5-Lipoxygenase Deficiency Reduces Acetaminophen-Induced Hepatotoxicity and Lethality

5-Lipoxygenase (5-LO) converts arachidonic acid into leukotrienes (LTs) and is involved in inflammation. At present, the participation of 5-LO in acetaminophen (APAP)-induced hepatotoxicity and liver damage has not been addressed. 5-LO deficient (5-LO-/-) mice and background wild type mice were chal...

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Published inBioMed research international Vol. 2013; no. 2013; pp. 1 - 13
Main Authors Cunha, Fernando Queiroz, Casagrande, Rúbia, Verri, Waldiceu A., Pinge-Filho, Phileno, da Silva, Rosiane V., Alves-Filho, José C., Cunha, Thiago Mattar, Crespigio, Jefferson, Pinho-Ribeiro, Felipe A., Cardoso, Renato D. R., Hohmann, Miriam S. N., Ferreira, Sergio Henrique
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Publishing Corporation 01.01.2013
John Wiley & Sons, Inc
Hindawi Limited
Subjects
Acetaminophen
Acetaminophen - adverse effects
Acetaminophen - pharmacology
Alanine Transaminase - blood
Alanine Transaminase - genetics
Analgesics, Non-Narcotic - adverse effects
Analgesics, Non-Narcotic - pharmacology
Analysis
Animals
Arachidonate 5-Lipoxygenase
Chemical and Drug Induced Liver Injury - enzymology
Chemical and Drug Induced Liver Injury - genetics
Chemical and Drug Induced Liver Injury - pathology
Cytokines - blood
Cytokines - genetics
Health aspects
Inflammation
Inflammation - chemically induced
Inflammation - enzymology
Inflammation - genetics
Inflammation - pathology
Ischemia
Membrane Glycoproteins - blood
Membrane Glycoproteins - genetics
Mice
Mice, Knockout
Mortality
NADPH Oxidase 2
NADPH Oxidases - blood
NADPH Oxidases - genetics
NF-E2-Related Factor 2 - blood
NF-E2-Related Factor 2 - genetics
Oxidation-Reduction - drug effects
Oxidative stress
Participation
Pathogenesis
Proteins
Risk factors
Rodents
Studies
Superoxides - blood
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Abstract 5-Lipoxygenase (5-LO) converts arachidonic acid into leukotrienes (LTs) and is involved in inflammation. At present, the participation of 5-LO in acetaminophen (APAP)-induced hepatotoxicity and liver damage has not been addressed. 5-LO deficient (5-LO-/-) mice and background wild type mice were challenged with APAP (0.3–6 g/kg) or saline. The lethality, liver damage, neutrophil and macrophage recruitment, LTB4, cytokine production, and oxidative stress were assessed. APAP induced a dose-dependent mortality, and the dose of 3 g/kg was selected for next experiments. APAP induced LTB4 production in the liver, the primary target organ in APAP toxicity. Histopathological analysis revealed that 5-LO-/- mice presented reduced APAP-induced liver necrosis and inflammation compared with WT mice. APAP-induced lethality, increase of plasma levels of aspartate aminotransferase and alanine aminotransferase, liver cytokine (IL-1β, TNF-α, IFN-γ, and IL-10), superoxide anion, and thiobarbituric acid reactive substances production, myeloperoxidase and N-acetyl-β-D-glucosaminidase activity, Nrf2 and gp91phox mRNA expression, and decrease of reduced glutathione and antioxidant capacity measured by 2,2′-azinobis(3-ethylbenzothiazoline 6-sulfonate) assay were prevented in 5-LO-/- mice compared to WT mice. Therefore, 5-LO deficiency resulted in reduced mortality due to reduced liver inflammatory and oxidative damage, suggesting 5-LO is a promising target to reduce APAP-induced lethality and liver inflammatory/oxidative damage.
