• Pediatric Gastroenterology, Hepatology & Nutrition
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• 제22권4호
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• pp.387-391
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• 2019

Tea is the most widely consumed beverage after water in the world. The consumption of iced tea has increased in Western countries and spiked among teenagers for enjoyment, freshening up and alertness. A teenager presented with symptoms of hepatitis. Liver ultrasound revealed sludge in the gallbladder. Laboratory investigations excluded all known causes of hepatotoxicity. Detail nutritional history revealed that the patient had been drinking 1.5-2 liters of black iced tea per day for the last three months. He was immediately advised to stop drinking any tea. Gradually all symptoms disappeared and two months after discontinuation of the tea, all liver enzymes returned to normal and the sludge in the gallbladder disappeared. This case report underlines the importance of a meticulous assessment of a child's dietary behavior when investigating a case of hepatotoxicity and raises awareness about the potential side effects of tea overconsumption.

• 약학회지
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• 제40권6호
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• pp.727-733
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• 1996

2-(Allylthio)pyrazine is effective in selectively suppressing constitutive and inducible expression of cytochrome P450 2E1. The effect of 2-(allylthio)pyrazine against potentiat ed chemical injury was studied in rats. Vitamin-A pretreatment of rats substantially increased carbon tetrachloride hepatotoxicity, as supported by an ~4-fold increase in serum alanine aminotransferase (ALT) activity. Concomitant pretreatment of rats with 2-(allylthio)pyrazine at the daily dose of 200mg/kg resulted in a 76% decrease in vitamin-A-potentiated hepatotoxicity, which supported the possibility that 2-(allylthio)pyrazine protects the liver against chemical-induced hepatic injury by the mechanism associated with Kupffer cell inactivation. Pyridine pretreatment caused substantial enhancement in carbon tetrachloride hepatotoxicity. 2-(Allylthio)pyrazine treatment of rats reduced the pyridine-potentiated toxicity in a dose-dependent manner. Animals treated with both pyridine and 2-(allylthio)pyrazine prior to intoxicating dose of CCl$_4$ resulted in 85% and 47% decreases in pyridine-increased triglycerides and cholesterol levels in the liver. The protective effect of 2-(allylthio)pyrazine on the DNA strand breakage induced by benzenetriol was assessed by measuring the conversion of supercoiled ${\Phi}x$-174 DNA to the open relaxed form. 2-(Allylthio)pyrazine blocked the benzenetriol-induced conversion of supercoiled DNA to open circular form in a dose-dependent manner. The presence of 2-(allylthio)pyrazine at the doses from I to 10mM in the incubation mixture containing 5 ${\mu}$M benzenetriol completely protected benzenetriol-induced DNA strand breakage with the EC50 for the 2-(allylthio)pyrazine blocking being noted as ~220 ${\mu}$M, whereas allyl disulfide exerted protecting effect at relatively high concentrations (i.e. ~850 ${\mu}$M), suggesting that 2-(allylthio)pyrazine effectively scavenges the reactive oxygen species. These results provide evidence that 2-(allylthio)pyrazine blocks vitamin A- or pyridine-potentiated CCl$_4$ hepatotoxicity and that the agent is active in protecting DNA by scavenging the reactive oxygen species.

• 대한수의학회지
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• 제45권2호
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• pp.255-261
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• 2005

