Developmental changes of adenosine deaminase, xanthine oxidase, and uricase in mouse tissues

This study was carried out to determine if Ginkgo Biloba Extract (GBE or Egb 761) exerts a beneficial effect against cisplatin-induced renal failure in rats. Sprague Dawley rats were divided into four groups. The first group (control) received orally 1 mL/kg/day of 0.9% saline by an oral carrier vehicle on days 1 to 10. The second group was injected with 7 mg/kg cisplatin intraperitoneally (i.p.) on the fourth day, once only. The third group (vit E=cisplatin) was administered 10 mg/kg/day i.p. vit E on 1 to 10 days with one dose of i.p. cisplatin (7 mg/kg) injection on the fourth day. The fourth group (GBE=cisplatin) was given GBE orally at 100 mg/mL/kg started on the first day up to the tenth day with one dose of cisplatin (7 mg/kg) injection on the fourth day. Cisplatin was found to lead a statistically significant increase in plasma BUN and creatinine levels, as well as urine micro total protein (MTP) levels, leading to acute renal failure (ARF) in rats. Renal xanthine oxidase (XO) activities increased in all groups (statistically significant in cisplatin=GBE-treated rats; P≤0.001). Adenosine deaminase (AD) activities were increased in cisplatin-treated rats, and decreased in cisplatin=GBE-treated (PB≤0.041) and cisplatin=vit E-treated (PB≤0.005) rats, compared to controls. Malondialdehyde (MDA), nitric oxide (NO) levels and myeloperoxidase (MPO) activities were increased in the kidney tissue of cisplatin-treated rats. Vit E improved plasma creatinine and urine MTP levels, together with tissue MDA, NO levels, and MPO activities. But GBE had no statistically significant effect on those parameters. These results indicate that increased XO, AD and MPO activities, as well as MDA and NO levels play a critical role in cisplatin nephrotoxicity. GBE has been shown to protect against cisplatin-induced nephrotoxicity. Toxicology and Industrial Health 2006; 22: 125-130.

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Electrophoretic analyses of alcohol dehydrogenase, aldehyde dehydrogenase, aldehyde oxidase, sorbitol dehydrogenase and xanthine oxidase from mouse tissues

Comparative Biochemistry and Physiology Part B Comparative Biochemistry ◽

10.1016/0305-0491(78)90134-7 ◽

1978 ◽

Vol 61 (3) ◽

pp. 339-346 ◽

Cited By ~ 14

Author(s):

Roger S. Holmes

Keyword(s):

Alcohol Dehydrogenase ◽

Xanthine Oxidase ◽

Aldehyde Dehydrogenase ◽

Aldehyde Oxidase ◽

Sorbitol Dehydrogenase ◽

Mouse Tissues

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Anti-Hyperuricemic Effects of Astaxanthin by Regulating Xanthine Oxidase, Adenosine Deaminase and Urate Transporters in Rats

Marine Drugs ◽

10.3390/md18120610 ◽

2020 ◽

Vol 18 (12) ◽

pp. 610

Author(s):

Yanzuo Le ◽

Xie Zhou ◽

Jiawen Zheng ◽

Fangmiao Yu ◽

Yunping Tang ◽

...

Keyword(s):

Uric Acid ◽

Xanthine Oxidase ◽

Adenosine Deaminase ◽

Transport Proteins ◽

Model Group ◽

Rat Models ◽

High Fructose ◽

Underlying Mechanisms ◽

Medicinal Drugs ◽

Mrna Expression Levels

This study was designed to investigate the effects and underlying mechanisms of Astaxanthin (AST) on high-fructose-induced hyperuricemia (HUA) from the perspectives of the uric acid (UA) synthesis and excretion in rat models. Following six weeks of a 10% fructose diet, the level of serum UA effectively decreased in the AST groups as compared to the model group. The enzymatic activities of xanthine oxidase (XOD) and adenosine deaminase (ADA) were significantly inhibited, and the mRNA expression levels of XOD and ADA significantly decreased after the AST administration. These results suggested that the AST reduced UA synthesis by inhibiting the mRNA expressions and enzyme activities of XOD and ADA, thereby contributing to HUA improvement. On the hand, the relative expressions of the mRNA and protein of kidney reabsorption transport proteins (GLUT9 and URAT1) were significantly down-regulated by AST, while that of the kidney secretion proteins (OAT1, OAT3 and ABCG2) were significantly up-regulated by AST. These results indicated that the AST promoted UA excretion by regulating the urate transport proteins, and thus alleviated HUA. This study suggested that the AST could serve as an effective alternative to traditional medicinal drugs for the prevention of fructose-induced HUA.

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Maternal and fetal plasma adenosine deaminase, xanthine oxidase and malondialdehyde levels in pre-eclampsia

Cell Biochemistry and Function ◽

10.1002/cbf.1152 ◽

2005 ◽

Vol 23 (4) ◽

pp. 279-283 ◽

Cited By ~ 30

Author(s):

Aysun Bay Karabulut ◽

Ayse Kafkaslı ◽

Feza Burak ◽

Engin M. Gozukara

Keyword(s):

Xanthine Oxidase ◽

Adenosine Deaminase ◽

Fetal Plasma ◽

Plasma Adenosine

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Inhibition of dipeptidyl peptidase-4 averts Free Fatty acids deposition in the hearts of oral estrogen-progestin contraceptive-induced hyperinsulinemic female rats

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2021-0043 ◽

2021 ◽

Author(s):

Tolulope Eniola Omolekulo ◽

Isaiah Woru Sabinari ◽

Emmanuel Damilare Areola ◽

Folasade O Ajao ◽

Olayinka Olawale Asafa ◽

...

Keyword(s):

Lipid Peroxidation ◽

Fatty Acids ◽

Uric Acid ◽

Free Fatty Acids ◽

Xanthine Oxidase ◽

Adenosine Deaminase ◽

Plasma Insulin ◽

Dipeptidyl Peptidase ◽

Female Rats ◽

Dipeptidyl Peptidase 4

Free fatty acids deposition in non-adipose tissues such as the heart is a characteristic of insulin resistant states which features hyperinsulinemia and dipeptidyl peptidase-4 (DPP-4) activation. Estrogen-progestin oral contraceptives (OC) treatment reportedly increased DPP-4 activity in rat tissue and DPP-4 inhibitors have anti-diabetic and anti-inflammatory properties. This study aims to investigate the effects of DPP-4 inhibition on cardiac free fatty acid (FFA) deposition in estrogen-progestin treated female rats.From our data, estrogen-progestin OC exposure in female rats led to elevated plasma insulin, cardiac DPP-4 activity, FFA and triglyceride (TG) accumulation, Triglyceride/high density lipoprotein (TG/HDL) ratio, adenosine deaminase/xanthine oxidase/uric acid pathway, lipid peroxidation, glycogen synthase activity and alanine phosphatase whereas cardiac glucose-6-phosphate dehydrogenase, Na/K-ATPase and nitric oxide (NO) were decreased. However, DPP-4 inhibition resulted in decreased plasma insulin, cardiac DPP-4 activity, FFA, TG and TG/HDL-C ratio and alkaline phosphatase. These were accompanied by reduced adenosine deaminase/xanthine oxidase/uric acid (ADA/XO/UA) pathway, lipid peroxidation and augmented NO and Na/K-ATPase in estrogen-progestin OC-treated rats.DPP-4 inhibition attenuated cardiac lipid deposition accompanied by reduced activity in the ADA/XO/UA pathway in estrogen-progestin OC-treated female rats. DPP-4 is therefore a plausible therapeutic target in cardiometabolic disorders

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