity, (2) vitamin E supplementation and immunity, (3) vitamin E and the decreased cellular immunity with aging, (4) vitamin E and T-cell differentiation in the thymus, (5) vitamin E and acquired immune deficiency syndrome (AIDS), and (6) vitamin E and the abnormal increase of host immune functions such as allergy and autoimmune diseases. In vitamin E deficiency most of the immune parameters show a downward trend, which is associated with increased infectious diseases and the incidence of tumors. In contrast, vitamin E supplementation has various beneficial effects on the host immune system. The decreased cellular immunity with aging or during the development of AIDS is markedly improved by the intake of a high vitamin E diet. In addition, vitamin E plays an important role in the differentiation of immature T cells in thymus. Vitamin E deficiency induces the decreased differentiation of immature T cells, which results in the early decrease of cellular immunity with aging in spontaneously hypertensive rats. Conversely, vitamin E supplementation induces a higher differentiation of immature T cells via increased positive selection by thymic epithelial cells, which results in the improvement of decreased cellular immunity in the aged. Furthermore, some reports have shown that vitamin E has an ability to modulate the development of allergy or autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus. Taken together, all of the evidence suggest that vitamin E is a potent vitamin for modulating not only decreased immunity shown in the aged but also abnormally increased host immune system in patients with allergy or autoimmune diseases.
The oXidation products of vitamin E, α-tocopherol, during the peroxidation of unsaturated lipids in the peroxidation of liposomal systems, human plasma, and some biological tissues have been reViewed. Free radical reactions of α-tocopherol take place via the α-tocopheroxyl radical as an intermediate. If suitable free radical is present, a non-radical product can be formed from the coupling of the free radical with the or-tocopheroxyl radical. The reaction products of α-tocopherol with lipid-peroxyl radicals, such as phosphatidylcholine-peroxyl radicals and cholesteryl ester-peroxyl radicals, are 8a-(lipid-dioxy)-α-tocopherones, which are hydrolyzed to or-tocopherylquinone. The other product-forming pathway yields 2, 3-and 5, 6-epoxy-α-tocopherylquinones and their precursors, epoxyhydroperoxy-α-tocopherylquinones. Other vitamin E compound, γ-tocopherol, is superior to α-tocopherol in the detoXification of reactive nitrogen oxide species and forms 5-nitro-γ-tocopherol as the reaction product. The oxidation products of vitamin E have been detectedin liposomal systems, plasma samples, a perfused rat liver model, and human atherosclerotic lesions. Thus, the formation of these products provides us with much information onthe antioxidant function of vitamin E in biological systems.
The adherence of monocytes to the vascular endothelial cells is an important early event in atherogenesis. Monocyte adherence to endothelial cells is induced by oxidized low density lipoprotein (LDL) and mediated by multiple cell adhesion molecules including vascular cell-adhesion molecule 1 (VCAM-1). Enhanced endothelial expression of these molecules by oxidized LDL has been shown to be a critical step in foam cell formation and the development of atherosclerosis. Recent studies have demonstrated that vitamin E inhibited the expression of mRNA and protein for VCAM-1 by endothelial cells in response to stimulation with oxidized LDL or inflammatory cytokines. Compared to α- tocopherol, α-tocotrienol displayed a more profound inhibitory effect on adhesion molecule expression and monocytic cell adherence. Among the isomers of tocotrienol, δ-tocotrienol was a potent and effective agent for the reduction of cellular VCAM-1 expression and monocytic cell adherence. The inhibitory effects of vitamin E analogs on the adhesiveness of endothelial cells correlated with their intracellular concentrations. Anti-atherogenic effects of tocotrienols may be derived from their properties of cholesterol-lowering effect, protein kinase C inhibition, and modulation of cyclooxygenase cascade. Although recent human studies have raised some doubts on the efficacy of vitamin E in the prevention of progression of atherosclerotic lesions, the experimental studies using tocotrienol strongly support its positive effect on the reduction of risk of atherogenesis. Further studies will be necessary for clarifying the anti-atherogenic effect of tocotrienol and its bioavailability after oral administration.