Bilirubin Powder CAS 635-65-4

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Bilirubin powder, CAS 635-65-4, molecular formula, C33H36N4O6, Also known as bilirubin or deep red bile, it is the main pigment in animal bile and one of the main components of gallstones. A chain shaped compound with four pyrrole rings and connected by a methylene group at its alpha position, belonging to the dienylcholine class, with a relative molecular weight of 584.7. It is usually a light orange or deep reddish brown crystal, insoluble in water, soluble in benzene, chloroform, carbon disulfide, acid and base, and slightly soluble in ether and ethanol. Bilirubin solid is relatively stable in a dry state, and its chloroform solution is also relatively stable in the dark. In alkaline solution or when encountering trivalent iron ions, it is extremely unstable and quickly oxidized to biliverdin. When heated, the color of bilirubin gradually darkens and does not melt, and its light green solution shows red fluorescence under ultraviolet light.

Bilirubin is mainly extracted from animal bile, and by-products such as bile calcium salts and bile acids can also be separated. People have developed various extraction methods based on the physicochemical properties of bilirubin, such as alcohol free extraction, concentration method, chromatography, resin method, one-step method, neutralization method, and so on. It is an important reagent in analytical chemistry and biochemical research, and also one of the raw materials for manufacturing artificial bezoar. In clinical medicine, it has the effects of sedation, shock relief, fever reduction, lowering blood pressure, and promoting red blood cell regeneration. It is one of the drugs used to treat leukemia. In addition, it has strong inhibitory effects on Japanese encephalitis virus and cancer cells. Has strong antioxidant properties and can inhibit some peroxidation damage in the body.

Excessive production of unconjugated bilirubin

 

This is mainly due to internal defects in red blood cells (such as deficiency of certain enzymes or abnormal hemoglobin) or damage to red blood cells by exogenous hemolytic factors (such as malaria, immune hemolysis, snake venom, aniline, etc.), causing a large amount of red blood cell damage and producing a large amount of unconjugated bilirubin. If it exceeds the processing capacity of liver cells, the unconjugated bilirubin in the blood increases, leading to jaundice. In some anemic patients, due to the proliferation of the bone marrow red blood cell system, there is an increase in ineffective red blood cell production in the bone marrow. These red blood cells are often destroyed in situ and cannot enter the bloodstream, or their survival time after entering the bloodstream is very short (several hours), resulting in an increase in unconjugated bilirubin.

Hemolytic jaundice is caused by excessive destruction of red blood cells leading to an increase in unconjugated bilirubin. The metabolic characteristics of its bile pigment are:
1. An increase in unconjugated bilirubin in serum is due to the liver's strong reserve capacity for processing unconjugated bilirubin powder, and the total bilirubin content in serum generally does not exceed 3-5 mg%. The qualitative test for serum bilirubin showed an indirect positive reaction.
2. Increased fecal urobilinogen is due to the liver's enhanced production of conjugated bilirubin, resulting in an increase in bilirubin excreted into the intestine.
3. Increased urinary (fecal) bilinogen and negative bilirubin.

Dysfunction of bilirubin uptake by liver cells

 

The obstruction of liver cell uptake of unconjugated bilirubin can be caused by the following reasons:
1. Due to damage to liver cells (such as viral hepatitis or drug poisoning), the function of liver cells to uptake unconjugated bilirubin is reduced.
2. The development of newborn liver is not yet complete, and there are few carrier proteins in liver cells, resulting in insufficient ability of liver cells to uptake bilirubin.
3. Gilbert's disease is a congenital, non hemolytic jaundice caused by impaired uptake of bilirubin by hepatic sinusoidal microvilli.

Clinical tests have found that the liver's ability to clear unconjugated bilirubin in such patients is only one-third of that of normal individuals, and their serum bilirubin generally does not exceed 3 mg% (in cases where serum bilirubin is higher than 5 mg% and severe cases, it has also been found that the activity of UDP glucuronosyltransferase in liver tissue is reduced).
The metabolic characteristics of bilirubin in liver cell uptake disorders are: an increase in unconjugated bilirubin in the blood, and an indirect positive reaction in the qualitative test of serum bilirubin; No bilirubin in urine; Low levels of urobilinogen in feces and urine excretion.

Bilirubin binding disorder in liver cells

 

Bilirubin binding disorders in liver cells can be caused by the following reasons:
1. Damage to liver cells (such as viral hepatitis or drug poisoning) leads to reduced production of glucuronic acid in the liver or inhibition of UDP glucuronosyltransferase.
2. Insufficient production of UDP glucuronosyltransferase in the liver of newborns (which gradually improves around 10 months after birth). Moreover, the gestational diol in maternal breast milk has an inhibitory effect on UDP glucuronosyltransferase.
3. Crigler Najar Syndrome: This is a non hemolytic, familial jaundice in newborns accompanied by nuclear jaundice. The experiment using isotope labeling of bilirubin proves that the liver cannot bind bilirubin with glucuronic acid. This is due to the lack of UDP glucuronosyltransferase in the liver.

