The kiwi (Actinidia deliciosa) is well known to contain anti-oxidants. In this study, we investigated the anti-oxidant effects of kiwi extract on carbon tetrachloride (CCl₄) induced liver injury in BALB/c mice. The radical scavenging effect of 80% methanol extract of Halla-Gold kiwi was observed. For the animal study, mice were randomly divided into four groups: normal group, CCl₄-induced model group, kiwi extract administered group, and silymarin treated group. The kiwi extract was provided daily for 10 days. At the 24 h after last administration, CCl₄ was injected. The kiwi extract showed strong inhibitory effect of DPPH radicals and superoxide scavenging. In animal study, administration of CCl₄ resulted in significantly elevated plasma levels of ALT and AST but they decreased in kiwiextract pretreated group. Anti-oxidant enzymes such as GSH-px and GSH-rd were restored in the kiwi extract treatment group. Histopathological degeneration was also prevented in the kiwi extract treated group compared with of the control group, which exhibited CCl₄-induced hepatotoxicity. On the basis of the obtained results, it can be concluded that kiwi extract showed protective effects, not only as anti-oxidant effects, but also in the protection of hepatotoxicity in CCl₄-intoxicated mice.

Several compounds and extracts isolated from a brown alga, Ishige (I.) okamurae, exhibit anti-oxidant and anti-inflammatory effects. The present study investigated whether the ethyl acetate (EtOAc) fraction of I. okamurae (EFIO) could ameliorate carbon tetrachloride (CCl₄)-induced hepatotoxicity in rats. Sprague-Dawley rats were intraperitoneally (i.p.) administered with EFIO at 10 or 50 mg/kg per day for 2 consecutive days before CCl₄ injection (3.3 mL/kg, i.p.). Twenty four hours later, the rats were anesthesized with diethyl ether and dissected. Pretreatment with EFIO significantly reduced the increased serum levels of alanine aminotransferase and aspartate aminotransferase in CCl₄-treated rats. Pretreatment with EFIO also significantly inhibited the reduced activities of superoxide dismutase and catalase in the CCl₄-injured liver. Histopathological evaluations showed that hemorrhage, hepatocyte necrosis, inflammatory cell infiltration, and fatty degeneration induced by CCl₄ treatment were ameliorated by the administration of EFIO. Additionally, liver immunohistochemical analyses revealed the marked reduction in ED1-positive monocyte-like macrophages in EFIO-pretreated rats given CCl₄. These results suggest that EFIO ameliorates CCl₄-induced liver injury, possibly through the inhibition of oxidative stress.

This study was carried out to find whether phenidone (1-phenyl-3-pyrazolidinone), a cyclooxygenase as well as a lipoxygenase inhibitor, exhibits the preventive effect on carbon tetrachloride (CCl₄)-induced acute liver injury in rats. Rats were pretreated with phenidone at a dose of 50 or 200 mg/kg (p.o.) once daily for 3 consecutive days before CCl₄ administration. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Malondialdehyde (MDA) production was determined as an index of lipid peroxidation in the liver and serum. The histopathological changes in the liver were also examined in each group. The reduction in body weights was significantly inhibited in the phenidone-treated group than in the CCl₄ control group. Significant increase in the relative liver weights of the phenidone-treated groups was observed compared with either the vehicle or CCl₄ groups. Elevation of serum AST and ALT activities occurred after CCl₄ treatment was significantly attenuated by the pretreatment with phenidone. The elevation of MDA levels in liver and serum were completely inhibited in phenidone-treated groups. The protective effects on phenidone-treated groups were confirmed histopathologically. These results suggest that phenidone may be a useful protector through modulation of hepatic inflammation in CCl₄-induced acute liver injury.

This study was carried out to evaluate the antitumor, hepatoprotective and antimutagenic activities on hot water extract of Phellinus gilvus (PGE). Growth of tumor in mice that were orally given 0.25, 0.5, 1.0, 2.0 gㆍkg-¹ dose of PGE was inhibited in a dose-dependant manner (p less than 0.05). The hepatoprotective effect of PGE in the carbon tetrachloride (CCl₄)-intoxicated rats was studied. In CCl₄+PGE groups, PGE was orally administered with 100 mg/kg/day dose 7 days before the treatment of CCl₄. The serum activity of aspartate aminotransferase and alanine aminotransferase in CCl₄+PGE group were decreased at a rate of 59.6% and 54.1% compared with those in CCl₄ group, respectively (p less than 0.05). Also, total cholesterol and triglyceride in CCl₄+PGE group were significantly decreased at a rate of 90% and 73.6% compared with those in CCl₄ group (p less than 0.05). In the Ames test, we confirmed PGE doesn't have any activity as a mutant, and PGE showed inhibitory effect against mutagenesis induced by 2-amino fluride and sodium azide in Salmonella typhimurium TA98, TA100 and TA 1535 in a dose-dependent manner. From the above results, we may suggest that PGE might have useful as a material for functional food and/or animal pharmaceutics.

This study investigated the protective effects of ethylene glycol-bis(β-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), an extracellular calcium chelator, and ethylenediaminetetraacetic acid (EDTA), which chelates calcium and most metal ions, against carbon tetrachloride (CCl₄)-induced acute hepatotoxicity in mice. Mice were treated with EGTA or EDTA at a dose of 20 (low) or 100 mg/kg (high) subcutaneously 1 h before CCl₄ administration. The mice were fasted and sacrificed 18 h after CCl₄ treatment.