Different parts of the plant Ficus glomerata Roxob was extracted with water and organic solvents. The effects of these extracts on blood sugar level of streptozotocin induced diabetic rats were studied. The pet ether extract of the stem bark of the plant reduced the blood sugar level significantly. Extracts from fruit and latex of the plant did not have any significant effect on blood sugar level of these diabetic rats. The pet ether extract of the stem bark completely inhibited the enzymes glucose-6-phosphatase and arginase and activated the enzyme glucose-6-phosphate dehydrogenase from rat liver. Extracts from fruit and latex inhibited only glucose-6-phosphatase but not arginase from rat liver. A number of components from pet ether extract of the stem bark were isolated and purified. The effect of these purified components on pure enzyme glucose-6-phosphate dehydrogenase were investigated. The chemical characterisation of some of these components were carried out.

The concentrations of interferon-alpha (IFN-alpha) in supernatants from cultures of Epstein-Barr virus (EBV) transformed B-lymphoblastoid cell lines derived from seven patients with congenital dyserythropoietic anaemia (CDA) type I were below the 95% confidence limits for those derived from six healthy subjects. In contrast, the concentrations of IFN-alpha in supernatants from cultures of EBV-transformed lymphoblastoid cell lines derived from four patients with other types of CDA and four patients with hereditary sideroblastic anaemia were normal. Supernatants from cultures of peripheral blood lymphocytes stimulated with phytohaemagglutinin or pokeweed mitogen contained less IFN-alpha when the cells were derived from patients with CDA type I than when derived from healthy subjects. Since patients with CDA type I show a substantial haematological response to treatment with IFN-alpha, the data suggest that impaired IFN-alpha production may be an important pathogenetic mechanism in CDA type I.

No abstract

Air-breathing magur catfish (Clarias magur) regularly face the problem of exposure to high environmental ammonia (HEA) as one of the major pollutants in their natural habitats that causes considerable toxic effects at the cellular level, including that of oxidative stress. The major objective of the present study was to demonstrate the antioxidant activity of endogenously produced nitric oxide (NO) to defend against ammonia-induced oxidative stress in primary hepatocytes of magur catfish during exposure to HEA. Exposure to NH 4 Cl (5 mmol l −1) led to a significant increase in intracellular ammonia concentration with a sharp rise of hydrogen peroxide (H 2 O 2) and malondialdehyde (MDA) concentrations within 3 h in primary hepatocytes, which decreased gradually at later stages of treatment. This phenomenon was accompanied by a significant increase in superoxide dismutase (SOD) and catalase (CAT) activity as a consequence of induction of corresponding genes. HEA exposure also led to the stimulation of NO production due to induction of inducible nitric oxide synthase (iNOS) activity, as a consequence of up-regulation of the nos2 gene. Most interestingly, when NO production by hepatocytes under ammonia stress was blocked by adding certain inhibitors [aminoguanidine and 3-(4methylphenylsulfonyl)-2-propenenitrile] to the culture medium, there was a further rise of H 2 O 2 and MDA concentrations in hepatocytes. These were accompanied by the lowering of SOD and CAT activity with less expression of corresponding genes. Thus, it can be contemplated that magur catfish use the strategy of stimulation of NO production, which ultimately induces the SOD-CAT enzyme system to defend against ammonia-induced oxidative stress.

No abstract

After the consumption of ethanol, acetaldehyde levels increase in the serum, and the serum develops a nondialyzable cytotoxic activity caused by the formation of unstable acetaldehyde-albumin complexes. The concentration of acetaldehyde in the serum and the cytotoxic activity in serum albumin 8.5 hr after six healthy volunteers began to drink 94 g of ethanol were significantly less when the ethanol was consumed as red wine than as white wine. The serum acetaldehyde was measured by a fluorigenic HPLC assay, and the cytotoxic activity in albumin was determined using two different assays based on dissimilar endpoints: (1) detachment of adherent A9 cells and (2) impairment of the ability of A9 cells to reduce tetrazolium. When serum obtained from five other healthy volunteers after the consumption of white wine was incubated at 37 degrees C for 3 hr with a number of dietary antioxidants at a concentration of 100 mumol/liter, the cytotoxicity of the albumin was markedly reduced. The antioxidants studied consisted of six flavonoids (kaempherol, fisetin, quercetin catechin, taxifolin, and coumarin) and three nonflavonoids (salicylic acid, tannic acid, and alpha-tocopherol). In the cases of alpha-tocopherol, a statistically significant reduction of cytotoxicity was observed at a concentration of 10 mumol/liter. In addition, the cytotoxicity of artificially prepared acetaldehyde-albumin complexes was significantly reduced when such complexes were incubated with 50 to 100 mumol/liter of kaempherol, fisetin, quercetin, coumarin or salicylic acid, or 10 mumol/liter of alpha-tocopherol at 37 degrees C for 3 hr. Evidently, in vitro, flavonoid and nonflavonoid dietary constituents reduce the amount of unstable acetaldehyde-albumin complexes found in both postalcohol serum and in artificially produced acetaldehyde-albumin complexes. The difference in the amount of unstable acetaldehyde-albumin complexes found in serum after the consumption of red and white wine may therefore be caused by the higher concentration of antioxidants, including flavonoids, in red wine than in white wine. Because acetaldehyde and acetaldehyde-albumin complexes have been implicated in the pathogenesis of alcohol-mediated tissue damage, these data suggest that dietary antioxidants may influence the biological consequences of excess alcohol consumption.

C57BL mice were depleted of macrophages by an intravenous injection of liposome-encapsulated dichloromethylene diphosphonate (DCMDP), and control mice were uninjected or injected with empty liposomes. One day after injection, a proportion of the DCMDP-treated and control mice was continuously exposed to ethanol vapor for 4 days. Albumin fractions were separated from the sera of both ethanol-unexposed and ethanol-exposed animals and tested for cytotoxicity against a monolayer of A9 cells using two indicators of cytotoxicity: detachment of adherent cells and a decrease in the ability of cells to reduce tetrazolium. The results show that, in mice exposed to ethanol, macrophages are a major source of the acetaldehyde in circulating cytotoxic acetaldehyde-albumin complexes and presumably also of free acetaldehyde.

Adherent-cell-depleted human marrow cells (MC) were cultured on their own or co-cultured with monolayers of blood-monocyte-derived macrophages or marrow-derived adherent cells with and without 2 mg ethanol/ml for 24 h. The incorporation of 3H-thymidine and 3H-leucine by MC cultured on their own was not significantly influenced by ethanol. By contrast, the incorporation of both radiolabelled compounds was significantly lower in MC from the co-cultures containing ethanol than from those not containing ethanol. This effect was mediated by a diffusible factor produced by macrophages in the ethanol-containing cultures and was independent of intercellular contact. Supernatants from ethanol-containing cultures of marrow-derived adherent cells displayed cytotoxic activity against A9 cells due to the presence of unstable acetaldehyde-albumin complexes. Ethanol inhibited rather than stimulated nitrite production in the MC/marrow-derived adherent cell co-culture system, suggesting that macrophage-derived nitric oxide did not play a role in causing the observed ethanol-related effects. The data indicate that, in the presence of ethanol, macrophages cause inhibition of the incorporation of 3H-thymidine and 3H-leucine into overlying MC, at least partly by oxidizing ethanol to acetaldehyde and releasing some of the potentially cytotoxic acetaldehyde thus formed extracellularly. Bone marrow macrophages may therefore play an important role in the pathogenesis of alcohol-related marrow damage in vivo.