Bioautography-guided isolation of antibacterial compounds of essential oils from Thai spices against histamine-producing bacteria

The outbreak of histamine fish poisoning has been being an issue in food safety and international trade. The growth of contaminated bacterial species including Morganella morganii which produce histidine decarboxylase causes histamine formation in fish during storage. Histamine, the main toxin, causes mild to severe allergic reaction. At present, there is no well-established solution for histamine fish poisoning. This study was performed to determine the antibacterial activity of essential oils from Thai spices against histamine-producing bacteria. Among the essential oils tested, clove, lemongrass and sweet basil oils were found to possess the antibacterial activity. Clove oil showed the strongest inhibitory activity against Morganella morganii, followed by lemongrass and sweet basil oils. The results indicated that clove, lemongrass and sweet basil oils could be useful for the control of histamine-producing bacteria. The attempt to identify the active components using preparative TLC and GC/MS found eugenol, citral and methyl chavicol as the active components of clove, lemongrass and sweet basil oils, respectively. The information from this study would be useful in the research and development for the control of histamine-producing bacteria in fish or seafood products to reduce the incidence of histamine fish poisoning

Inhibition of gastric acid secretion by Ya-hom in isolated mouse whole stomach

Background: Ya-hom, the traditional Thai formula for abdominal discomfort treatment has, been reported to inhibit gastric acid secretion in gastric fistula rats. However, the mechanism underlying its action remains unclear.Objective: To investigate the gastric acid inhibitory action of Ya-hom and its mechanism of action by using an isolated mouse whole stomach model.Methods: The gastric acid secretion of isolated mouse whole stomach was stimulated by histamine (5.0 μM) or bethanechol (10 or 100 μM) after adding the inhibitors (atropine 1 μM, ranitidine 10 μM, indomethacin 0.1 μM or L-NAME 300 μM) and/or Ya-hom to the serosal solution. The effluent perfusate was collected continuously in 10-minute fractions for 120 minutes after stimulation.Results: Re-dissolved lyophilized Ya-hom extract at doses of 2.5, 5.0, 10.0, and 20.0 mg/mL inhibited histamine-stimulated gastric acid secretion in a dose-dependent manner. Inhibition of Ya-hom (10 mg/mL) was also observed in the presence of atropine (1 μM), which was used to eliminate effects of endogenous acetylcholine. Ya-hom inhibited bethanechol-stimulated gastric acid secretion in the presence and absence of ranitidine. While the inhibitory action of Ya-hom on histamine-stimulated gastric secretion was not affected by indomethacin, it was attenuated by concomitant treatment with the nitric oxide synthase inhibitor (L-NAME).Conclusion: Ya-hom did not stimulate gastric acid secretion in the isolated mouse whole stomach. Ya-hom significantly inhibited gastric acid secretion after this was stimulated via histamine or bethanechol. Nitric oxide stimulation plays an important role in the inhibitory action of Ya-hom.