Pretreatment of male BALB/c mice with β-ionone potentiates thioacetamide-induced hepatotoxicity

Jeong, Tae Cheon; Gu, Hee Kyoung; Park, Jong-Il; Yun, Hyo-In; Kim, Hyoung-Chin; Ha, Chang-Su; Roh, Jung Koo

doi:10.1016/s0378-4274(98)00386-5

Cited by 13 publications

(3 citation statements)

References 15 publications

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“…This differential distribution of ROS positive hepatocytes is likely to be due to a difference in the metabolism of the two compounds. Whereas DEN is metabolically activated by Cyp2E1 which is more abundant in zone 3 hepatocytes (26), TAA can be converted to more toxic metabolites via a thioacetamide S-oxide intermediate by several enzymes including Cyp2B (27), whose spatial distribution in the liver is affected by exposure to different chemicals and growth factors (28). Increased H 2 O 2 accumulation in livers of TAA-treated p38 α Δ hep mice was also detected using the ROS indicator 5-[and-6]-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate (CM-H 2 DCFDA) (Fig.…”

Section: Resultsmentioning

confidence: 99%

p38α Inhibits Liver Fibrogenesis and Consequent Hepatocarcinogenesis by Curtailing Accumulation of Reactive Oxygen Species

et al. 2013

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Most hepatocellular carcinomas (HCCs) develop in the context of severe liver fibrosis and cirrhosis caused by chronic liver inflammation, which also results in accumulation of reactive oxygen species (ROS). In this study, we examined whether the stress activated protein kinase p38α (Mapk14) controls ROS metabolism and development of fibrosis and cancer in mice given thioacetamide (TAA) to induce chronic liver injury. Liver-specific p38α ablation was found to enhance ROS accumulation, which appears to be exerted through the reduced expression of anti-oxidant protein heat shock protein (HSP) 25 (Hspb1), a mouse homologue of HSP27. Its re-expression in p38α-deficient liver prevents ROS accumulation and TAA-induced fibrosis. p38α-deficiency increased expression of SOX2, a marker for cancer stem cells, and the liver oncoproteins c-Jun (Jun) and Gankyrin (Psmd10) and led to enhanced TAA-induced hepatocarcinogenesis. The up-regulation of SOX2 and c-Jun was prevented by administration of the antioxidant butylated hydroxyanisole. Intriguingly, the risk of human HCC recurrence is positively correlated with ROS accumulation in liver. Thus, p38α and its target HSP25/HSP27 appear to play a conserved and critical hepatoprotective function by curtailing ROS accumulation in liver parenchymal cells engaged in oxidative metabolism of exogenous chemicals. Augmented oxidative stress of liver parenchymal cells may explain the close relationship between liver fibrosis and hepatocarcinogenesis.

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Section: Resultsmentioning

confidence: 99%

p38α Inhibits Liver Fibrogenesis and Consequent Hepatocarcinogenesis by Curtailing Accumulation of Reactive Oxygen Species

et al. 2013

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“…Fulminant hepatic failure was induced by intraperitoneal injection of thioacetamide (TAA) (150 mg/kg, Sigma ) [23, 24]. Mice were randomly divided into 2 groups: group 1 (phosphate buffer saline (PBS); n = 36) and group 2 (2 × 10 6 iPSCs; n = 23) via tail vein injection.…”

Section: Methodsmentioning

confidence: 99%

Investigation of Hepatoprotective Activity of Induced Pluripotent Stem Cells in the Mouse Model of Liver Injury

Chiang

Chang

Huang

et al. 2011

BioMed Research International

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To date liver transplantation is the only effective treatment for end-stage liver diseases. Considering the potential of pluripotency and differentiation into tridermal lineages, induced pluripotent stem cells (iPSCs) may serve as an alternative of cell-based therapy. Herein, we investigated the effect of iPSC transplantation on thioacetamide- (TAA-) induced acute/fulminant hepatic failure (AHF) in mice. Firstly, we demonstrated that iPSCs had the capacity to differentiate into hepatocyte-like cells (iPSC-Heps) that expressed various hepatic markers, including albumin, α-fetoprotein, and hepatocyte nuclear factor-3β, and exhibited biological functions. Intravenous transplantation of iPSCs effectively reduced the hepatic necrotic area, improved liver functions and motor activity, and rescued TAA-treated mice from lethal AHF. 1,1′-dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanine perchlorate cell labeling revealed that iPSCs potentially mobilized to the damaged liver area. Taken together, iPSCs can effectively rescue experimental AHF and represent a potentially favorable cell source of cell-based therapy.

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“…Carbon tetrachloride is deposited in various tissues such as liver, brain, and testes because of the solubility in lipid and crossing of the cell membranes ( 38 ). Detoxification enzymes of the cytochrome P450 cause the production of secondary active and toxic metabolites, which can damage the testis and other body tissues ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of methanolic extract of Berberis integerrima Bunge. root on carbon tetrachloride-induced testicular injury in Wistar rats

Rafiee

Nejati

Heidari

et al. 2016

IJRM

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Background:Tissue protective effect of compounds with antioxidant properties has been demonstrated. The alkaloids found in barberry root are considered as antioxidants.Objective:According to barberry protective effects in different tissues, in this study, the protective effect of Berberis integerrima Bge. root )MEBIR) was evaluated against CCl4-induced testicular damages in Wistar rats.Materials and Methods:40 mature male rats were randomly divided into 5 groups: 1: Normal control, 2: Sham: received CCl4 diluted in olive oil (50% v/v; 1ml/kg bw), intraperitoneally, twice a week for 4 weeks, 3 and 4: Sham rats treated with MEBIR (250 and 500 mg/kg bw) for 28 days, 5: Sham rats treated with silymarin (50 mg/kg bw) for 28 days. After 28 days, serum testosterone level, absolute testis weight, catalase activity, malondialdehyde level, and histological parameters were investigated.Results: In the treated rats with MEBIR (250 and 500 mg/kg bw) or silymarin (50 mg/kg bw), there was a significant increase in the absolute testis weight, testosterone level, seminiferous tubules diameter (p<0.001), thickness of the epithelium, tubule differentiation index) p<0.001), spermiogenesis index (p<0.001), the activity of catalase, and a significant decrease in interstitial tissue thickness (p<0.001) and malondialdehyde level in comparison with CCl4-treated group. The effect of the MEBIR at dose of 500 mg/kg bw is more than that of the standard drug, silymarin (50 mg/kg bw).Conclusion:From the results, it is suggested that the protective effects of MEBIR is possibly due to antioxidant effects of its bioactive compounds.

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Pretreatment of male BALB/c mice with β-ionone potentiates thioacetamide-induced hepatotoxicity

Cited by 13 publications

References 15 publications

p38α Inhibits Liver Fibrogenesis and Consequent Hepatocarcinogenesis by Curtailing Accumulation of Reactive Oxygen Species

p38α Inhibits Liver Fibrogenesis and Consequent Hepatocarcinogenesis by Curtailing Accumulation of Reactive Oxygen Species

Investigation of Hepatoprotective Activity of Induced Pluripotent Stem Cells in the Mouse Model of Liver Injury

Protective effect of methanolic extract of Berberis integerrima Bunge. root on carbon tetrachloride-induced testicular injury in Wistar rats

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