Immunosuppression in adult female B6C3F1 mice by chronic exposure to ethanol in a liquid diet

Holsapple, Michael P.; Eads, Micah; Stevens, Wayne; Wood, Steve; Kaminski, Norbert E.; Morris, Dale L.; Poklis, Alphonse; Kamiński, E.; Jordan, Stephen D.

doi:10.1016/0162-3109(93)90064-w

Cited by 13 publications

(4 citation statements)

References 40 publications

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“…In models that involve mice as the experimental subject of ETOH consumption, fatty change in the liver is rarely seen. Results of two reports have shown that in mice fed an ETOH diet providing 30% or 36% of calories a mild microvesicular steatosis ultimately developed, but a relatively long feeding time (28–30 days) was required for its development [19,20]. In contrast to these study findings, it has been shown that mice provided an ETOH‐containing diet given by a continuous, intragastric technique develop a severe steatosis and a modest increase in serum levels of alanine aminotransferase (ALT) after 30 days of feeding [21].…”

Section: Introductionmentioning

confidence: 99%

Initiation of alcoholic fatty liver and hepatic inflammation with a specific recall immune response in alcohol-consuming C57Bl/6 mice

Slukvin

Boor

Jerrells

2001

Clinical and Experimental Immunology

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SUMMARYWhether immunological responses are involved in initiation and progression of alcoholic liver disease is unclear. We describe a mouse model of alcoholic liver injury characterized by steatosis and hepatic inflammation initiated by a recall immune response. Mice immune to Listeria monocytogenes fed a liquid diet containing ethanol and challenged with viable bacteria developed steatosis within 24 h and, at a later time, elevated serum alanine aminotransferase levels, indicating more liver damage in this group. Listeria antigen also induced steatosis and increased serum alanine aminotransferase levels in immune ethanol-consuming mice. The production of tumour necrosis factor by a recall immune response in this model is a major, but not the only, component in initiation of alcoholic liver disease.

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Section: Introductionmentioning

confidence: 99%

Initiation of alcoholic fatty liver and hepatic inflammation with a specific recall immune response in alcohol-consuming C57Bl/6 mice

Slukvin

Boor

Jerrells

2001

Clinical and Experimental Immunology

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“…Mice were pair-fed; that is, caloric intake by the LED or cLED-fed mice determined the caloric intake for the LCD or cLCD-fed mice for the subsequent day. The murine ethanol feeding regimen we and others use typically results in blood alcohol levels in the 0.1% to 0.15% range, which closely parallels levels that cause inebriation in humans (Holsapple et al, 1993;Jayasinghe et al, 1992;Mikszta et al, 1995;Schodde et al, 1996).…”

Section: Diets and Feedingmentioning

confidence: 75%

Ethanol Consumption and the Susceptibility of Mice to Listeria monocytogenes Infection

Salerno¹,

Waltenbaugh²,

Cianciotto³

2001

Alcoholism Clin & Exp Res

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“…For examples, 3-methylcholanthrene and β-naphthoflavone, well-known inducers of CYP 1A enzymes, could not be used as model inducers in studying the role of metabolism in toxicant-induced toxicity in vivo due to their intrinsic toxicity (White et al ., 1985). Ethanol and dexamethasone, inducers of CYP 2E1 and CYP 3A enzymes, respectively, are also immunosuppressive themselves (Sabbele et al ., 1987; Holsapple et al ., 1993). Therefore, developing new CYP inducers capable of inducing specific CYP enzyme(s) without or with low toxicity in vivo at the dose for CYP induction is of importance.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Diallyl Sulfide against Thioacetamide-Induced Toxicity: A Possible Role of Cytochrome P450 2E1

Kim

Lee

Kang

et al. 2014

Biomolecules & Therapeutics

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Effects of diallyl sulfide (DAS) on thioacetamide-induced hepatotoxicity and immunotoxicity were investigated. When male Sprague-Dawley rats were treated orally with 100, 200 and 400 mg/kg of DAS in corn oil for three consecutive days, the activity of cytochrome P450 (CYP) 2E1-selective p-nitrophenol hydroxylase was dose-dependently suppressed. In addition, the activities of CYP 2B-selective benzyloxyresorufin O-debenzylase and pentoxyresorufin O-depentylase were significantly induced by the treatment with DAS. Western immunoblotting analyses also indicated the suppression of CYP 2E1 protein and/or the induction of CYP 2B protein by DAS. To investigate a possible role of metabolic activation by CYP enzymes in thioacetamide-induced hepatotoxicity, rats were pre-treated with 400 mg/kg of DAS for 3 days, followed by a single intraperitoneal treatment with 100 and 200 mg/kg of thioacetamide in saline for 24 hr. The activities of serum alanine aminotransferase and aspartate aminotransferase significantly elevated by thioacetamide were protected in DAS-pretreated animals. Likewise, the suppressed antibody response to sheep erythrocytes by thioacetamide was protected by DAS pretreatment in female BALB/c mice. Taken together, our present results indicated that thioacetamide might be activated to its toxic metabolite(s) by CYP 2E1, not by CYP 2B, in rats and mice.

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Immunosuppression in adult female B6C3F1 mice by chronic exposure to ethanol in a liquid diet

Cited by 13 publications

References 40 publications

Initiation of alcoholic fatty liver and hepatic inflammation with a specific recall immune response in alcohol-consuming C57Bl/6 mice

Initiation of alcoholic fatty liver and hepatic inflammation with a specific recall immune response in alcohol-consuming C57Bl/6 mice

Ethanol Consumption and the Susceptibility of Mice to Listeria monocytogenes Infection

Protective Effects of Diallyl Sulfide against Thioacetamide-Induced Toxicity: A Possible Role of Cytochrome P450 2E1

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