The biosynthesis of S-(3-hexan-1-ol)-glutathione (3MH-S-glut) and S-(3-hexan-l-ol)-L-cysteine (3MH-S-cys), which act as flavour precursors in wines, in Vitis vinifera grapes exposed to various environmental stress conditions is reported here. Ultraviolet (UV-C) irradiation, water deficit, and biological stimulation up-regulated 3MH-S-glut and 3MH-S-cys biosynthesis in grape leaves. 3MH-S-glut and 3MH-S-cys contents in grape berries were increased by cold shock, heat shock, UV-C irradiation, and biological stimulation. The results suggest that environmental stress enhances the biosynthesis of both flavour precursors in grapevine. The transcription of VvGST1, VvGST3, VvGST4, and GGT in grapevine exposed to the stress conditions was increased markedly compared with that in control grapevine. Also, UV irradiation increased GST (glutathione S-transferase) and GGT (γ-glutamyl transferase) enzyme activities in grape berries. Recombinant VvGST3 and VvGST4, but not VvGST1, mediated the synthesis of 3MH-S-glut from reduced glutathione and trans-2-hexenal in vitro. The enzymatic mediation of flavour precursor production is a novel function of plant GSTs and may result in the detoxification of damaged grape cells under stress conditions.

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Rhesus monkeys (Macaca mulatta) chronically administered opioids were more susceptible to simian immunodeficiency virus (SIV) strain mac239 (SIVmac239) infection than those without prior exposure to opioids. Increased plasma viremia in morphine-dependent monkeys allowed SIV to be detected in the animals' peripheral blood mononuclear cells (PBMC) without cocultivation with a tissue culture cell line. In contrast, virus titers from the PBMC of morphine-naive SIVmac239-infected animals were undetectable in the absence of cocultivation. PBMC isolated from noninfected animals and treated with morphine sulfate in vitro produced an increase in the expression of beta-chemokine receptor 5 (CCR5). Because both SIVmac239 and human immunodeficiency virus (HIV) require CCR5 for cell entry, the unique role of morphine in promoting SIV infection may provide a mechanism to account for the high incidence of HIV disease among drug-using populations.

BACKGROUND Curcumin, the yellow pigment in turmeric, has been shown to prevent tumor progression in a variety of tissues in rodents. The authors investigated the effect of curcumin on human carcinoma cell lines to determine whether constitutive interleukin‐8 (IL‐8) production of tumor cells was correlated with nuclear factor κB (NF‐κB) activation and cell growth activity. METHODS A human pancreatic carcinoma cell line, SUIT‐2, was incubated with various concentrations of curcumin for 2 hours. Biologic features, including IL‐8 production, DNA binding activity, transactivation of NF‐κB, cell growth activity, cell viability, and the expression of IL‐8 receptors (CXCR1 and CXCR2) were analyzed. RESULTS The constitutive production of IL‐8 was inhibited by curcumin at concentrations of 10–100 μM in a dose dependent manner. NF‐κB activity was reduced significantly by curcumin treatment. Pretreatment with curcumin inhibited the growth rate of carcinoma cells significantly. Such cell growth inhibition by curcumin was not recovered by exogenous recombinant IL‐8. The investigation of expression in IL‐8 receptors, CXCR1 and CXCR2, revealed that the expression of both receptors was enhanced remarkably by curcumin. Exogenous IL‐8 could not recover this enhancement of IL‐8 receptors. These results suggest that curcumin inhibits IL‐8‐induced receptor internalization. CONCLUSIONS The authors concluded that curcumin contributed not only to the inhibition of IL‐8 production but also to signal transduction through IL‐8 receptors. These data suggest that curcumin reduces numerous IL‐8 bioactivities that contribute to tumor growth and carcinoma cell viability. From this point of view, curcumin is a potent anticancer agent that inhibits the production of proinflammatory cytokines, including IL‐8, by tumor cells. Cancer 2002;95:1206–14. © 2002 American Cancer Society. DOI 10.1002/cncr.10812