CY could induce free radical production, followed by cytotoxicity and oxidative stress. As shown in Table 1, Table 2 and Table 3, CY significantly reduced the T-AOC, SOD, CAT and GSH-Px activities in hearts, livers and kidneys. In comparison with MC group, AHG administration could enhance the T-AOC, SOD, CAT and GSH-Px in different tissues dose-dependently. Particularly, the level of T-AOC, SOD, CAT and GSH-Px were almost recovered to normal level when treated with AHG at the concentration of 10 mg/kg (p < 0.01). Meanwhile, Table 1, Table 2 and Table 3 showed the significant increases in MDA levels in the hearts, livers and kidneys in mice of CY-treated group (p < 0.01), while AHG treatment at 1, 5, and 10 mg/kg could cause a dose-dependent decrease in the accumulation of tissue MDA. In addition, when the dose of AHG reached to 10 mg/kg, the contents of MDA were recovered to the normal levels. The results suggested that AHG can enhance anti-oxidative activities in liver, kidney and heart.