Studies on the Mechanism of Antibody Formation
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The present investigation was made to clarify the action of adrenalin on the formation of inosine, which was identified as antibody-promoting factor. The results obtained were as follows.Adrenalin displayed its action at two locations in the course of metabolic degradation of ATP and adenosine. At one location, it accelerated the degradation from ATP or adenosine to inosine and hypoxanthine, and at the other it inhibited the conversion from inosine and hypoxanthine to xanthine. Especially, when adrenalin and adenosine were used together, inosine and hypoxanthine were found to have increased about 1.7 times after incubation for 40-60 minutes, but xanthine did not behave in the same manner. The optimal rate of adrenalin was 100μg per ml of basic medium.Keywords:
Hypoxanthine
Inosine
Xanthine
CSF obtained for clinical purposes from newborn, children and adults has been analysed by high pressure liquid chromatography for hypoxanthine, xanthine, inosine, uridine and urate. Large rises in hypoxanthine and to a lesser extent xanthine occur for about 24 h after hypoxia. High concentrations were associated with later evidence of brain damage or subsequent death. Changes in CSF could be independent of those in plasma. Small or negligible rises were associated with localised and generalised infections including bacterial meningitis, fits, or both. Marked and rapid rises were found after death. These estimations may "predict" the extent of brain damage or brain death.
Hypoxanthine
Xanthine
Inosine
Hypoxia
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To find the association between purine metabolites and diabetic complications in rats.Alloxan was administered to induce diabetes in rats. After 30 days, the levels of uric acid, inosine, xanthine, hypoxanthine and AMP were assessed in both plasma and liver tissues using HPLC technique.A significant increase in xanthine, hypoxanthine, AMP levels (p < .001 and t-value 2.78) and inosine in plasma and liver tissues (p < .05 and t-value 2.11) with a concomitant increase in uric acid levels (p < .001 and t-value 2.80) was observed in diabetic group.Purine metabolites like uric acid and other intermediate products of purine metabolism are increased in diabetes. These results can be used in addition or separately in evaluating the progression of diabetes.
Hypoxanthine
Xanthine
Inosine
Purine metabolism
Alloxan
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The present investigation was made to clarify the action of adrenalin on the formation of inosine, which was identified as antibody-promoting factor. The results obtained were as follows.Adrenalin displayed its action at two locations in the course of metabolic degradation of ATP and adenosine. At one location, it accelerated the degradation from ATP or adenosine to inosine and hypoxanthine, and at the other it inhibited the conversion from inosine and hypoxanthine to xanthine. Especially, when adrenalin and adenosine were used together, inosine and hypoxanthine were found to have increased about 1.7 times after incubation for 40-60 minutes, but xanthine did not behave in the same manner. The optimal rate of adrenalin was 100μg per ml of basic medium.
Hypoxanthine
Inosine
Xanthine
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Inosine
Hypoxanthine
Adenine nucleotide
Adenosine monophosphate
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Citations (142)
Abstract Isocratic reverse-phase high performance liquid chromatography techniques were developed to resolve and quantitate the purine nucleosides adenosine (Ado) and inosine (Ino) and their metabolites hypoxanthine (Hyp), xanthine (Xan), and uric acid (UA) in the cerebrospinal fluid of the rat. The moving phase composition for resolving hypoxanthine, xanthine and uric acid was a 0.22 M, pH 5.8 phosphate buffer. The moving phase composition for resolving adenosine and inosine was a 0.22 M, pH 6.8 phosphate buffer, 7% methanol (v/v) and 2.5 mM tetrabutylammonium phosphate. The observed cerebrospinal fluid concentrations in the rat were: Ado = 35 ± 9 nM (s.e.m.), Ino = 359 ± 85 nM, Hyp = 243 ± 77 nM, Xan = 1340 ± 423 nM and UA = 6130 ± 678 nM.
Hypoxanthine
Inosine
Xanthine
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The concentration of xanthine and hypoxanthine was measured in 8 portions of SAGM red cell concentrates during 4 wk storage. The concentration of xanthine increased from 4.2 to 35.1 mumol/l and the concentration of hypoxanthine increased from 16.8 to 165.2 mumol/l (mean values). Previous studies have demonstrated several important effects of purine bases--among these a reduced cytotoxicity of purine antimetabolites. It is concluded that further studies are necessary to investigate the clinical role of purines in stored blood products.
Hypoxanthine
Xanthine
Purine metabolism
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Inosine
Hypoxanthine
Xanthine
Purine metabolism
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The phenomenon of decreased serum uric acid (UA) levels in patients with Parkinson’s disease (PD) and its relationship with purine metabolic pathways remain unclear. We compared inosine, hy-poxanthine, xanthine, and UA levels in serum and cerebrospinal fluid (CSF) of PD patients with those of controls, and investigated the effect of changes in the purine metabolic system on UA levels in PD. Overall, 134 samples (serum, 45 PD patients and 30 controls; CSF, 39 PD patients and 20 controls), were analyzed using liquid chromatography-tandem mass spectrometry. A general linear model (GLM) was used to investigate relationships among purine metabolites. Compared to controls, PD patients had significantly lower UA levels in the serum and CSF, and serum and CSF UA levels were significantly correlated. Additionally, in PD, decreased serum hypoxanthine levels were observed with decreased CSF inosine and hypoxanthine levels, suggesting the involvement of the purine recycling system. GLM analysis indicated that the reduced UA levels in PD were mainly due to sources other than the purine metabolic system, such as exercise, nutritional indices, muscle volume, or adipose tissue. Our results highlight the impairment of purine recycling pathways in PD, as evidenced by the decreased serum hypoxanthine and CSF inosine.
Hypoxanthine
Inosine
Xanthine
Purine metabolism
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Citations (1)
The present investigation was made to clarify the action of adrenalin on the formation of inosine, which was identified as antibody-promoting factor. The results obtained were as follows.Adrenalin displayed its action at two locations in the course of metabolic degradation of ATP and adenosine. At one location, it accelerated the degradation from ATP or adenosine to inosine and hypoxanthine, and at the other it inhibited the conversion from inosine and hypoxanthine to xanthine. Especially, when adrenalin and adenosine were used together, inosine and hypoxanthine were found to have increased about 1.7 times after incubation for 40-60 minutes, but xanthine did not behave in the same manner. The optimal rate of adrenalin was 100μg per ml of basic medium.
Hypoxanthine
Inosine
Xanthine
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