Historically, botanicals have been reported to possess good antioxidative activities as demonstrated by their free radical scavenging property rendering their usage in liver protection. In this study, we describe the potential use of MAP, a standardized blend comprising three extracts from Myristica fragrans, Astragalus membranaceus, and Poria cocos, in ameliorating chemically induced acute liver toxicities. Acetaminophen (APAP) and carbon tetrachloride (CCl)-induced acute liver toxicity models in mice were utilized. Hepatic functional tests from serum collected at T24, histopathology analysis, and merit of blending three standardized extracts were evaluated. MAP administered at doses of 150-400 mg/kg showed statistically significant and dose-correlated inhibitions of serum alanine aminotransferase (ALT) ranging from 30.8% (P ≤ .05) to 88.1% (P = .0001) in the APAP and 66.9% (P = .002) to 83.7% (P = .0002) in the CClmodels, respectively. Moreover, MAP resulted in up to 75.7%, 60.9%, and 33.3% reductions in serum aspartate aminotransferase (AST), bile acid, and total bilirubin, respectively. Mice treated with oral doses of composition of MAP at 300 mg/kg showed statistically significant reduction in hepatocyte necrosis when compared with vehicle control. Unexpected synergistic protection of liver damage was also observed. Therefore, the composition, MAP, could be potentially utilized as an effective hepatic detoxifying agent for the protection of liver damage.

The effect of carrot extract on carbon tetrachloride (CCl4)-induced acute liver damage was evaluated. The increased serum enzyme levels (viz., glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, alkaline phosphatase, sorbitol and glutamate dehydrogenase) by CCl4-induction were significantly lowered due to pretreatment with the extract. The extract also decreased the elevated serum bilirubin and urea content due to CCl4 administration. Increased activities of hepatic 5'-nucleotidase, acid phosphatase, acid ribonuclease and decreased levels of succinic dehydrogenase, glucose-6-phosphatase and cytochrome P-450 produced by CCl4 were reversed by the extract in a dose-responsive way. Results of this study revealed that carrot could afford a significant protective action in the alleviation of CCl4-induced hepatocellular injury.

We examined the hepatoprotective activity of Inonotus obliquus water extract (IO-W) against tert-butyl hydroperoxide (t-BHP)-induced oxidative liver injury in the primary cultured rat hepatocyte. The 50% radical scavenging concentrations (SC50s) of IO-W for radical-scavenging activity against 2,2'-azino-bis-(3-ethylbenzothi- azoline-6-sulfonic acid) (ABTS) and 1,1-diphenyl-2-picryl-hydrazyl (DPPH) were 5.19 mg/mL and 0.39 mg/mL, respectively. IO-W pretreatment to the primary cultured hepatocytes significantly (p<0.05) protected the cells from t-BHP-induced cytotoxic injury even at a low concentration of IO-W (10µg/mL). The cellular leakage of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH), as well as malondialdehyde (MDA) formation caused by t-BHP were significantly (p<0.05) suppressed by IO-W pretreatment (>100µg/ mL). In conclusion, this study demonstrates that IO-W exhibited hepatoprotective activity against t-BHP-induced oxidative liver injury in the primary cultured hepatocyte probably via its abilities of quenching free radicals, inhibiting the leakage of ALT, AST, and LDH, and decreasing MDA formation.

BACKGROUND:Lead toxicity is a public health concern. Lead is one of the dispensable and non-biodegradable heavy metals and is toxic even at low concentrations.

OBJECTIVE:This study was to investigate the effect of oral administration of Vitamin C and Vitamin E on lead-induced hepatotoxicity and oxidative stress in the brain of rats.

METHODS:Thirty Sprague-Dawley albino male albino rats (115.58 +/- 4.96g) were divided equally into five groups. The rats were fed rat chow and water ad libitum. Group 1 rats served as control and were orally administered 2ml saline every day for 7 weeks. Group 2 rats received orally 2ml lead acetate solution (60mg/kg body weight) every day for 7 weeks. Group3 rats received orally 2ml lead acetate solution (60mg/kg body weight) and vitamin C (40mg/kg body weight) every other day for 7 weeks. Group 4 rats received orally 2ml lead acetate solution (60mg/kg body weight) and vitamin E (150mg/kg body weight)every day for 7weeks. Group 5 received orally lead acetate solution at 60mg/kg body weight and vitamin C (40mg/kg body weight)and vitamin E (150mg/kg body weight) every other day for 7weeks. Three rats from each group were sacrificed after the fourth week. The remaining rats were sacrificed after the seventh week. Changes in body weight, liver weight, brain weight, activities of liver function enzymes (aspartate amino transferase (AST), alanine amino transferase (ALT) and alkaline phosphatase(ALP) in the serum at week 4 and week 7 were assayed.The oxidative stress markers (reduced glutathione (GSH), nitric oxide(NO), malondialdehyde(MDA), levels, catalase(CAT) and superoxide dismutase (SOD) activities) were determined in the brain of rats. Serum lead level of rats was also determined.

RESULTS:The lead Pb exposed rats caused a significant (p<0.01) increase in bioavailable lead in the blood (p<0.05) as compared to the control. AST, ALT and ALPactivities were significantly increased (p<0.05) in the serum of rats exposed to lead as compared to the control. NO and MDA levels were significantly increased (p<0.05) in the brain of rats exposed to lead, while GSH level, SOD and CAT activities were significantly reduced (p<0.05) in the brain of rats exposed to lead when compared with the control.

CONCLUSION:Data of the study indicate that oral administration of vitamin C and vitamin E significantly reduced the blood lead concentration, ameliorates the hepatic damage and significantly reduced the oxidative stress in the brain of rats.