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Article: Chloramphenicol succinate, a competitive substrate and inhibitor of succinate dehydrogenase: Possible reason for its toxicity

TitleChloramphenicol succinate, a competitive substrate and inhibitor of succinate dehydrogenase: Possible reason for its toxicity
Authors
Ambekar, CSLee, JSKCheung, BMYChan, LCLiang, RKumana, CR
KeywordsChloramphenicol succinate
Human bone marrow and liver
Metabolism
Rat liver and kidney mitochondria
Succinate dehydrogenase
Issue Date2004
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/toxinvit
Citation
Toxicology In Vitro, 2004, v. 18 n. 4, p. 441-447 How to Cite?
DOI: http://dx.doi.org/10.1016/j.tiv.2003.12.010
AbstractFrom our previous study [Eur. J. Clin. Pharmacol. 56 (2000) 405] we hypothesized that chloramphenicol succinate (CAPS) may be a competitive substrate for succinate dehydrogenase (SDH). It may be oxidized by SDH to release chloramphenicol (CAP), which may inhibit SDH by feed back mechanism. The present ex-vivo/in vitro study was aimed to investigate this possibility by using human tissues (bone marrow and liver samples) and animal tissues (rat liver and kidney). The effect of different SDH activators and specific inhibitors was studied on CAPS metabolism by SDH. The metabolites and reduction products were detected by using HPLC. In marrow samples, CAPS was slowly oxidized to form CAP. The formation of CAP (oxidation product) was enhanced by FAD and low malonate and inhibited by high malonate and 3-NPA. Similar results were obtained with mitochondria from human and rat tissues. These studies suggest that CAPS could be a competitive oxidative substrate and the metabolite CAP could be an inhibitor at the reduction site. Therefore, SDH could be a target molecule responsible for CAPS induced toxicity. © 2004 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/91592
ISSN
0887-2333
2021 Impact Factor: 3.685
2020 SCImago Journal Rankings: 0.834
ISI Accession Number ID
WOS:000222155000006
References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorAmbekar, CSen_HK
dc.contributor.authorLee, JSKen_HK
dc.contributor.authorCheung, BMYen_HK
dc.contributor.authorChan, LCen_HK
dc.contributor.authorLiang, Ren_HK
dc.contributor.authorKumana, CRen_HK
dc.date.accessioned2010-09-17T10:21:52Z-
dc.date.available2010-09-17T10:21:52Z-
dc.date.issued2004en_HK
dc.identifier.citationToxicology In Vitro, 2004, v. 18 n. 4, p. 441-447en_HK
dc.identifier.issn0887-2333en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91592-
dc.description.abstractFrom our previous study [Eur. J. Clin. Pharmacol. 56 (2000) 405] we hypothesized that chloramphenicol succinate (CAPS) may be a competitive substrate for succinate dehydrogenase (SDH). It may be oxidized by SDH to release chloramphenicol (CAP), which may inhibit SDH by feed back mechanism. The present ex-vivo/in vitro study was aimed to investigate this possibility by using human tissues (bone marrow and liver samples) and animal tissues (rat liver and kidney). The effect of different SDH activators and specific inhibitors was studied on CAPS metabolism by SDH. The metabolites and reduction products were detected by using HPLC. In marrow samples, CAPS was slowly oxidized to form CAP. The formation of CAP (oxidation product) was enhanced by FAD and low malonate and inhibited by high malonate and 3-NPA. Similar results were obtained with mitochondria from human and rat tissues. These studies suggest that CAPS could be a competitive oxidative substrate and the metabolite CAP could be an inhibitor at the reduction site. Therefore, SDH could be a target molecule responsible for CAPS induced toxicity. © 2004 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/toxinviten_HK
dc.relation.ispartofToxicology in Vitroen_HK
dc.subjectChloramphenicol succinateen_HK
dc.subjectHuman bone marrow and liveren_HK
dc.subjectMetabolismen_HK
dc.subjectRat liver and kidney mitochondriaen_HK
dc.subjectSuccinate dehydrogenaseen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBone Marrow - drug effects - physiologyen_HK
dc.subject.meshChloramphenicol - analogs & derivatives - analysis - pharmacology - toxicityen_HK
dc.subject.meshChromatography, High Pressure Liquiden_HK
dc.subject.meshHumansen_HK
dc.subject.meshKidney - drug effects - physiologyen_HK
dc.subject.meshLiver - drug effects - physiologyen_HK
dc.subject.meshMitochondria - drug effects - physiologyen_HK
dc.subject.meshOxidation-Reductionen_HK
dc.subject.meshOxidative Stressen_HK
dc.subject.meshProtein Synthesis Inhibitors - analysisen_HK
dc.subject.meshRatsen_HK
dc.subject.meshSuccinate Dehydrogenase - antagonists & inhibitors - pharmacologyen_HK
dc.titleChloramphenicol succinate, a competitive substrate and inhibitor of succinate dehydrogenase: Possible reason for its toxicityen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, BMY:mycheung@hku.hken_HK
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_HK
dc.identifier.emailLiang, R:rliang@hku.hken_HK
dc.identifier.authorityCheung, BMY=rp01321en_HK
dc.identifier.authorityChan, LC=rp00373en_HK
dc.identifier.authorityLiang, R=rp00345en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.tiv.2003.12.010en_HK
dc.identifier.pmid15130601-
dc.identifier.scopuseid_2-s2.0-2342593351en_HK
dc.identifier.hkuros87678-
dc.identifier.hkuros101472-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2342593351&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume18en_HK
dc.identifier.issue4en_HK
dc.identifier.spage441en_HK
dc.identifier.epage447en_HK
dc.identifier.isiWOS:000222155000006-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridAmbekar, CS=55278609200en_HK
dc.identifier.scopusauthoridLee, JSK=7601479992en_HK
dc.identifier.scopusauthoridCheung, BMY=7103294806en_HK
dc.identifier.scopusauthoridChan, LC=7403540707en_HK
dc.identifier.scopusauthoridLiang, R=26643224900en_HK
dc.identifier.scopusauthoridKumana, CR=7005112381en_HK
dc.identifier.issnl0887-2333-

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