The purpose of this study is to compare hepatotoxicity of each treatment for dermatophytosis; one is the administration of the ketoconazole only and the other, ketoconazole with diphenyl-dimeththyl-dicarboxylate. Have chosen the range of 14-24 months of healthy dogs divided by two groups (group 1 and group 2) for the experiment of which test proved positive in dermatophytosis diagnosis and showed normal reaction in terms of physical examination, blood chemistry and especially of liver function. Group 1 was administrated ketoconazole orally at 10 mg/kg/day and of same dose of ketoconazole with diphenyl-dimethyl-dicarboxylate for group 2. After administering, we have tested two groups by blood collecting every one week in order to check the differences of hepatotoxicity state through AST, ALT and r-GTP, the barometers of liver function which lasted for 12 weeks. Moreover, tested Indocyanine Green (ICG), known as susceptible gauge of function of excretion before starting the experiment and tested ICG as well after 12 weeks. The experiment of result the value of group 1 in AST, ALT and r-GTP has been highly rised after administering ketoconazole for 10 weeks meanwhile, of group 2 has shown a steady state troughout the whole experiment. For ICG test, we injected 0.5 mg/kg of ICG into a vein for both groups and tested the retention rate at regular interval of 15, 30, 45 minutes. The results of retention rate in two groups were similar to before the drug administration. However, after 12 weeks the retention rate of group 1 has been delayed, on the other hand, retention rate of group 2 were a steady state. In conclusion, the administration of ketoconazole only for a long period of time induced hepatotoxicity where as, the administration of ketoconazole with diphenyl-dimethyl-dicarboxylate didn't induce hepatotoxicity. Therefore, when doctors prescribes for a dog with dermatophytosis should not administrate ketoconnazole itself but with diphenyl-dimethyl-dicarboxylate and one who has abnormal condition of liver function should not be prescribed ketoconazole treatment. If there is a case needed to prescribe ketoconazole treatment, the regular monitoring should be accompanied by at the same time.

• 한국생명과학회:학술대회논문집
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• 한국생명과학회 2008년도 제49회 학술심포지움 및 국제학술대회
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• pp.30.2-30.2
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• 2008

• Journal of Ginseng Research
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• 제12권2호
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• pp.173-181
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• 1988

We have studied the mechanism by examing the effect of ginseng on the epoxide hydrolase which is catabolized the reactive intermetabolite of bromobenzene, and bromobenzene-induced hepatotoxicity. It was observed that ginseng saponin fraction protects against bromo benzene-induced hepatotoxicity in mice as evidenced 1. increased the epoxide hydrolase activity, 2. lower serum transaminase activity, 3. decreased the formation of lipid peroxide. These results suggested that the inducing effect of ginseng on the epoxide hydrolase is believed to be a possible detoxication mechanism for the bromobenzene toxicity in mice.

• 약학회지
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• 제23권1호
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• pp.41-49
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• 1979

By intraperitoneal administration of thioacetamide to rats, acute liver injury was produced. In these rats, the level of serum GOT and GPT activities showed a remarkable increase and the principal histopathologic change was centrilobular hepatic necrosis. In this study, combined administration of silymarin with promethazine hydrochloride to the rats with acute liver injury which was produced by thioacetamide inhibited the increase of serum transaminase activities and protected the histopathologic change, showing comparatively more improved results than simple administration of silymarin alone. On the basis of these results, it is suggested that promethazine hydrochloride potentiates the effectiveness of silymarin in acute thioacetamide hepatotoxicity of rats.

• 한국생명과학회:학술대회논문집
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• 한국생명과학회 2007년도 제48회 학술심포지움 및 추계국제학술대회
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• pp.124.2-124.2
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• 2007

See Full Text

• 한국생명과학회:학술대회논문집
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• 한국생명과학회 2007년도 제48회 학술심포지움 및 추계국제학술대회
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• pp.125.1-125.1
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• 2007

See Full Text

• Toxicological Research
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• 제9권2호
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• pp.253-262
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• 1993

The effects of dichloromethane (DCM) on carbon tetrachloride (CT) toxicity were examined in adult male rats. A concomitant treatment of rats with DCM (0.3, 0.6, 1.2 g/kg, po) significantly potentiated the hepatotoxicity of CT (1.0 g/kg, po) as determined by increase in serum GPT (glutamic pyruvic transaminase), GOT (glutamic oxaloacetic transaminase), and SDH (sorbitol dehydrogenase) activity 24 hr following the treatments. Serum LDH (lactate dehydrogenase) activity was increased by either DCM or CT treatment.

• Toxicological Research
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• 제9권2호
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• pp.133-145
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• 1993

The present study examined the effects of butylated hydroxyanisole (BHA) on acetaminophen (AA)-induced hepatotoxicity in male rats and also examined the effects of these compounds on the biliary excretion of phenolphthalein (PP) and the hepatic glucuronidation. Male Sprague-Da-wley rats were pretreated with BHA (0.75% in diet for 10 days) were given single dose of AA (600mg/kg, ip) and liver function was determined 24 hr later. Serum activity of alanine aminotransferase (ALT) and histopathology were used as indices of hepatotoxicity.