AbstractList 5-Lipoxygenase (5-LO) converts arachidonic acid into leukotrienes (LTs) and is involved in inflammation. At present, the participation of 5-LO in acetaminophen (APAP)-induced hepatotoxicity and liver damage has not been addressed. 5-LO deficient (5-LO⁻/⁻) mice and background wild type mice were challenged with APAP (0.3-6 g/kg) or saline. The lethality, liver damage, neutrophil and macrophage recruitment, LTB₄, cytokine production, and oxidative stress were assessed. APAP induced a dose-dependent mortality, and the dose of 3 g/kg was selected for next experiments. APAP induced LTB4 production in the liver, the primary target organ in APAP toxicity. Histopathological analysis revealed that 5-LO⁻/⁻ mice presented reduced APAP-induced liver necrosis and inflammation compared with WT mice. APAP-induced lethality, increase of plasma levels of aspartate aminotransferase and alanine aminotransferase, liver cytokine (IL-1β, TNF-α , IFN- γ, and IL-10), superoxide anion, and thiobarbituric acid reactive substances production, myeloperoxidase and N-acetyl-β-D-glucosaminidase activity, Nrf2 and gp91(phox) mRNA expression, and decrease of reduced glutathione and antioxidant capacity measured by 2,2'-azinobis(3-ethylbenzothiazoline 6-sulfonate) assay were prevented in 5-LO⁻/⁻ mice compared to WT mice. Therefore, 5-LO deficiency resulted in reduced mortality due to reduced liver inflammatory and oxidative damage, suggesting 5-LO is a promising target to reduce APAP-induced lethality and liver inflammatory/oxidative damage.
5-Lipoxygenase (5-LO) converts arachidonic acid into leukotrienes (LTs) and is involved in inflammation. At present, the participation of 5-LO in acetaminophen (APAP)-induced hepatotoxicity and liver damage has not been addressed. 5-LO deficient (5-LO-/-) mice and background wild type mice were challenged with APAP (0.3-6 g/kg) or saline. The lethality, liver damage, neutrophil and macrophage recruitment, LTB4, cytokine production, and oxidative stress were assessed. APAP induced a dose-dependent mortality, and the dose of 3 g/kg was selected for next experiments. APAP induced LTB4 production in the liver, the primary target organ in APAP toxicity. Histopathological analysis revealed that 5-LO-/- mice presented reduced APAP-induced liver necrosis and inflammation compared with WT mice. APAP-induced lethality, increase of plasma levels of aspartate aminotransferase and alanine aminotransferase, liver cytokine (IL-1β, TNF-α, IFN-γ, and IL-10), superoxide anion, and thiobarbituric acid reactive substances production, myeloperoxidase and N-acetyl-β-D-glucosaminidase activity, Nrf2 and [superscript] gp91 phox [/superscript] mRNA expression, and decrease of reduced glutathione and antioxidant capacity measured by 2, [superscript] 2 [variant prime] [/superscript] -azinobis(3-ethylbenzothiazoline 6-sulfonate) assay were prevented in 5-LO-/- mice compared to WT mice. Therefore, 5-LO deficiency resulted in reduced mortality due to reduced liver inflammatory and oxidative damage, suggesting 5-LO is a promising target to reduce APAP-induced lethality and liver inflammatory/oxidative damage.
5-Lipoxygenase (5-LO) converts arachidonic acid into leukotrienes (LTs) and is involved in inflammation. At present, the participation of 5-LO in acetaminophen (APAP)-induced hepatotoxicity and liver damage has not been addressed. 5-LO deficient (5-LO -/- ) mice and background wild type mice were challenged with APAP (0.3–6 g/kg) or saline. The lethality, liver damage, neutrophil and macrophage recruitment, LTB 4 , cytokine production, and oxidative stress were assessed. APAP induced a dose-dependent mortality, and the dose of 3 g/kg was selected for next experiments. APAP induced LTB 4 production in the liver, the primary target organ in APAP toxicity. Histopathological analysis revealed that 5-LO -/- mice presented reduced APAP-induced liver necrosis and inflammation compared with WT mice. APAP-induced lethality, increase of plasma levels of aspartate aminotransferase and alanine aminotransferase, liver cytokine (IL-1 β , TNF- α , IFN- γ , and IL-10), superoxide anion, and thiobarbituric acid reactive substances production, myeloperoxidase and N-acetyl- β -D-glucosaminidase activity, Nrf2 and gp91 phox mRNA expression, and decrease of reduced glutathione and antioxidant capacity measured by 2, 2 ′ -azinobis(3-ethylbenzothiazoline 6-sulfonate) assay were prevented in 5-LO -/- mice compared to WT mice. Therefore, 5-LO deficiency resulted in reduced mortality due to reduced liver inflammatory and oxidative damage, suggesting 5-LO is a promising target to reduce APAP-induced lethality and liver inflammatory/oxidative damage.
