An extract of Japanese green tea, one of the most popular drinks in Japan, was an inhibitor of the growth of Streptococcus mutans, a bacterium responsible for causing dental caries. The analysis of the extract revealed that the main antibacterial componentsof the extract were several polyphenolic compounds, especially gallocatechin (GC), epigallocatechin (EGC), and epigallocatechin gallate (EGCg). GC was the most active component and its minimum inhibitory concentration against the bacterium was around 250 ug per ml.

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The mechanism of farnesol (FOH)-induced growth inhibition ofSaccharomyces cerevisiae was studied in terms of its promotive effect on generation of reactive oxygen species (ROS). The level of ROS generation in FOH-treated cells increased five- to eightfold upon the initial 30-min incubation, while cells treated with other isoprenoid compounds, like geraniol, geranylgeraniol, and squalene, showed no ROS-generating response. The dependence of FOH-induced growth inhibition on such an oxidative stress was confirmed by the protection against such growth inhibition in the presence of an antioxidant such as α-tocopherol, probucol, orN-acetylcysteine. FOH could accelerate ROS generation only in cells of the wild-type grande strain, not in those of the respiration-deficient petite mutant ([rho 0]), which illustrates the role of the mitochondrial electron transport chain as its origin. Among the respiratory chain inhibitors, ROS generation could be effectively eliminated with myxothiazol, which inhibits oxidation of ubiquinol to the ubisemiquinone radical by the Rieske iron-sulfur center of complex III, but not with antimycin A, an inhibitor of electron transport that is functional in further oxidation of the ubisemiquinone radical to ubiquinone in the Q cycle of complex III. Cellular oxygen consumption was inhibited immediately upon extracellular addition of FOH, whereas FOH and its possible metabolites failed to directly inhibit any oxidase activities detected with the isolated mitochondrial preparation. A protein kinase C (PKC)-dependent mechanism was suggested to exist in the inhibition of mitochondrial electron transport since FOH-induced ROS generation could be effectively eliminated with a membrane-permeable diacylglycerol analog which can activate PKC. The present study supports the idea that FOH inhibits the ability of the electron transport chain to accelerate ROS production via interference with a phosphatidylinositol type of signal.

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A series of sesquiterpene dialdehydes was isolated from the East African medicinal plants Warburgia stuhlmannii and Warburgia ugandensis (Canellaceae) as antibiotics, particularly against Saccharomyces cerevisiae, Candida utilis, and Sclerotinia libertiana. Among these sesquiterpene dialdehydes, polygodial [1] exhibited the most potent activity. When tested on S. cerevisiae, polygodial proved to be fungicidal rather than fungistatic. When the cells of S. cerevisiae are treated in vitro with polygodial for 10 min, the cell membrane becomes severely damaged, and many vesicles, possibly formed from the fragmented cell membrane, can be observed within the cytoplasm. The observation of cell membrane lesions led us to propose a rather innovative hypothesis: the use of polygodial to facilitate the transmembrane transport of exogenous chemicals into cells. For example, polygodial could be combined with an antibiotic having poor cell membrane permeability in an effort to increase its antibiotic activity by increasing its ability to gain entrance into the cell. We report here that a remarkably enhanced efficacy was obtained when actinomycin D was used in combination with polygodial. We believe polygodial may be acting as an "advance scout," punching holes in the plasma membrane and gaining an entrance into the cell for an antibiotic previously less effective because of problems with cell membrane permeability.

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Background:The sphingolipids ceramide and sphingosine 1-phosphate (S1P) control various cellular functions, including proliferation, cell death, and autophagy. Results: Binding of S1P to its receptor S1P 3 counteracts ceramide-mediated autophagy by activating the mammalian target of rapamycin (mTOR) pathway. Conclusion: Sphingolipid rheostat between ceramide and S1P plays an important role in regulating mTOR-controlled autophagy. Significance: We provide new insights into novel regulatory mechanisms in autophagy induction.