Amino acid transport in isolated rat hepatocytes

Kilberg, Michael S.

doi:10.1007/bf01871236

Cited by 217 publications

(97 citation statements)

References 87 publications

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“…These features are not those of the L-like system proposed for pre-compaction methionine uptake, which is not inhibited by glycine (Borland & Tasca, 1974;Holmberg & Johnson, 1979). They are features of the glycine-specific mechanism described for several other preparations (Eavenson & Christensen, 1967;Kilberg, 1982).…”

Section: Discussionmentioning

confidence: 70%

Glycine transport in mouse eggs and preimplantation embryos

Hobbs¹,

Kaye²

1985

Reproduction

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Summary. In pre-compaction embryos glycine was taken up by the glycine-specific gl y\ x=r eq-\ system, which is concentrative, weakly exchangeable and dependent on Na+. After compaction glycine uptake increased, apparently due to the expression of the A\ x=r eq-\ transport system and its reactivity with glycine. Studies of the metabolic fate of carbon from glycine indicated conversion to serine and alanine. These changes are interpreted to show that glycine could provide carbon for intermediary energy metabolism, resulting in CO2, as well as for macromolecular synthesis.

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Section: Discussionmentioning

confidence: 70%

Glycine transport in mouse eggs and preimplantation embryos

Hobbs¹,

Kaye²

1985

Reproduction

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“…And last, there is no evidence for a second saturable component in the cerebro vascular influx of isoleucine or cyc10leucine (Ta kasato et aI., 1983). If a second saturable component existed fo r leucine, the transport system would have to be leucine specific, a possibility that was considered unlikely (C hri stensen, 1969;Kilberg, 1982).…”

Section: Discussionmentioning

confidence: 99%

Regional Cerebrovascular Transport of Leucine as Measured by the in situ Brain Perfusion Technique

Smith

Takasato

Sweeney

et al. 1985

J Cereb Blood Flow Metab

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Summary: Leucine influx into six brain regions was de termined in anesthetized rats with the in situ brain per fusion technique using either saline or plasma perfusate.This technique has several advantages over other methods such as the brain uptake index (BUI) technique.The concentration dependence of L-Ieucine influx was best described by a model with a saturable and a nonsat urable component. For the saturable component, Villa, equaled 10,67 ± 0.21 x 10-4 fLmol S-l g I and Kill equaled 0.0257 ± 0.0009 fLmol ml-I, whereas the con stant of non saturable diffusion (Kd) equaled 0.957 ± 0.067 x 10-4 S -I in the parietal lobe during saline per fusion. V rna' was higher in the cortical lobes than in other brain areas, probably owing to a greater capillary surface area. There were no regional differences in Kill or Kd. The apparent Kill for L-Ieucine during plasma perfusion wasThe cerebrovascular endothelium. in addition to restricting the exchange of ions. proteins, and hy drophilic nonelectrolytes, has specific transport systems for rapid transfer of essential nutrients from plasma to brain (Rapoport, 1976 port (Takasato et aI., [984). First, the perfusion technique is 100 times more sensitive than the BU[ technique for the measurement of cerebrovascular permeability. Second, the rat� 01' regional cerebral perfusion is measured directly during perfusion, whereas the cerebral flow rate of the B UI intraca rotid bolus has never been determined experimen tally. Third, with the perfusion technique, there is negligible mixing of perfusate with blood before the perfusion fluid reaches the brain capillaries (Taka sato et aI., [984). In contrast, the assumption that the B U [ intracarotid bolus does not mix with blood before reaching the capillaries has never been ver ified experimentally (Fenstermacher et aI., 198 I).Minimal mixing is important, owing to the sensi tivity of cerebrovascular amino acid transport to competition effects (Rapoport, [976; Pard ridge . 1977a). Fourth, the perfusion technique, unlike the intravenous injection method, allows virtually ab solute control of solute concentrations in brain cap illaries. And last, the perfusion method, unlike the intravenous injection method, is not subject to er-

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“…24 However, the observation that the neuronal glycine receptor antagonist, strychnine, shares the same cytoprotective action of glycine in either hepatocytes and kidney tubular cells 22,25 indicates that the action of glycine may not be ascribed to an effect on cell metabolism.…”

Section: 3mentioning

confidence: 99%

Glycine protects against hepatocyte killing by KCN or hypoxia by preventing intracellular Na+ overload in the rat

et al. 1997

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exposed to endotoxin shock. 7 Although the cytoprotective Glycine has been shown to prevent hepatocyte death ineffect of glycine is well established, the mechanisms involved duced by anoxia and by several toxic agents. However, the still must be fully clarified. Cytoprotection by glycine, in fact, mechanisms responsible for such a cytoprotective effect have is not related to the preservation of intracellular ATP, nor not yet been entirely clarified. We have previously shown that does it require protein synthesis or mitochondrial metaboan uncontrolled increase in intracellular Na / is critical for lism of the amino acid. 1,3 Moreover, glycine does not prevent hepatocyte killing induced by adenosine triphosphate (ATP) intracellular acidification consequent to ATP depletion, 3,8 depletion. We herein report that protection by glycine (2 and it does not interfere with the accumulation of unesterimmol/L) against cytotoxicity induced in isolated rat hepatofied fatty acids in isolated renal proximal tubular cells. 9 Recyte by potassium cyanide (KCN) or hypoxia was associated cently, glycine has been shown to inhibit nonlysosomal prowith the prevention of cytosolic Na / accumulation. The additeolysis in rat hepatocytes exposed to potassium cyanide tion of the Na / ionophore, monensin, abolished the effects of (KCN) or anoxia, suggesting that it might protect against glycine on both Na / increase and cytotoxicity. Pretreating hepatocellular injury by preventing the activation of degradahepatocytes with the glycine-receptor antagonist, strychnine tive proteolytic processes. the intracellular acidification consequent to mitochondrial dysfunctions, whereas the block of Na / efflux is mainly The small, neutral amino acid, glycine, has been shown to caused by the inhibition of the Na / /K / ATPase activity conseprevent irreversible cell injury caused by adenosine triphosquent to ATP depletion. 16 Consistently, the incubation of phate (ATP) depletion in rabbit renal proximal tubular isolated hepatocytes in a bicarbonate-free buffer or in an cells, 1,2 rat hepatocytes, 3,4 and human endothelial cells. 5 acidic medium (pH 6.5) greatly reduced Na / overload and Moreover, glycine addition minimizes reperfusion injury of cell killing by the redox cycling agent, menadione, 16 which is rat liver in a low-flow/reflow liver perfusion model, 6 while known to damage mitochondria and cause ATP depletion.12 feeding a glycine-containing diet improves the survival of rat These observations have prompted us to investigate whether the cytoprotective activity of glycine against the hepatotoxic action of anoxia or KCN poisoning might be asAbbreviations: ATP, adenosine triphosphate; KCN, potassium cyanide; NPPB, 5-cribed to an effect on Na / accumulation.nitro-2-(3-phenylpropylamino) benzoic acid.

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Amino acid transport in isolated rat hepatocytes

Cited by 217 publications

References 87 publications

Glycine transport in mouse eggs and preimplantation embryos

Glycine transport in mouse eggs and preimplantation embryos

Regional Cerebrovascular Transport of Leucine as Measured by the in situ Brain Perfusion Technique

Glycine protects against hepatocyte killing by KCN or hypoxia by preventing intracellular Na+ overload in the rat

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