Search

Acute p.o. administration of 99.5% ethanol (0.1 ml) to fasted mice produced heart toxicity. Pretreatment with p.o. administration of tetramethylpyrazine (TMP) could prevent such toxicity effectively and dose-dependently. The maximal antioxidative effect against 99.5% ethanol-induced heart toxicity could be observed at 1 hour after TMP administration. In order to further investigate the heart protective mechanism of TMP, both lipid peroxidation level in vivo and superoxide scavenging activity were conducted. TMP exhibited a dose- dependently anti-lipid peroxidation effect in mice heart homogenate, and results indicated that 99.5% ethanol-induced intoxicated mice hearts have higher malonic dialdehyde (MDA) levels compared with those in TMP administrated mice hearts. These results suggest that the potentially heart protective mechanism of TMP could be contributed, at least in part, to its prominent anti-lipid peroxidation and anti-free radical formation effects, hence it could protect the heart from lipid peroxidation-induced heart toxicity. [ABSTRACT FROM AUTHOR]

Angelica archangelica (AAA) has been effectively used in folk medicines as a remedy against stomachal and intestinal disturbances, arthritic disease, etc. However, there is still lack of scientific proof about its antioxidant capability. This study aimed at investigating the effects of total AAA against chronic ethanol-induced hepatotoxicty. ICR mice were divided into five groups, each consisting of 10 animals. A single dose of ethanol (70%, 0.1 ml, p.o.) was used to induce hepatotoxicity in these mice which resulted in a significant elevation of the activities of serum GOT and GPT. Treatment of mice with AAA (10, 25, and 50 mg/kg p.o.) after 2 weeks ameliorated the ethanol- induced hepatotoxicity effects. Hepatotoxicity was evidenced by a significant increase in hepatic lipid peroxidation manifested as the presence of malondialdehyde. It was found that AAA inhibits the malondialdehyde formation in mouse liver homogenates both in vitro and in vivo. AAA is cytoprotective agent effective against chronic ethanol-induced hepatotoxicity, possibly through inhibition of the production of oxygen free radicals that cause lipid peroxidation, and hence indirectly protects the liver from oxidative stress. [ABSTRACT FROM AUTHOR]

Acute administration of absolute ethanol (10 ml/kg) per os to fasted mice produced extensive renal failure as measured by a rise in blood urea nitrogen and creatinine. Pretreatment with oral administration of tetramethylpyrazine (TMP) prevented such failure. The maximal effect against absolute ethanol-induced renal failure could be observed 1 h after TMP administration. In order to further investigate the renal protective mechanism of TMP, experiments on lipid peroxidation and superoxide scavenging activity were conducted. Renal homogenates made from mice treated with ethanol showed that TMP pretreatment had an antioxidant effect. Mice in acute renal failure had higher malonic dialdehyde concentrations than those pretreated with TMP. The renal protective mechanism of TMP was attributed, in part, to its prominent superoxide scavenging effect, which protects the kidney from superoxide-induced renal damage.Copyright © 2002 National Science Council, ROC and S. Karger AG, Basel [ABSTRACT FROM AUTHOR]