5-Lipoxygenase (5-LO) converts arachidonic acid into leukotrienes (LTs) and is involved in inflammation. At present, the participation of 5-LO in acetaminophen (APAP)-induced hepatotoxicity and liver damage has not been addressed. 5-LO deficient (5-LO −/− ) mice and background wild type mice were challenged with APAP (0.3–6 g/kg) or saline. The lethality, liver damage, neutrophil and macrophage recruitment, LTB 4 , cytokine production, and oxidative stress were assessed. APAP induced a dose-dependent mortality, and the dose of 3 g/kg was selected for next experiments. APAP induced LTB 4 production in the liver, the primary target organ in APAP toxicity. Histopathological analysis revealed that 5-LO −/− mice presented reduced APAP-induced liver necrosis and inflammation compared with WT mice. APAP-induced lethality, increase of plasma levels of aspartate aminotransferase and alanine aminotransferase, liver cytokine (IL-1 β , TNF- α , IFN- γ , and IL-10), superoxide anion, and thiobarbituric acid reactive substances production, myeloperoxidase and N-acetyl- β -D-glucosaminidase activity, Nrf2 and gp91 phox mRNA expression, and decrease of reduced glutathione and antioxidant capacity measured by 2,2′-azinobis(3-ethylbenzothiazoline 6-sulfonate) assay were prevented in 5-LO −/− mice compared to WT mice. Therefore, 5-LO deficiency resulted in reduced mortality due to reduced liver inflammatory and oxidative damage, suggesting 5-LO is a promising target to reduce APAP-induced lethality and liver inflammatory/oxidative damage.
5-Lipoxygenase (5-LO) converts arachidonic acid into leukotrienes (LTs) and is involved in inflammation. At present, the participation of 5-LO in acetaminophen (APAP)-induced hepatotoxicity and liver damage has not been addressed. 5-LO deficient (5-LO-/-) mice and background wild type mice were challenged with APAP (0.3–6 g/kg) or saline. The lethality, liver damage, neutrophil and macrophage recruitment, LTB4, cytokine production, and oxidative stress were assessed. APAP induced a dose-dependent mortality, and the dose of 3 g/kg was selected for next experiments. APAP induced LTB4 production in the liver, the primary target organ in APAP toxicity. Histopathological analysis revealed that 5-LO-/- mice presented reduced APAP-induced liver necrosis and inflammation compared with WT mice. APAP-induced lethality, increase of plasma levels of aspartate aminotransferase and alanine aminotransferase, liver cytokine (IL-1β, TNF-α, IFN-γ, and IL-10), superoxide anion, and thiobarbituric acid reactive substances production, myeloperoxidase and N-acetyl-β-D-glucosaminidase activity, Nrf2 and gp91phox mRNA expression, and decrease of reduced glutathione and antioxidant capacity measured by 2,2′-azinobis(3-ethylbenzothiazoline 6-sulfonate) assay were prevented in 5-LO-/- mice compared to WT mice. Therefore, 5-LO deficiency resulted in reduced mortality due to reduced liver inflammatory and oxidative damage, suggesting 5-LO is a promising target to reduce APAP-induced lethality and liver inflammatory/oxidative damage.
5-Lipoxygenase (5-LO) converts arachidonic acid into leukotrienes (LTs) and is involved in inflammation. At present, the participation of 5-LO in acetaminophen (APAP)-induced hepatotoxicity and liver damage has not been addressed. 5-LO deficient (5-LO super(-/-) ) mice and background wild type mice were challenged with APAP (0.3-6 g/kg) or saline. The lethality, liver damage, neutrophil and macrophage recruitment, LTB sub(4) , cytokine production, and oxidative stress were assessed. APAP induced a dose-dependent mortality, and the dose of 3 g/kg was selected for next experiments. APAP induced LTB sub(4) production in the liver, the primary target organ in APAP toxicity. Histopathological analysis revealed that 5-LO super(-/-) mice presented reduced APAP-induced liver necrosis and inflammation compared with WT mice. APAP-induced lethality, increase of plasma levels of aspartate aminotransferase and alanine aminotransferase, liver cytokine (IL-1 beta , TNF- alpha , IFN- gamma , and IL-10), superoxide anion, and thiobarbituric acid reactive substances production, myeloperoxidase and N-acetyl- beta -D-glucosaminidase activity, Nrf2 and super(gp91phox) mRNA expression, and decrease of reduced glutathione and antioxidant capacity measured by 2, super(2') -azinobis(3-ethylbenzothiazoline 6-sulfonate) assay were prevented in 5-LO super(-/-) mice compared to WT mice. Therefore, 5-LO deficiency resulted in reduced mortality due to reduced liver inflammatory and oxidative damage, suggesting 5-LO is a promising target to reduce APAP-induced lethality and liver inflammatory/oxidative damage.
