1 The e ects of ethyl alcohol and wine (red and white) on haemostatic parameters and experimental thrombosis were studied in rats; NO was evaluated as a possible mediator of these e ects. 2 We found that red wine (12% alcohol) supplementation (8.4+0.4 ml d 71 in drinking water, for 10 days) induced a marked prolongation of`template' bleeding time (BT) (258+13 vs 132+13 s in controls; P50.001), a decrease in platelet adhesion to ®brillar collagen (11.6+1.0 vs 32.2+1.3%; P50.01) and a reduction in thrombus weight (1.45+0.33 vs 3.27+0.39 mg; P50.01). 3 Alcohol-free red wine showed an e ect similar to red wine. In contrast, neither ethyl alcohol (12%) nor white wine (12% alcohol) a ected these systems. 4 All these e ects were also observed after red wine i.v. injection (1 ml kg 71 of 1 : 4 dilution) 15 min before the experiments.5 The e ects of red wine were prevented by the NO inhibitor, N o nitro-L-arginine-methyl ester (L-NAME). L-arginine, not D-arginine, reversed the e ect of L-NAME on red wine infusion. 6 Red wine injection induced a 3 fold increase in total radical-trapping antioxidant parameter values of rat plasma with respect to controls, while white wine and alcohol did not show any e ect. 7 Our study provides evidence that red wine modulates primary haemostasis and prevents experimental thrombosis in rats, independently of its alcohol content, by a NO-mediated mechanism.

Benzothiazoles are a part of the molecular structure of a large number of natural products, biocides, drugs, food flavors, and industrial chemicals. They also appear in the environment mainly as a result of their production and use as rubber vulcanization accelerators. A new headspace solid-phase microextraction (HS-SPME) method for analysis of benzothiazole (BTH) in wine is described. This method is fast, inexpensive, and does not require solvents. The detection limit of BTH in wine was 45 ppt with linearity up to 100 ppb. The quantification of BTH is performed by the standard additions method and does not require the use of an internal standard. We have analyzed 12 wines from different grape varieties grown in several regions, using SPME extraction and gas chromatography-mass spectrometry (GC-MS) detection. Under these experimental conditions, benzothiazole was found in all wines analyzed. Concentration levels in samples varied from 0.24 microg/L (Vermentino) to 1.09 microg/L (Franciacorta).

Our previous studies are reviewed and at the same time preliminary experimental observation to the topic of endocrine end-points in autoimmune disease is introduced. To this end, we have used rheumatoid arthritis (RA), including synovial fluids and primary cultures of synovial macrophages, as a model system in order to investigate (a) expression and subcellular localization of high-affinity sites of steroid binding in immune effector cells; (b) steroid metabolic profiles in both male and female RA patients, as compared to healthy subjects; and (c) activities of key steroid enzymes that govern intratissue accumulation of sex hormones. In RA tissues and cells, the concurrent evidence for (1) androgen and/or estrogen receptors, (2) high concentrations of biologically active steroids, (3) key enzymes of steroid metabolism, and (4) significant changes of estrogen to androgen ratio, all strongly suggests that individual immune cells, including synovial macrophages, may behave as steroid-sensitive cells, namely, they may represent a target for sex steroids, supporting the hypothesis of a potential endocrine regulation of the immune response also in RA disease. In this respect, definition of several endocrine end-points may have important implications for the treatment of rheumatic disease and other immunological disorders.

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We have previously reported that gap junction-mediated intercellular communication (GJIC) can be restored in junctionally deficient human prostate epithelial cells, also suggesting that GJIC activity is regulated by estrogen. In the present work, we report studies on sex steroid regulation of GJIC and proliferative activity in both nontumoral (Chang liver, CL) and malignant (HepG2, Huh7) human liver cells. Junctional activity and liver cell growth were measured using the scrape-loading/dye-transfer (SL/DT) and the MTS assay, respectively. Using the SL/DT, only Huh7 cells exhibited a moderate degree of junctional activity in basic conditions, while neither CL nor HepG2 cells showed functional GJIC. Under exactly the same experimental approach used for prostate studies, we observed that, once again, both estrogen (either estradiol or estrone) and FK induce a significant increase of GJIC in Huh7 cells, while exposure of HepG2 cells to FK produces only a limited rise of junctional activity in this cell line. However, estrogen induced a significant increase and reduction of the proliferative activity of CL and Huh7 cells, respectively, while growth of HepG2 cells was not affected. While the above evidence suggests that estrogens are primarily implicated in growth regulation and communication of both prostate and liver epithelial cells, it also implies that compounds able to restore GJIC in junctionally deficient cells or prevent its disruption in junctionally proficient cells may be used for development of new strategies in the prevention and/or treatment of several human malignancies, including hepatocellular carcinoma (HCC).