Xanthine oxidase (XOD) is one of the important enzymes in nucleic acid metabolism, which can catalyze hypoxanthine to produce uric acid and hydrogen peroxide. It is a flavinase containing molybdenum, non heme iron, inorganic sulfide and fad. It is a form of xanthine oxidoreductase. Xanthine oxidoreductase is an enzyme producing reactive oxygen species. It is a kind of enzyme with low specificity, which can not only catalyze hypoxanthine to xanthine and then to uric acid, but also directly catalyze xanthine to uric acid.
The enzyme mainly exists in the liver, spleen and milk of mammals, but can not be detected in the serum of normal people. XOD is released into serum earlier than ALT in the process of hepatocyte injury. Therefore, the increase of XOD activity in serum can sensitively reflect acute liver injury.
XOD activity usually increased significantly in the early stage of jaundice, about 30-50 times of the upper limit of normal, and then decreased to the normal level as jaundice subsided. The positive rate of XOD was higher than that of ALT (90.4%) and AST (81.8%). In other liver diseases such as liver cirrhosis, amebic liver disease and hepatic echinococcosis, the serum XOD activity did not increase or slightly increased. Therefore, XOD can be regarded as a sensitive and specific index for the diagnosis of acute liver injury.
XOD is also helpful to distinguish the types of jaundice. Clinical observation showed that the serum XOD in patients with hepatocellular jaundice increased significantly, while the activity of XOD in patients with obstructive jaundice and hemolytic jaundice was almost normal or only slightly increased, generally less than 1 mu / L.
The common diseases with high XOD are as follows:
1. Acute hepatitis is significantly higher than chronic hepatitis.
2. Infectious mononucleosis often increases.
The activation of xanthine oxidase (XOD) can cause uric acid metabolism disorder and aggravate glucose metabolism disorder.
When XOD is activated, it can also produce superoxide radicals and hydrogen peroxide, leading to oxidative stress.
Xanthine oxidase (XOD) uses molecular oxygen as electron acceptor to catalyze the oxidation of purine, pterin, aldehydes and other heterocyclic compounds, and produce reactive oxygen species (ROS) such as hydrogen peroxide and superoxide radicals. Reactive oxygen species can induce oxidative stress in cells.
Pre receptor and post receptor defects are the main pathogenesis of insulin resistance. The former is mainly manifested by the abnormal binding of insulin to target tissue receptors, including the relative deficiency of insulin and its receptors, the structural changes of insulin and its receptors, etc.; the latter is mainly manifested by the dysfunction of insulin signaling pathway, etc.
Under oxidative stress, it interferes with the signal transduction of insulin binding to receptor mainly by stimulating the inflammatory signal transduction pathway and c-Jun N-terminal kinase pathway. The main reactive oxygen species produced by xanthine oxidase activation is O2, which can inhibit the functional expression of insulin receptor.
The sensitivity of insulin receptor and the integrity of its structure and function are shown by the consumption of glucose. When the number or structure and function of insulin receptors change, the sensitivity of insulin receptors will change accordingly.
In recent years, the incidence of gout and diabetes is increasing year by year. With xanthine oxidase (XO) and α - glucosidase as the main enzyme targets of hyperuricemia and hyperglycemia, exploring the inhibitory effect and mechanism of natural plant ingredients with low toxicity and little side effect on XO and α - glucosidase has gradually become a research hotspot. XO inhibitors can reduce the content of uric acid in the body by inhibiting the activity of xanthine oxidase, which is widely used in clinical treatment.
Therefore, some xanthine oxidase inhibitors can effectively reduce the level of uric acid. However, patients with hyperuricemia do not fully develop gout. Therefore, the development of gout in patients with hyperuricemia can be predicted by regular detection of xanthine oxidase, uric acid and erythrocyte sedimentation rate.
