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The project aimed to provide scientific basis to international claims of Teschke et al. (2003) and Schmidt et al. (2002) stating that Kava (Piper methysticum) is responsible for cases of liver complications in areas in which consumption is regularly practiced, making it a hepatotoxin. Thirty C57BL/6 mice had been acclimatized as Kava root chips were subjected to extraction using water as solvent. Twenty mice (4 groups of 5 replicates) were given varying (25 mg/kg BW, 50 mg/kg BW, 100 mg/kg BW, 125 mg/kg BW) concentrations of the crude Kava extract, and methylenedioxybenzene or Safrole (a hepatotoxin) was used as positive control for 5 mice (with concentrations of 0.5 mg/kg BW for 2 mice, 0.75 mg/kg BW for another 2, and 1 mg/kg BW for the remaining), all of which was given once intravenously. After one week, all mice were subjected to serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), and alkaline phosphatase (ALP) liver function tests. One-way ANOVA with a confidence level of 95% was then implemented to determine whether there was a significant difference among the results. The test’s conclusions significantly differed from the said claims made about the hepatotoxicity of the Kava root, thus making them debatable.