Abstract:
:Transport of alpha-ketoisocaproate (KIC), a ketoacid originating from leucine and proposed to be involved in the buffering of glutamate in neurones, was studied in neuroblastoma NB-2a cells. The accumulated KIC was mostly transaminated to leucine, while free keto-acid was detectable either only after prolonged times or after inhibiting transaminase with aminooxyacetate. Accumulation of KIC was found to be inhibited by other branched-chain ketoacids, while lactate and beta-hydroxybutyrate were ineffective. The transport of KIC, resembling a facilitated diffusion, was decreased by phloretin, alpha-cyano-4-hydroxycinnamate, 4,4'-diisothiocyano-2,2'-stilbenedisulphonate, and p-chlorimercuribenzoate. The process of accumulation did not resemble a symport with protons; therefore an involvement of the known proton-coupled monocarboxylate transporters (MCT) was excluded. Distribution of KIC suggests a mechanism involving a cotransport with 2 [Na+].
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Bachowska-Mac M,Nehlig A,Nałecz MJ,Nałecz KAdoi
10.1006/bbrc.1997.7001subject
Has Abstractpub_date
1997-08-08 00:00:00pages
63-7issue
1eissn
0006-291Xissn
1090-2104pii
S0006291X97970017journal_volume
237pub_type
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