Bacterial lipopolysaccharide enhances aflatoxin B1 hepatotoxicity in rats by a mechanism that depends on tumor necrosis factor α

Barton, Charles C.; Barton, Eva X.; Ganey, Patricia E.; Kunkel, Steven L.; Roth, Robert A.

doi:10.1053/jhep.2001.20643

Cited by 74 publications

(35 citation statements)

References 51 publications

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“…Our results seem to differ with those of Roth et al where concurrent inflammation render the liver considerably more sensitive to the hepatotoxic effects of AFB1 [4]. Enhancement of AFB1-induced hepatotoxicity by LPS depends on tumor necrosis factor α [3]. In addition, synergistic liver injury from LPS is suggested in rats of exposure with monocrotaline [25].…”

Section: Discussioncontrasting

confidence: 99%

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Co-Exposure Effects of LPS with Various Aflatoxin B1 Doses in Isolated Perfused Rat Liver Model

Koohi

Staji

Hayati

et al. 2017

IJT

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Section: Discussioncontrasting

confidence: 99%

“…LPS can translocate from the GI lumen into the blood and therefore liver and others organ become exposed. Exposure to nontoxic doses of bacterial endotoxin (LPS) can cause the liver more sensitive to injury from hepatotoxic chemicals [3,4].…”

Section: Introductionmentioning

confidence: 99%

Co-Exposure Effects of LPS with Various Aflatoxin B1 Doses in Isolated Perfused Rat Liver Model

Koohi

Staji

Hayati

et al. 2017

IJT

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“…The other inflammatory responses were measured at 5 hours after LPS challenges and compared to those of the non-treated control group. The measurement time points of 5 hours (11) and the LPS dose of 5 mg/kg (12) were chosen to obtain maximum levels of cytokine production.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of a methanol extract from Pulsatilla koreana in lipopolysaccharide-exposed rats

Lee

Ko³

2012

BMB Reports

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To investigate the therapeutic effect of a Korean herbal medicine Pulsatilla koreana as an anti-septic agent, anti-inflammatory effects of the herbal medicine were determined in lipopolysaccharide (LPS)-exposed rats. Treatment with a methanol extract from Pulsatilla koreana significantly inhibited LPS-induced inflammatory responses. Results from ELISA analysis showed that Pulsatilla koreana decreased the plasma and hepatic levels of pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α while increased the level of anti-inflammatory cytokine IL-10 in LPS-exposed rats. Pulsatilla koreana also decreased the plasma levels of other inflammatory mediators such as NO3

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“…Experimental studies have indeed revealed critical interactions between LPS and a number of unrelated xenobiotics and identified some critical mediators including TNFα, eicosanoids, and neutrophil products (Roth et al, 1997;Barton et al, 2000).…”

Section: Proinflammatory Conditionsmentioning

confidence: 99%

Animal Models of Human Disease in Drug Safety Assessment

Boelsterli

2003

J. Toxicol. Sci.

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-Animal models of human disease have been widely used in drug discovery, but they are rarely utilized in toxicological research and screening (except for transgenic models in carcinogenicity testing). Although genetic and/or acquired pathophysiological alterations associated with a particular disease may greatly exacerbate toxic responses to drugs in certain patient subsets, these pre-existing pathological conditions are usually not considered in preclinical safety assessment. Examples of disease-related determinants of susceptibility include disruption of the cytokine network in pro-inflammatory conditions, mitochondrial alterations and oxidative stress in certain neurodegenerative diseases, altered antioxidant defense in certain viral infections, and altered gene expression and mitochondrial dysfunction in type 2 diabetes. Hence, if cellular stress caused by drugs or metabolites and the disease-related effects are superimposed, then an individual can become sensitized to potential drug toxicity. Animal models of modest inflammation indeed can potentiate the toxicity of certain drugs. Similarly, rodent models of type 2 diabetes predispose the animals to hepatotoxic effects of thiazolidinediones antidiabetics. In conclusion, it is suggested that tailor-made and simplified models be adopted and increasingly used, in spite of clear limitations, as optimal substrates for satellite toxicity studies to facilitate candidate selection, help predict rare and unexpected toxicity, and identify new biomarkers.

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Bacterial lipopolysaccharide enhances aflatoxin B1 hepatotoxicity in rats by a mechanism that depends on tumor necrosis factor α

Cited by 74 publications

References 51 publications

Co-Exposure Effects of LPS with Various Aflatoxin B1 Doses in Isolated Perfused Rat Liver Model

Co-Exposure Effects of LPS with Various Aflatoxin B1 Doses in Isolated Perfused Rat Liver Model

Anti-inflammatory effects of a methanol extract from Pulsatilla koreana in lipopolysaccharide-exposed rats

Animal Models of Human Disease in Drug Safety Assessment

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