The sources of bile pigment in the rat: studies of the "early labeled" fraction.

Robinson, Stephen H.; Tsong, Maria; Brown, B. W.; Schmid, Rudi

doi:10.1172/jci105463

Cited by 78 publications

(40 citation statements)

References 55 publications

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“…This early-labeled pigment fraction is observed within the first few days after the administration of a labeled heme precursor such as glycine-2-14C, when labeled erythrocytes are just beginning to enter the peripheral blood (3,4). Recent studies have shown that the early pigment fraction is heterogeneous in origin and consists of an initial sharp peak followed by a more prolonged second component (5)(6)(7)(8).…”

Section: (12)mentioning

confidence: 99%

“…The initial peak appears to be derived exclusively from extra-erythroid sources (6,7), primarily from the turnover of nonhemoglobin hemes in the liver (9)(10)(11)(12). In rats the later or plateau component also is largely independent of erythroid sources under normal conditions (7), but contains a small erythropoietic component which is substantially augmented when red cell production is either accelerated or abnormal (7).…”

Section: (12)mentioning

confidence: 99%

“…In rats the later or plateau component also is largely independent of erythroid sources under normal conditions (7), but contains a small erythropoietic component which is substantially augmented when red cell production is either accelerated or abnormal (7). It has been suggested that the erythropoietic fraction normally has a larger role in other species (13)(14)(15).…”

Section: (12)mentioning

confidence: 99%

“…The production of early-labeled bilirubin and hemoglobin heme was measured in rats with external bile drainage according to previously described techniques (7). Bile duct cannulation was performed under ether anesthesia, and 2-3 hr later the rats received 50 ACi glycine-2-"C intravenously.…”

Section: (12)mentioning

confidence: 99%

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Hemolysis of “stress” reticulocytes: a source of erythropoietic bilirubin formation

Robinson¹,

Tsong²

1970

J. Clin. Invest.

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Section: (12)mentioning

confidence: 99%

Section: (12)mentioning

confidence: 99%

Section: (12)mentioning

confidence: 99%

Section: (12)mentioning

confidence: 99%

See 2 more Smart Citations

Hemolysis of “stress” reticulocytes: a source of erythropoietic bilirubin formation

Robinson¹,

Tsong²

1970

J. Clin. Invest.

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“…The quantity of the radiolabeled compounds injected in these experiments far exceeds the trace amounts used in past in vivo studies (28)(29)(30)(31)(32) [5-'4C]DOVA, 0.14% of the radiolabel was recovered as hepatic heme. These data indicate that under the conditions of these experiments, DOVA and glycine are converted to hepatic heme with similar efficiency.…”

Section: Resultsmentioning

confidence: 91%

Biosynthesis of 5-aminolevulinic acid and heme from 4,5-dioxovalerate in the rat.

Morton¹,

Kushner²,

Straka³

et al. 1983

J. Clin. Invest.

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A B S T R A C T We previously demonstrated an alternate pathway for the biosynthesis of 5-aminolevulinic acid (ALA) in bovine liver mitochondria and of tetrapyrroles in suspensions of rat hepatocytes (1980. J. Biol. Chem. 255: 3742;. Proc. Natl. Acad. Sci. USA. 78: 5335). This pathway involves a transamination reaction that incorporates the intact 5-carbon skeleton of 4,5-dioxovaleric acid (DOVA) into ALA.We investigated this alternate pathway in vivo by the intraperitoneal injection of DOVA into rats. 3.4%, respectively, of the radioactivity as hepatic heme after 3 h. These doses of radiolabeled DOVA, glycine, and ALA were injected into rats with phenylhydrazine-induced anemia. Recovery of radioactivity after 3 h as splenic (erythroid) heme was 0.35% for DOVA, 0.072% for glycine, and 0.25% for ALA. These studies establish that the intact 5-carbon skeleton of DOVA can be incorporated into ALA and heme in vivo.

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Phenobarbital does not increase early labeling of bilirubin from 4-[14C]-δ-aminolevulinic acid in man and rat

et al. 1991

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delta-Aminolevulinic acid-4-[14C] and [3H]-bilirubin were administered intravenously to five patients with Gilbert's syndrome and four healthy control subjects on two occasions: before and on days 10 through 14 of a course of phenobarbital (2.5 mg/kg/day). The resulting curves of [3H]-bilirubin and [14C]-bilirubin in plasma were analyzed by computer to determine a number of parameters of physiological interest. As expected, phenobarbital produced a highly significant fall in the plasma concentration of unconjugated bilirubin as a result of a significant increase in hepatic bilirubin clearance in all subjects; plasma bilirubin turnover was unaltered. Surprisingly, the drug produced no change in the incorporation of [14C]-delta-aminolevulinic acid into [14C]-early labeled bilirubin. To explain this unexpected finding, the effects of phenobarbital (75 mg/kg/day for 6 days) on incorporation of [14C]-delta-aminolevulinic acid and 2-[14C]-glycine into [14C]-early labeled bilirubin and on the activity of the enzyme delta-aminolevulinic acid synthase were studied in nonfasted, adult, male Sprague-Dawley rats. At the dose and duration of treatment used, phenobarbital administration increased total hepatic delta-aminolevulinic acid synthase activity and produced a significant increase of 70% in the incorporation of [14C]-glycine into early labeled bilirubin. By contrast, no increase in the incorporation of [14C]-delta-aminolevulinic acid into early labeled bilirubin was observed. These data suggest that delta-aminolevulinic acid is an inappropriate precursor for studies of the rate of heme biosynthesis, presumably because it bypasses delta-aminolevulinic acid synthase, the physiological rate-limiting enzyme in the heme biosynthetic pathway.

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The sources of bile pigment in the rat: studies of the "early labeled" fraction.

Cited by 78 publications

References 55 publications

Hemolysis of “stress” reticulocytes: a source of erythropoietic bilirubin formation

Hemolysis of “stress” reticulocytes: a source of erythropoietic bilirubin formation

Biosynthesis of 5-aminolevulinic acid and heme from 4,5-dioxovalerate in the rat.

Phenobarbital does not increase early labeling of bilirubin from 4-[14C]-δ-aminolevulinic acid in man and rat

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