The antioxidative and hepatoprotective potentials of two anthraquinones, alaternin (2-hydroxy-emodin) and emodin, to scavenge and/or inhibit hydroxyl radicals generated by the Fenton reaction and to protect tacrine-induced cytotoxicity in human liver derived HepG2 cells were evaluated, respectively. The inhibitory activity on hydroxyl radical generated in a cell-free chemical system (FeSO$_4$/$H_2O$$_2$) was investigated by a fluorescence spectrophotometer using a highly fluorescent probe, 2$^1$,7$^1$-dichlorofluorescein. The hydroxyl radical scavenging activity was determined by electron spin resonance spectroscopy using 5,5-dimethy-1-pyrroline-N-oxide as hydroxyl radicals trapping agents. Tacrine-induced HepG2 cell toxicity was determined by a 3-［4,5-dimethylthiazole-2yl］-2,5-diphenyltertrazolium bromide assay. Although the scavenging activity of alaternin on hydroxyl radical was similar to that of emodin in dose-dependent pat-terns, the inhibitory activity exhibited by the former on hydroxyl radical generation was stron-ger than that of the latter, with $IC_{50}$/ values of 3.05$pm$0.26 $mu$M and 13.29$pm$3.20 $mu$M, respectively. In addition, the two anthraquinones, alaternin and emodin showed their hepatoprotective activ-ities on tacrine-induced cytotoxicity, and the EC$_{50}$ values were 4.02 11M and 2.37 $mu$M, respec-tively. Silymarin, an antihepatotoxic agent used as a positive control exhibited the EC$_{50}$ value of 2.00 $mu$M. These results demonstrated that both alaternin and emodin had the simultaneous antioxidant and hepatoprotective activities.ies.