pubmed-article:3800962 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:3800962 | lifeskim:mentions | umls-concept:C0205054 | lld:lifeskim |
pubmed-article:3800962 | lifeskim:mentions | umls-concept:C0007262 | lld:lifeskim |
pubmed-article:3800962 | lifeskim:mentions | umls-concept:C0441472 | lld:lifeskim |
pubmed-article:3800962 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
pubmed-article:3800962 | lifeskim:mentions | umls-concept:C0046565 | lld:lifeskim |
pubmed-article:3800962 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:3800962 | lifeskim:mentions | umls-concept:C0629352 | lld:lifeskim |
pubmed-article:3800962 | lifeskim:mentions | umls-concept:C0046566 | lld:lifeskim |
pubmed-article:3800962 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:3800962 | pubmed:dateCreated | 1987-1-30 | lld:pubmed |
pubmed-article:3800962 | pubmed:abstractText | The effects of 2-tetradecylglycidic acid (TDGA), TDGA-CoA and TDGA-carnitine were examined in purified hepatic CPT (carnitine palmitoyltransferase) and in hepatic mitochondria and inverted submitochondrial vesicles derived from Sprague-Dawley rats. Since TDGA has been reported as a specific inhibitor of carnitine palmitoyltransferase-A (CPT-A), the focus was on kinetics and inhibition of CPT-A, and the relationship of this key enzyme to beta-oxidation. After administration of TDGA in vivo to overnight-starved rats, the Vmax. of CPT in intact mitochondria and in inverted vesicles (CPT-B) was depressed by 66%. The S0.5 for palmitoyl-CoA and Km for carnitine were unchanged. The I50 (concn. giving 50% inhibition) for malonyl-CoA was significantly increased from 20 to 141 microM in intact mitochondria, but unchanged (199 versus 268 microM) in inverted vesicles. The addition in vitro of TDGA-CoA (0-1.0 microM) gave I50 values of 0.29 and 0.27 microM (S.E.M. = 0.19) in intact mitochondria from fed and 48 h-starved rats, and 0.81 and 1.57 microM (S.E.M. = 0.29) for inverted vesicles derived from fed and starved rats. Addition in vitro of TDGA-carnitine to mitochondria from starved rats yielded an I50 value of 27.7 mM (S.E.M. = 12.2) for L-[methyl-14C]carnitine release from palmitoyl-L-[methyl-14C]carnitine and 0.64 mM (S.E.M. = 0.07) for palmitoyl-L-[methyl-14C]carnitine formation from L-[methyl-14C]carnitine in intact mitochondria. Inverted vesicles were not measurably sensitive to TDGA-carnitine up to 500 microM for the assay of L-[methyl-14C]carnitine release, but were as sensitive as intact mitochondria when inhibition was determined in the direction of palmitoyl-L-[methyl-14C]carnitine formation (I50 = 0.54 +/- 0.07 microM). When TDGA-CoA was added to intact mitochondria, then incubated for 5 min at room temperature and subsequently washed out, Vmax. of CPT decreased from 5.8 to 3.5 (S.E.M. = 0.6) in intact mitochondria, and from 17.2 to 6.3 (S.E.M. = 4.8) in inverted vesicles. The Km for L-carnitine and the S0.5 for palmitoyl-CoA increased 2-fold with TDGA-CoA pretreatment in both intact mitochondria and inverted vesicles. Detergent solubilization (0.05% Triton X-100) resulted in a complete loss of TDGA-CoA sensitivity (up to 1.0 microM measured). Sonicated mitochondria exhibited an I50 of 0.72 +/- 0.03 microM.(ABSTRACT TRUNCATED AT 400 WORDS) | lld:pubmed |
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pubmed-article:3800962 | pubmed:language | eng | lld:pubmed |
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pubmed-article:3800962 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:3800962 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:3800962 | pubmed:month | Sep | lld:pubmed |
pubmed-article:3800962 | pubmed:issn | 0264-6021 | lld:pubmed |
pubmed-article:3800962 | pubmed:author | pubmed-author:BradtP TPT | lld:pubmed |
pubmed-article:3800962 | pubmed:author | pubmed-author:BradyL JLJ | lld:pubmed |
pubmed-article:3800962 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:3800962 | pubmed:day | 15 | lld:pubmed |
pubmed-article:3800962 | pubmed:volume | 238 | lld:pubmed |
pubmed-article:3800962 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:3800962 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:3800962 | pubmed:pagination | 801-9 | lld:pubmed |
pubmed-article:3800962 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:3800962 | pubmed:year | 1986 | lld:pubmed |
pubmed-article:3800962 | pubmed:articleTitle | Action in vivo and in vitro of 2-tetradecylglycidic acid, 2-tetradecylglycidyl-CoA and 2-tetradecylglycidylcarnitine on hepatic carnitine palmitoyltransferase. | lld:pubmed |
pubmed-article:3800962 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:3800962 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:3800962 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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