Protective effect of diallyl sulfone against acetaminophen-induced hepatotoxicity in mice

Lin, Marie C.M.; Wang, Er Jia; Patten, Chris; Lee, Mao Jung; Xiao, Fang; Reuhl, Kenneth R.; Yang, Chung S.

doi:10.1002/(sici)1522-7146(1996)11:1<11::aid-jbt2>3.0.co;2-y

Cited by 35 publications

(15 citation statements)

References 25 publications

(42 reference statements)

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“…Analysis of Acetaminophen Metabolism-Quantitative determination of the acetaminophen metabolites in plasma was carried out by a modified high pressure liquid chromatography method as previously published (15).…”

Section: Methodsmentioning

confidence: 64%

Acetaminophen Toxicity

Mirochnitchenko¹,

Weisbrot-Lefkowitz²,

Reuhl

et al. 1999

Journal of Biological Chemistry

109

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Acetaminophen is one of the most extensively used analgesics/antipyretics worldwide, and overdose or idiopathic reaction causes major morbidity and mortality in its victims. Research into the mechanisms of toxicity and possible therapeutic intervention is therefore essential. In this study, the response of transgenic mice overexpressing human antioxidant enzymes to acute acetaminophen overdose was investigated. Animals overexpressing superoxide dismutase or plasma glutathione peroxidase demonstrated dramatic resistance to acetaminophen toxicity. Intravenous injection of glutathione peroxidase provided normal mice with nearly complete protection against a lethal dose of acetaminophen. Surprisingly, animals overexpressing intracellular glutathione peroxidase in the liver were significantly more sensitive to acetaminophen toxicity compared with nontransgenic littermates. This sensitivity appears to be due to the inability of these animals to efficiently recover glutathione depleted as a result of acetaminophen metabolism. Finally, the results suggest that glutathione peroxidase overexpression modulates the synthesis of several acetaminophen metabolites. Our results demonstrate the ability of glutathione peroxidase levels to influence the outcome of acetaminophen toxicity.

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Section: Methodsmentioning

confidence: 64%

Acetaminophen Toxicity

Mirochnitchenko¹,

Weisbrot-Lefkowitz²,

Reuhl

et al. 1999

Journal of Biological Chemistry

109

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“…실제로 여러 가지 질병을 예방 하고 치료하는데 효과가 있어 많은 연구의 대상이 되고 있는 데, 이는 마늘이 함유하고 있는 다량의 유기 황화합물 (organosulfur compounds) 때문인 것으로 알려지고 있다 [5,10]. 특히, diallyl disulfide (DADS)는 마늘의 주요한 유기 황화합물 성분으로서 화학적 간독성에 대한 보호와 [17,28] 항 박테리아 [3] 및 항동맥경화 [19] 등에 효과를 보이는 것으로 보 고되고 있다. 또한 DADS는 다양한 암세포의 G2/M 세포주기 를 억제시키고 [12,20,22], 미토콘드리아의 Bcl-2 family 및 reactive oxygen species (ROS)의 증가를 유도함으로써 세포사 멸(apoptosis)을 일으켜 결과적으로 암세포의 증식을 억제하 는 것으로도 알려져 있다 [9,15,23,29].…”

Section: 서 론unclassified

Effect of Diallyl Disulfide on Heme Oxygenase-1 Expression in Human Hepatoma Cell Line HepG2

Kim¹,

Lee²,

Park³

2011

Journal of Life Science

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Diallyl disulfide (DADS), the most prevalent oil-soluble organosulfur compound in garlic, is known to have diverse biological activities, including anticarcinogenic, antiatherosclerotic, antiinflammatory, and antioxidant actions. In this study, we investigated the effect of DADS on the expression of heme oxygenase-1 (HO-1) in human liver hepatoma cell line HepG2. Treatment of HepG2 cells by DADS evoked a dose-dependent growth inhibition without significant toxicity to the cells, and also induced the expression of transcription factor Nrf2.

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“…An animal study in mice indicated that garlic -derived diallyl sulfone (DASO2) decreased the plasma concentrations of oxidative acetaminophen metabolites but not of nonoxidative acetaminophen metabolites [99] , due to the inhibition of CYP2E1, which is the major enzyme responsible for the bioactivation of acetaminophen [100] . Diallyl sulfone signifi cantly inhibited acetaminophen oxidation to N -acetyl -p -benzoquinone imine (the toxic metabolite of acetaminophen) in liver microsomes [99] . This provides an explanation for the protective effect of diallyl sulfone on acetaminophen -induced hepatotoxicity [99] .…”

Section: The Effect Of Garlic On Analgesics (Acetaminophen)mentioning

confidence: 99%