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  • 1995-1999  (4)
  • L-Tryptophan  (3)
  • COMPOUND 40/80  (1)
  • 1
    ISSN: 1438-2199
    Keywords: Amino acids ; L-Tryptophan ; Serum albumin ; Transport ; L-Tryptophan depletion ; α-Methyl-DL-tryptophan ; Analbuminemic rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The role of serum albumin in the transport of orally administered L-tryptophan (Trp) into rat tissues was examined using analbuminemic and Sprague-Dawley (SD) rats with and without a-methyl-DL-tryptophan (AMT)-induced Trp depletion. Trp was orally administered to rats 16h after AMT or 0.85% NaCl administration, when liver tryptophan 2,3-dioxygenase and protein synthetic activities in AMT-treated rats were similar to those of 0.85% NaCl-treated rats. After oral Trp administration, regardless of the presence or absence of Trp depletion, free serum Trp concentrations were similar in the analbuminemic and SD rats, while total serum Trp concentrations were lower in analbuminemic rats than in SD rats. Although liver, brain, and muscle Trp concentrations after oral Trp administration under Trp depletion were lower in analbuminemic rats than in SD rats, the ratio of the liver Trp concentration in analbuminemic rats to that in SD rats was smaller than that of the brain or muscle Trp concentration. These results suggest that variations in serum albumin levels could affect the transport of orally administered Trp into the liver of rats with Trp depletion.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1438-2199
    Keywords: Amino acids ; L-Tryptophan ; Albumin ; Non-esterified fatty acids ; Puromycin aminonucleoside ; Experimental nephrosis (rat)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is known that total L-tryptophan (Trp) levels decrease with a decrease in albumin-bound Trp levels and an increase in free Trp levels in the plasma or serum of nephrotic children. We, therefore, examined the change of serum Trp levels following the development and recovery of acute nephrosis in 6-week-old male Wistar rats injected once with puromycin aminonucleoside (100mg/kg body weight) and checked the levels of 16 amino acids including Trp in the serum and the levels of Trp in the liver, kidney, and urine under nephrotic conditions. In this study, the development and recovery of nephrosis were checked by the changes of levels of urinary protein and serum protein and albumin. Total serum Trp and albumin-bound serum Trp levels decreased with the development of nephrosis and these decreased levels returned to the normal level with its recovery. In contrast, free serum Trp levels increased with the development of nephrosis and this increased level returned to the normal level with its recovery. In the serum of nephrotic rats, the decrease of albumin-bound Trp levels and the increase of free Trp levels were well consistent with a decrease in albumin levels and an increase in the level of non-esterified fatty acids which are known to weaken the binding of Trp to albumin and among 16 amino acids studied, only Trp showed a significant change in its levels. Trp levels increased in the liver and kidney but not in the urine under nephrotic conditions. These results indicate that the change of serum Trp levels should be closely related to the condition of nephrosis and that although serum Trp is lost under nephrotic conditions, the lost serum Trp is accumulated in the liver and kidney.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1438-2199
    Keywords: L-Tryptophan ; Transport ; Metabolism ; Liver ; Carbon tetrachloride ; Experimental liver cirrhosis (rat)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the serum of rats with liver cirrhosis induced by 12-week intermittent carbon tetrachloride (CCl4) injection, free L-tryptophan (Trp) levels increased with decreases in total Trp, albumin-bound Trp, and albumin levels. In the serum of the cirrhotic rats, there were no changes in the ratio of albumin-bound Trp to albumin and the level of free fatty acids which are known to weaken the binding of Trp to albumin. In the liver of the cirrhotic rats, there were increases in protein and free Trp (i.e., non-protein Trp) contents and a decrease in total tryptophan 2,3-dioxygenase (TDO) activity. The decreased TDO activity was mainly due to the reduction of apo-TDO activity. When [3H]Trp was injected into the portal vein of the cirrhotic and control rats, radioactivity derived from the injected [3H]Trp in the liver was higher in the cirrhotic rats than in the control rats at 10min after the injection, while the radioactivity in the serum was lower in the former rats than in the latter rats. These results indicate that the increased Trp is easily taken up into the cirrhotic liver, and suggest that the Trp taken up into the cirrhotic liver could be utilized for the maintenance of synthesis of proteins in the tissue through the reduction of Trp metabolism due to reduced TDO activity in the tissue.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-2568
    Keywords: COMPOUND 40/80 ; MAST CELL DEGRANULATOR ; GASTRIC MUCOSA ; MUCOSAL LESION RAT ; ACTIVE OXYGEN METABOLISM ; OXIDATIVE STRESS ; BLOOD FLOW ; ISCHEMIA-REPERFUSION
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relationship between the changes of activeoxygen metabolism and blood flow and the formation,progression, and recovery of lesions was examined in thegastric mucosa of rats treated once with compound 48/80, a mast cell degranulator. Gastricmucosal lesions appeared 0.5 hr after compound 48/80treatment, became worst at 3 hr, and recovered fairlywell at 12 hr. Increases in gastric mucosal lipidperoxide content and xanthine oxidase andmyeloperoxidase activities and decreases in gastricmucosal vitamin E and hexosamine contents andSe-dependent glutathione peroxidase activity occurredwith the formation and progression of gastric mucosal lesions.These changes were attenuated with the recovery of thelesion. Gastric mucosal nonprotein SH content decreasedwith the formation of gastric mucosal lesions, and this decreased SH content returned to nearthe original level with lesion progression. No changesin gastric mucosal superoxide dismutase and catalaseactivities occurred with the formation, progression, and recovery of gastric mucosal lesions.Gastric mucosal blood flow decreased with the formationof gastric mucosal lesions, and this decreased bloodflow recovered with lesion progression. Serum serotonin concentration, an index of mast celldegranulation, increased with the formation of gastricmucosal lesions, and this increased serotonin level wasattenuated with lesion progression and recovery.Pretreatment with ketotifen, a connective tissue mast cellstabilizer, prevented the formation of gastric mucosallesions, the increases of gastric mucosal lipid peroxidecontent, xanthine oxidase and myeloperoxidase activities, and serum serotonin level; and thedecreases of gastric mucosal nonprotein SH content,glutathione peroxidase activity, and blood flow found at0.5 hr after compound 48/80 treatment. These results indicate that the changes of gastric mucosalactive oxygen metabolism and blood flow are closelyrelated to the formation, progression, and recovery ofgastric mucosal lesions in rats with a single compound 48/80 treatment. The present results alsosuggest that this compound 48/80-induced gastric mucosalinjury could be a kind of ischemia-reperfusion-inducedinjury occurring through degranulation of connective tissue mast cells.
    Type of Medium: Electronic Resource
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