THE METABOLISM OF DL-HYDROXYPROLINE-2-C14 IN THE RAT

1954 ◽  
Vol 32 (1) ◽  
pp. 154-160 ◽  
Author(s):  
R. Gianetto ◽  
L. P. Bouthillier

DL-Hydroxyproline-2-C14 was synthesized with an over-all yield of about three per cent as calculated on the amount of carbon dioxide employed as radioactive starting material. DL-Hydroxyproline-2-C14 given to three normal rats by intraperitoneal injection was shown to be slowly metabolized. A scheme is suggested for the conversion of this amino acid into glutamic and aspartic acids.

1954 ◽  
Vol 32 (3) ◽  
pp. 154-160 ◽  
Author(s):  
R. Gianetto ◽  
L. P. Bouthillier

DL-Hydroxyproline-2-C14 was synthesized with an over-all yield of about three per cent as calculated on the amount of carbon dioxide employed as radioactive starting material. DL-Hydroxyproline-2-C14 given to three normal rats by intraperitoneal injection was shown to be slowly metabolized. A scheme is suggested for the conversion of this amino acid into glutamic and aspartic acids.


2010 ◽  
Vol 4 (5) ◽  
pp. 771-775 ◽  
Author(s):  
Ugochukwu E. Aronu ◽  
Hallvard F. Svendsen ◽  
Karl Anders Hoff

1961 ◽  
Vol 39 (11) ◽  
pp. 1717-1735 ◽  
Author(s):  
P. G. Scholefield

The cumulative entry of amino acids into Ehrlich ascites carcinoma cells is due to the presence of active transport systems, each with its own specific range of substrates. Several amino acids and amino acid analogues may have an affinity for the same transport system and thus may inhibit transport of other amino acids by acting as competitive inhibitors or competitive substrates. Loss of methionine from ascites cells takes place by a diffusion process which obeys Fick's law. Leucine accumulation by ascites cells is small and is increased on addition of certain other amino acids. The increase is not due to inhibition of leucine oxidation as increase in the rate of production of radioactive carbon dioxide from labeled leucine also occurs. Kinetic aspects of these results are discussed.


ChemInform ◽  
2007 ◽  
Vol 38 (23) ◽  
Author(s):  
Chaorong Qi ◽  
Huanfeng Jiang ◽  
Zhaoyang Wang ◽  
Bo Zou ◽  
Shaorong Yang

2011 ◽  
Vol 114 (1) ◽  
pp. 85-91 ◽  
Author(s):  
Rami Abu Fanne ◽  
Taher Nassar ◽  
Achinoam Mazuz ◽  
Otailah Waked ◽  
Samuel N. Heyman ◽  
...  

Object The severity of neurological impairment following traumatic brain injury (TBI) is exacerbated by several endogenous processes, including hyperglycemia, hypotension, and the generation of glutamate. However, in addition to controlling hyperglycemia, insulin has pleiotropic effects on tissue metabolism, which include reducing the concentration of the neurotoxic amino acid glutamate, making it unclear whether insulin's beneficial effects are attributable to the establishment of euglycemia per se. In the present study, the authors asked if reducing glutamate via approaches that do not lower glucose levels would improve neurological outcome following TBI. Methods Glucagon activates gluconeogenesis by increasing the hepatic uptake of amino acids such as glutamate and facilitating their conversion to glucose. Glucagon was administered as a single intraperitoneal injection before or after closed head injury (CHI). Neurological function, brain histological features, blood glutamate and glucose levels, and CSF glutamate concentrations were measured. Results A single intraperitoneal injection of glucagon (25 μg) into mice 10 minutes before or after CHI reduced lesion size by about 60% (p < 0.0001) and accelerated neurological recovery. The neuroprotective effect of glucagon was related to gluconeogenesis by decreasing the concentration of the neuroexcitatory amino acid glutamate in the circulation from 207 ± 32.1 μmol/L in untreated mice to 101.11 ± 21.6 μmol/L in treated mice (p < 0.001); a similar effect occurred in the CSF. The neuroprotective effect of glucagon was seen notwithstanding the attendant increase in blood glucose, the final substrate of gluconeogenesis. Conclusions Glucagon exerts a marked neuroprotective effect post-TBI by decreasing CNS glutamate. Glucagon was beneficial despite increasing blood glucose. Favorable effects also occurred when glucagon was given prior to TBI, suggesting its involvement in the preconditioning process. Thus, glucagon may be of value in providing neuroprotection when administered after TBI or prior to certain neurosurgical or cardiac interventions in which the incidence of perioperative ischemia is high.


1957 ◽  
Vol 35 (1) ◽  
pp. 55-62
Author(s):  
S. H. Zbarsky ◽  
A. R. P. Paterson

The metabolism of 2-C14-adenine has been studied in the rat. Following intraperitoneal injection of the labelled material, isotope was found in the adenine and guanine of the visceral nucleic acids. Allantoin was the major radioactive metabolite excreted in the urine, and radioactive adenine and uric acid were also shown to be present. The finding of radioactivity in the urinary urea indicated a significant metabolic conversion of the 2-carbon of adenine to carbon dioxide. This result agreed with the finding of 8.5–9.4% of the injected radioactivity in the respiratory carbon dioxide. Possible mechanisms whereby carbon 2 of adenine may be metabolized to carbon dioxide are discussed.


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