scholarly journals Some observations on the role of copper ions in the reduction of phosphomolybdate by ascorbic acid and their application in the determination of inorganic orthophosphate

1957 ◽  
Vol 65 (4) ◽  
pp. 709-716 ◽  
Author(s):  
J. L. Peel ◽  
B. C. Loughman
Keyword(s):  
1994 ◽  
Vol 303 (3) ◽  
pp. 935-939 ◽  
Author(s):  
P Ou ◽  
S P Wolff

Erythrocytes exposed to ascorbic acid in the presence of aminotriazole undergo a dose- and time-dependent inactivation of endogenous catalase which is proportional to environmental hydrogen peroxide (H2O2) concentrations. The production of H2O2 seems to be dependent upon the availability of transition metal chelatable by o-phenanthroline (OPT), although the kinetics of catalase inactivation and H2O2 production by externally added copper ions in the presence of OPT is complex. Furthermore, although glucose is also able to undergo a transition-metal-catalysed oxidation yielding H2O2, the production of H2O2 by glucose seems to be a minor process by comparison with ascorbic acid oxidation. Indeed, on the basis of these data, transition-metal-catalysed ascorbic acid oxidation is likely to be a more important source of oxidative stress in the diabetic state than hyperglycaemia.


2012 ◽  
Vol 11 (2) ◽  
pp. 25
Author(s):  
A. J. Abd

Determination of reliable biochemical parameters of experimental diabetic rabbit by alloxane monohydrates and role of diatery antioxidants (ascorbic acid, vit. A, and α-tocopherole) supplementation were investigated. Body weight gain, blood (plasma) chemistries, antioxidant enzymes and histopathological lesion were determined over 10 week in new Zealand white rabbits: control T1 group, diabetic T2 group, diabetic and ascorbic acid T3 group, diabetic and Vit. A T4 group, diabetic and α-tocopherole T5 animals group . each of dietary ascorbic acid, vit. A and α-tocopherole that given to animals of T3, T4 and T5 respectively were significantly (P≤0.01) reduced glucose level in blood than T2 diabetic group, also these antioxidants improve levels of cholesterol and triglyceride. Enzymatic activity of liver glutathione peroxidase and superoxide dismutase were significantly increasd more than of diabetic animals T2. histopathological structures of liver and pancrease confirm these results which indicate mild congestion and less degenerative signs in hepatocytes with mild degeneration of langerhans islets, generally oxidative stress resulted from diabetes and may diminished by administration of antioxidant ascorbic acid, Vit. A and α-tocopherole supplementation, and α-tocopherole group was the best group


Planta Medica ◽  
2010 ◽  
Vol 76 (12) ◽  
Author(s):  
A Copra-Janicijevic ◽  
E Sofic ◽  
L Klepo ◽  
A Topcagic ◽  
I Tahirovic ◽  
...  

1987 ◽  
Vol 26 (01) ◽  
pp. 1-6 ◽  
Author(s):  
S. Selvaraj ◽  
M. R. Suresh ◽  
G. McLean ◽  
D. Willans ◽  
C. Turner ◽  
...  

The role of glycoconjugates in tumor cell differentiation has been well documented. We have examined the expression of the two anomers of the Thomsen-Friedenreich antigen on the surface of human, canine and murine tumor cell membranes both in vitro and in vivo. This has been accomplished through the synthesis of the disaccharide terminal residues in both a and ß configuration. Both entities were used to generate murine monoclonal antibodies which recognized the carbohydrate determinants. The determination of fine specificities of these antibodies was effected by means of cellular uptake, immunohistopathology and immunoscintigraphy. Examination of pathological specimens of human and canine tumor tissue indicated that the expressed antigen was in the β configuration. More than 89% of all human carcinomas tested expressed the antigen in the above anomeric form. The combination of synthetic antigens and monoclonal antibodies raised specifically against them provide us with invaluable tools for the study of tumor marker expression in humans and their respective animal tumor models.


1981 ◽  
Author(s):  
M Yamamoto ◽  
K Watanabe ◽  
Y Ando ◽  
H Iri ◽  
N Fujiyama ◽  
...  

It has been suggested that heparin caused potentiation of aggregation induced by ADP or epinephrine. The exact mechanism of heparin-induced platelet activation, however, remained unknown. In this paper, we have investigated the role of anti-thrombin III ( AT ) in heparin-induced platelet activation using purified AT and AT depleted plasma. When ADP or epinephrine was added to citrated PRP one minute after addition of heparin ( 1 u/ml, porcine intestinal mucosal heparin, Sigma Co. USA ), marked enhancement of platelet aggregation was observed, compared with the degree of aggregation in the absence of heparin. However, in platelet suspensions prepared in modified Tyrode’s solution, heparin exhibited no potentiating effect on platelet aggregation induced by epinephrine or ADP. Potentiation of epinephrine- or ADP-induced platelet aggregation by heparin was demonstrated when purified AT was added to platelet suspensions at a concentration of 20 μg/ml. AT depleted plasma, which was prepared by immunosorption using matrix-bound antibodies to AT, retained no AT, while determination of α1-antitrypsinα2- macroglobulin and fibrinogen in AT depleted plasma produced values which corresponded to those of the original plasma when dilution factor was taken into account. The activities of coagulation factors were also comparable to those of the original plasma. Heparin exhibited potentiating effect on ADP- or epinephrine-induced aggregation of platelets in original plasma, but no effect in AT depleted plasma. When purified AT was added back to AT depleted plasma at a concentration of 20 μg/ml, potentiation of platelet aggregation by heparin was clearly demonstrated.Our results suggest that effect of heparin on platelet aggregation is also mediated by anti-thrombin III.


1971 ◽  
Vol 26 (02) ◽  
pp. 275-288 ◽  
Author(s):  
S Chattopadhyay ◽  
D. D Johnson ◽  
G. J Millar ◽  
L. B Jaques

SummaryRats were subjected to the following procedures: No treatment, Stressor (10% NaCl i.p.), Warfarin for 7 days, Stressor followed by Warfarin; and groups were sacrificed at intervals for assessment of spontaneous hemorrhage and of adrenal ascorbic acid concentration. There was no hemorrhage in the no treatment and stressor groups; some hemorrhage in the warfarin group; profound hemorrhage with Warfarin + Stressor. The adrenal ascorbic acid concentration was found to be lower, 8 h and again 5 days after stress, and remained lower in the warfarin + stress animals. Warfarin had no effect on adrenal ascorbic acid level.In another series of experiments in which the stress consisted of an electric current to the cage floor for 6 sec over 15 min, rats were sacrificed daily for determination of serum corticosterone concentration and occurrence of spontaneous hemorrhage. There was a statistically significant increase of serum corticosterone concentration with stress, warfarin and combined warfarin and stress treatments (P< 0.001 for all three variables). There was a significant correlation (r = 0.96 and 0.89, P< 0.01) for serum corticosterone concentration with hemorrhage score and incidence of hemorrhage in stressed rats receiving warfarin, but not in those receiving only warfarin. The results indicate an activation, rather than an exhaustion, of the pituitary-adrenal axis during the combined action of anticoagulant and stress, which results in the development of spontaneous hemorrhage.


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