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  • Articles: DFG German National Licenses  (4)
  • Cysteine  (2)
  • Mitochondria  (2)
  • 1
    Electronic Resource
    Electronic Resource
    S-[2-Carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine in normal human urine (1991)
    Springer
    Amino acids 1 (1991), S. 259-262 
    Details
    ISSN: 1438-2199
    Keywords: Amino acids ; Human urine ; Paper electrophoresis ; Cysteine ; Imidazole compound
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A compound, which had the same mobility on a high-voltage paper electrophoretogram and the sameR F value on a thin-layer chromatogram as those ofS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine (I), was partially purified from human urine by ion-exchange column chromatography. The compound gave a signal at m/z 260 on its FAB mass spectrum, which was assigned as MH+ of compound I. These results suggest that the urinary compound is compound I and it is a physiological precursor of 3-[(carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic acid [Kinuta et al., (1991) Biochem J 275: 617–621].
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00806924
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    l-Cysteine metabolism via 3-mercaptopyruvate pathway and sulfate formation in rat liver mitochondria (1992)
    Springer
    Amino acids 2 (1992), S. 143-155 
    Details
    ISSN: 1438-2199
    Keywords: Amino acids ; Cysteine metabolism ; 3-Mercaptopyruvate pathway ; Sulfate formation ; Mitochondria ; Glutathione
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have studied the 3-mercaptopyruvate pathway (transamination pathway) ofl-cysteine metabolism in rat liver mitochondria.l-Cysteine and other substrates at 10 mM concentration were incubated with mitochondrial fraction at pH 8.4, and sulfate and thiosulfate were determined by ion chromatography. Whenl-cysteine alone was incubated, sulfate formed was 0.7µmol per mitochondria from one g of liver per 60 min. Addition of 2-oxoglutarate and GSH resulted in more than 3-fold increase in sulfate formation, and thiosulfate was formed besides sulfate. The sum (A + 2B) of sulfate (A) and thiosulfate (B) formed was approximately 7-times that withl-cysteine alone. Incubation with 3-mercaptopyruvate resulted in sulfate and thiosulfate formation, and sulfate was formed with thiosulfate. These reactions were stimulated with glutathione. Sulfate formation froml-cysteinesulfinate and 2-oxoglutarate was not enhanced by glutathione and thiosulfate was not formed. These findings indicate thatl-cysteine was metabolized and sulfate was formed through 3-mercaptopyruvate pathway in mitochondria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00806085
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effect ofN-acetylcysteine administration on cysteine and glutathione contents in liver and kidney and in perfused liver of intact and diethyl maleate-treated rats (1994)
    Springer
    Amino acids 7 (1994), S. 255-266 
    Details
    ISSN: 1438-2199
    Keywords: Amino acids ; N-Acetylcysteine ; Cysteine ; Glutathione ; Diethyl maleate ; Perfused rat liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effect ofN-acetyl-l-cysteine (NAC) administration on cysteine and glutathione (GSH) contents in rat liver and kidney was studied using intact and diethyl maleate (DEM)-treated rats and perfused rat liver. Cysteine contents increased rapidly, reaching peak at 10 min after intraperitoneal NAC administration. In liver mitochondria it increased slowly, reaching peak at 60 min. GSH content did not change significantly in these tissues. However, in liver and kidney depleted of GSH with DEM, NAC administration restored GSH contents in 60 and 120 min, respectively. Perfusion with 10 mM NAC resulted in 76% increase in liver cysteine content, but not in GSH content. Liver perfusion of DEM-injected rats with 10 mM NAC restored GSH content by 15%. Present findings indicate that NAC is an effective precursor of cysteine in the intact liver and kidney and in the perfused rat liver, and that NAC stimulated GSH synthesis in GSH-depleted tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00807701
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Increase in cystathionine content in rat liver mitochondria after D,L-propargylglycine administration (1995)
    Springer
    Amino acids 9 (1995), S. 111-122 
    Details
    ISSN: 1438-2199
    Keywords: Amino acids ; Cystathionine ; Mitochondria ; Propargylglycine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intraperitoneal administration of D,L-propargylglycine to rats resulted in an increase in the cystathionine content of whole liver and liver mitochondria. Cystathionine in mitochondria was identified by amino acid analysis, thin layer chromatography, high-voltage paper electrophoresis and liquid chromatography-mass spectrometry. The cystathionine content of whole liver was 5.37 ± 1.59µmol per g of fresh liver at 14 h after the administration of 50 mg of D,L-propargylglycine per kg of body weight, while 0.07 ± 0.02µmol of cystathionine per g of fresh liver was detected in the control rats. The cystathionine content of liver mitochondria from both groups of rats was 9.40 ± 1.20 and 0.19 ± 0.04 nmol of cystathionine per mg of protein, respectively. The mitochondrial cystathionine increased dose-dependently with the increase of D,L-propargylglycine administered. The increase was proportional to the time after the administration up to 12 h, and then decreased. The increase of cystathionine in the liver mitochondria was linearly proportional to that in the whole liver. These results suggest that cystathionine in liver mitochondria is in an equilibrium with that in the cytosol.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00805832
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    Paper (German National Licenses)
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