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Article: Protective effects of garlic and related organosulfur compounds on acetaminophen-induced hepatotoxicity in mice

TitleProtective effects of garlic and related organosulfur compounds on acetaminophen-induced hepatotoxicity in mice
Authors
Issue Date1996
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taap
Citation
Toxicology And Applied Pharmacology, 1996, v. 136 n. 1, p. 146-154 How to Cite?
AbstractIn previous studies, we have demonstrated that diallyl sulfide, a flavor component of garlic, protects against chemically induced hepatotoxicity. The present study examined the activities of fresh garlic homogenates (FGH) and related organosulfur compounds in the protection against acetaminophen (APAP)-induced hepatotoxicity and the possible mechanisms involved in this protection. When FGH (5 g/kg) was administered to Swiss-Webster mice 2 hr prior to, or immediately after, an APAP treatment (0.2 g/kg), APAP-induced hepatotoxicity was essentially prevented as indicated by serum levels of alanine aminotransferase and lactate dehydrogenase and by liver histopathology. Partial protection was observed with a lower dose of FGH (0.5 g/kg). FGH also prevented APAP-induced hepatic glutathione depletion in a dose-dependent manner. FGH significantly inhibited the formation of APAP-oxidized metabolites, as indicated by decreased plasma levels of oxidized APAP metabolites. The amount of APAP excreted as oxidized metabolites in the 24 hr urine samples was also significantly lower in the mice pretreated with FGH. FGH supernatant inhibited cytochrome P450-dependent APAP oxidation in microsomal incubations. The results suggest that the protection against APAP-induced hepatotoxicity by FGH is mainly due to its inhibition of P450-mediated APAP bioactivation. Several garlic-derived organosulfur compounds and structurally related compounds were examined for their abilities to protect against APAP-induced hepatotoxicity. An S-allyl structure appears to be a common feature for most sulfides to inhibit P450 2E1-dependent activity and to display good protective activities.
Persistent Identifierhttp://hdl.handle.net/10722/167551
ISSN
2015 Impact Factor: 3.847
2015 SCImago Journal Rankings: 1.593
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, EJen_US
dc.contributor.authorLi, Yen_US
dc.contributor.authorLin, Men_US
dc.contributor.authorChen, Len_US
dc.contributor.authorStein, APen_US
dc.contributor.authorReuhl, KRen_US
dc.contributor.authorYang, CSen_US
dc.date.accessioned2012-10-08T03:08:25Z-
dc.date.available2012-10-08T03:08:25Z-
dc.date.issued1996en_US
dc.identifier.citationToxicology And Applied Pharmacology, 1996, v. 136 n. 1, p. 146-154en_US
dc.identifier.issn0041-008Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/167551-
dc.description.abstractIn previous studies, we have demonstrated that diallyl sulfide, a flavor component of garlic, protects against chemically induced hepatotoxicity. The present study examined the activities of fresh garlic homogenates (FGH) and related organosulfur compounds in the protection against acetaminophen (APAP)-induced hepatotoxicity and the possible mechanisms involved in this protection. When FGH (5 g/kg) was administered to Swiss-Webster mice 2 hr prior to, or immediately after, an APAP treatment (0.2 g/kg), APAP-induced hepatotoxicity was essentially prevented as indicated by serum levels of alanine aminotransferase and lactate dehydrogenase and by liver histopathology. Partial protection was observed with a lower dose of FGH (0.5 g/kg). FGH also prevented APAP-induced hepatic glutathione depletion in a dose-dependent manner. FGH significantly inhibited the formation of APAP-oxidized metabolites, as indicated by decreased plasma levels of oxidized APAP metabolites. The amount of APAP excreted as oxidized metabolites in the 24 hr urine samples was also significantly lower in the mice pretreated with FGH. FGH supernatant inhibited cytochrome P450-dependent APAP oxidation in microsomal incubations. The results suggest that the protection against APAP-induced hepatotoxicity by FGH is mainly due to its inhibition of P450-mediated APAP bioactivation. Several garlic-derived organosulfur compounds and structurally related compounds were examined for their abilities to protect against APAP-induced hepatotoxicity. An S-allyl structure appears to be a common feature for most sulfides to inhibit P450 2E1-dependent activity and to display good protective activities.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taapen_US
dc.relation.ispartofToxicology and Applied Pharmacologyen_US
dc.subject.meshAcetaminophen - Administration & Dosage - Toxicity - Urineen_US
dc.subject.meshAlanine Transaminase - Blooden_US
dc.subject.meshAllyl Compoundsen_US
dc.subject.meshAnalgesics, Non-Narcotic - Administration & Dosage - Toxicity - Urineen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntioxidants - Administration & Dosage - Pharmacologyen_US
dc.subject.meshBiotransformationen_US
dc.subject.meshCytochrome P-450 Cyp2e1en_US
dc.subject.meshCytochrome P-450 Enzyme System - Metabolismen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshGarlic - Metabolismen_US
dc.subject.meshGlutathione - Metabolismen_US
dc.subject.meshL-Lactate Dehydrogenase - Blooden_US
dc.subject.meshLiver - Drug Effects - Enzymology - Pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMicrosomes, Liver - Drug Effects - Enzymologyen_US
dc.subject.meshOxidation-Reductionen_US
dc.subject.meshOxidoreductases, N-Demethylating - Metabolismen_US
dc.subject.meshPlant Extracts - Pharmacologyen_US
dc.subject.meshPlant Oils - Administration & Dosage - Pharmacologyen_US
dc.subject.meshPlants, Medicinalen_US
dc.subject.meshSulfides - Pharmacologyen_US
dc.subject.meshSulfur - Pharmacologyen_US
dc.titleProtective effects of garlic and related organosulfur compounds on acetaminophen-induced hepatotoxicity in miceen_US
dc.typeArticleen_US
dc.identifier.emailLin, M:mcllin@hkucc.hku.hken_US
dc.identifier.authorityLin, M=rp00746en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1006/taap.1996.0018en_US
dc.identifier.pmid8560468-
dc.identifier.scopuseid_2-s2.0-0030030355en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030030355&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume136en_US
dc.identifier.issue1en_US
dc.identifier.spage146en_US
dc.identifier.epage154en_US
dc.identifier.isiWOS:A1996TR05900018-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWang, EJ=7403414471en_US
dc.identifier.scopusauthoridLi, Y=27170950800en_US
dc.identifier.scopusauthoridLin, M=7404816359en_US
dc.identifier.scopusauthoridChen, L=7409444486en_US
dc.identifier.scopusauthoridStein, AP=36745429600en_US
dc.identifier.scopusauthoridReuhl, KR=7006483839en_US
dc.identifier.scopusauthoridYang, CS=36037810500en_US

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