Audience Academic
Author da Silva, Rosiane V.
Ferreira, Sergio Henrique
Verri, Waldiceu A.
Alves-Filho, José C.
Cunha, Thiago Mattar
Hohmann, Miriam S. N.
Casagrande, Rúbia
Cunha, Fernando Queiroz
Pinge-Filho, Phileno
Crespigio, Jefferson
Cardoso, Renato D. R.
Pinho-Ribeiro, Felipe A.
AuthorAffiliation 2 Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Avenida Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil
1 Department of Pathology, Biological Science Centre, State University of Londrina, Rodovia Celso Garcia Cid Pr 445, Km 380. Cx. Postal 6001, 86051-990 Londrina PR, Brazil
3 Department of Pharmaceutical Sciences, Health Sciences Centre, State University of Londrina, Rodovia Celso Garcia Cid Pr 445, Km 380, Cx. Postal 10011, 86051-990 Londrina, PR, Brazil
AuthorAffiliation_xml – name: 1 Department of Pathology, Biological Science Centre, State University of Londrina, Rodovia Celso Garcia Cid Pr 445, Km 380. Cx. Postal 6001, 86051-990 Londrina PR, Brazil
– name: 2 Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Avenida Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil
– name: 3 Department of Pharmaceutical Sciences, Health Sciences Centre, State University of Londrina, Rodovia Celso Garcia Cid Pr 445, Km 380, Cx. Postal 10011, 86051-990 Londrina, PR, Brazil
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/24288682$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright Copyright © 2013 Miriam S. N. Hohmann et al.
COPYRIGHT 2013 John Wiley & Sons, Inc.
Copyright © 2013 Miriam S. N. Hohmann et al. Miriam S. N. Hohmann et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright © 2013 Miriam S. N. Hohmann et al. 2013
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– notice: COPYRIGHT 2013 John Wiley & Sons, Inc.
– notice: Copyright © 2013 Miriam S. N. Hohmann et al. Miriam S. N. Hohmann et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Snippet 5-Lipoxygenase (5-LO) converts arachidonic acid into leukotrienes (LTs) and is involved in inflammation. At present, the participation of 5-LO in acetaminophen...
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SubjectTerms Acetaminophen
Acetaminophen - adverse effects
Acetaminophen - pharmacology
Alanine Transaminase - blood
Alanine Transaminase - genetics
Analgesics, Non-Narcotic - adverse effects
Analgesics, Non-Narcotic - pharmacology
Analysis
Animals
Arachidonate 5-Lipoxygenase
Chemical and Drug Induced Liver Injury - enzymology
Chemical and Drug Induced Liver Injury - genetics
Chemical and Drug Induced Liver Injury - pathology
Cytokines - blood
Cytokines - genetics
Health aspects
Inflammation
Inflammation - chemically induced
Inflammation - enzymology
Inflammation - genetics
Inflammation - pathology
Ischemia
Membrane Glycoproteins - blood
Membrane Glycoproteins - genetics
Mice
Mice, Knockout
Mortality
NADPH Oxidase 2
NADPH Oxidases - blood
NADPH Oxidases - genetics
NF-E2-Related Factor 2 - blood
NF-E2-Related Factor 2 - genetics
Oxidation-Reduction - drug effects
Oxidative stress
Participation
Pathogenesis
Proteins
Risk factors
Rodents
Studies
Superoxides - blood
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Title 5-Lipoxygenase Deficiency Reduces Acetaminophen-Induced Hepatotoxicity and Lethality
URI https://search.emarefa.net/detail/BIM-1030734
https://dx.doi.org/10.1155/2013/627046
https://www.ncbi.nlm.nih.gov/pubmed/24288682
https://www.proquest.com/docview/1461248752
https://search.proquest.com/docview/1464507855
https://pubmed.ncbi.nlm.nih.gov/PMC3832964
Volume 2013
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