scholarly journals Kinetics of Inhibition of Xanthine Oxidase by Globularia alypum and its Protective Effect against Oxonate-Induced Hyperuricemia and Renal Dysfunction in Mice

Author(s):  
Boussoualim Naouel ◽  
Trabsa hayat ◽  
Krache Iman ◽  
Arrar Lekhmissi ◽  
Baghiani Abderrahmane
1966 ◽  
Vol 16 (01/02) ◽  
pp. 277-295 ◽  
Author(s):  
A Silver ◽  
M Murray

SummaryVarious investigators have separated the coagulation products formed when fibrinogen is clotted with thrombin and identified fibrinopeptides A and B. Two other peaks are observed in the chromatogram of the products of coagulation, but these have mostly been dismissed by other workers. They have been identified by us as amino acids, smaller peptides and amorphous material (37). We have re-chromatographed these peaks and identified several amino acids. In a closed system of fibrinogen and thrombin, the only reaction products should be fibrin and peptide A and peptide B. This reasoning has come about because thrombin has been reported to be specific for the glycyl-arginyl peptide bond. It is suggested that thrombin also breaks other peptide linkages and the Peptide A and Peptide B are attacked by thrombin to yield proteolytic products. Thrombin is therefore probably not specific for the glycyl-arginyl bond but will react on other linkages as well.If the aforementioned is correct then the fibrinopeptides A and B would cause an inhibition with the coagulation mechanism itself. We have shown that an inhibition does occur. We suggest that there is an autoinhibition to the clotting mechanism that might be a control mechanism in the human body.The experiment was designed for coagulation to occur under controlled conditions of temperature and time. Purified reactants were used. We assembled an apparatus to record visually the speed of the initial reaction, the rate of the reaction, and the density of the final clot formed after a specific time.The figures we derived made available to us data whereby we could calculate and plot the information to show the mechanism and suggest that such an inhibition does exist and also further suggest that it might be competitive.In order to prove true competitive inhibition it is necessary to fulfill the criteria of the Lineweaver-Burk plot. This has been done. We have also satisfied other criteria of Dixon (29) and Bergman (31) that suggest true competitive inhibition.


Author(s):  
Perumal Elangovan ◽  
Ramalingam Ramakrishnan ◽  
Kasinathan Amudha ◽  
Abdulkadhar Mohamed Jalaludeen ◽  
Gunasekaran Karuna Sagaran ◽  
...  

2009 ◽  
Vol 70 (5) ◽  
pp. 633-639 ◽  
Author(s):  
Gregory A. Bannikov ◽  
Jeffrey Lakritz ◽  
Christopher Premanandan ◽  
John S. Mattoon ◽  
Eric J. Abrahamsen

2019 ◽  
Vol 20 (19) ◽  
pp. 4680 ◽  
Author(s):  
Yu Mizuno ◽  
Takeshi Yamamotoya ◽  
Yusuke Nakatsu ◽  
Koji Ueda ◽  
Yasuka Matsunaga ◽  
...  

Hyperuricemia has been recognized as a risk factor for insulin resistance as well as one of the factors leading to diabetic kidney disease (DKD). Since DKD is the most common cause of end-stage renal disease, we investigated whether febuxostat, a xanthine oxidase (XO) inhibitor, exerts a protective effect against the development of DKD. We used KK-Ay mice, an established obese diabetic rodent model. Eight-week-old KK-Ay mice were provided drinking water with or without febuxostat (15 μg/mL) for 12 weeks and then subjected to experimentation. Urine albumin secretion and degrees of glomerular injury judged by microscopic observations were markedly higher in KK-Ay than in control lean mice. These elevations were significantly normalized by febuxostat treatment. On the other hand, body weights and high serum glucose concentrations and glycated albumin levels of KK-Ay mice were not affected by febuxostat treatment, despite glucose tolerance and insulin tolerance tests having revealed febuxostat significantly improved insulin sensitivity and glucose tolerance. Interestingly, the IL-1β, IL-6, MCP-1, and ICAM-1 mRNA levels, which were increased in KK-Ay mouse kidneys as compared with normal controls, were suppressed by febuxostat administration. These data indicate a protective effect of XO inhibitors against the development of DKD, and the underlying mechanism likely involves inflammation suppression which is independent of hyperglycemia amelioration.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Hiroki Omizo ◽  
Yoshifuru Tamura ◽  
Chikayuki Morimoto ◽  
Masaki Ueno ◽  
Yuto Hayama ◽  
...  

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