 

This type of jaundice is highly harmful, and most children die from nuclear jaundice, also known as bilirubin encephalopathy. Due to the high toxicity of unconjugated bilirubin, high concentrations of unconjugated bilirubin can inhibit oxidative phosphorylation. In addition, unconjugated bilirubin is lipophilic and has a high affinity for tissues with high lipid content; In addition, the development of the blood-brain barrier in newborns or infants is not yet complete, and unconjugated bilirubin is prone to penetrate brain tissue and deposit in nerve cells, especially in the basal ganglia, thalamus, and hippocampus, which are deeply stained by bilirubin (hence called nuclear jaundice), causing central nervous system dysfunction, manifested as mental fatigue, drowsiness, decreased or increased muscle tone, and even leading to kyphosis, muscle spasms, and rigidity.

Bilirubin binding disorder in muscle cells and metabolic characteristics of bilirubin:
(1) Elevated unconjugated bilirubin in serum (Grigler Najar type I syndrome, complete deficiency of UDP glucuronosyltransferase, serum unconjugated bilirubin can reach 25-45mg%), and the qualitative test for serum bilirubin shows an indirect positive reaction.
(2) There is no bilirubin in the urine.
(3) Due to the reduced production of conjugated bilirubin, the excretion of urobilinogen from feces and urine is significantly reduced.

Dysregulation of bilirubin secretion by liver cells

 

Intrahepatic bilirubin is composed of cholesterol, bile salts, phospholipids, water, and electrolytes to form liver bile, which is secreted into the bile ducts through the Golgi complex and microvilli. Simple or selective bilirubin secretion disorders are rare. Dubin Johnson syndrome and Rotor syndrome are two very similar chronic idiopathic jaundice that can occur in the same family. The metabolic characteristics of its bile pigment are: an increase in serum conjugated bilirubin, showing a direct positive reaction; Positive bilirubin in urine. At the same time, liver cells also have obstacles in the excretion of sodium tetrabromophthalate (BSP), but bile acid secretion and bile flow are normal, without bile stasis. It is currently believed that this may be due to congenital defects in the secretion of bilirubin and negative ion dyes by liver cells. Bilirubin cannot be directed towards the bile ducts and flows back into the sinusoids, resulting in an increase in conjugated bilirubin in the serum.

Brief introduction of bilirubin powder generation process:

① The aging red blood cells are destroyed in the mononuclear phagocyte system. First, globin is removed and haemoglobin is separated;

② Heme, under the action of heme oxygenase of microsomes in mononuclear phagocytes, epoxidates and breaks heme porphyrins, releasing CO and iron, and

It forms biliverdin and heme oxygenase. It exists in mononuclear phagocyte system cells such as liver, spleen, bone marrow or macrophages. Traditional Chinese medicine | education network collects and collates it in

Microsomes belong to mixed function oxidase, and the reaction needs molecular oxygen, and NADPH, NADPH cytochrome P450 reductase coexist;

③ Biliverdin generates bilirubin IXA under the catalysis of biliverdin reductase, which exists in the soluble part of mononuclear phagocyte system cells

With NADPH as coenzyme.

Biliverdin is formed from heme in the body, then reduced to bilirubin, and further combined and excreted. Such a complex process only takes 12 minutes in total to produce bilirubin.

Production of bilirubin:

1. Primary acidification: add half water to the calcium salt of bile pigment, stir it into a paste, pass the 80 mesh sieve, add 0.5 ~ 1% sodium bisulfite according to the amount of calcium salt, slowly add 1:1 dilute hydrochloric acid under constant stirring, acidify it to pH 1 ~ 2, and release acid water for precipitation and filtration.

2. Secondary acidification: add a small amount of ethanol to the precipitate, stir it into a paste, and then add about 10 times

90 ~ 95% ethanol and wash once, then suck off the supernatant, take the precipitate and filter it dry with silk cloth,

The result is crude bilirubin.

3. Refining: add 6 ~ 10 times of chloroform and extract it in three times (i.e. condense the distilled water into

Part of the liquid flows into the raw material and is distilled out again. To improve the purity of distillate) each reflux

After extracting for 2-3 hours, separate the lower chloroform extract, combine the three chloroform extracts, distill and recover chloroform until bile red is recrystallized. Add an appropriate amount of 95% ethanol and continue distillation to remove the residual chloroform in the solution. Bilirubin is filtered by suction, ethanol is filtered off, washed once with a small amount of slightly heated 95% ethanol and distilled water, and then washed twice with a small amount of absolute ethanol, acetone and ether. After vacuum drying, excellent bilirubin was obtained. Stored away from light, the yield is 3 ~ 5 / 10000, and the content is 90%. The above fresh pig bile is processed into bile pigment calcium salt in time, which is relatively stable. Bilirubin in bile will not be oxidized to biliverdin. It can be stored at room temperature for a long time, but it should be mold proof. Therefore, bile should be collected and processed immediately after slaughter to improve the yield of bilirubin.

Bilirubin powder is a kind of bile pigment in the middle of dimethylsichuan. It is a reddish brown pigment body. It is insoluble in water, insoluble in alcohol, ether and soluble in alkali. The maximum absorption is 432 nm (in alkali) and 540 nm (in chloroform). Bile of humans and carnivores is abundant. There are two types of blood bilirubin in the red purple Hijman van den Bergh reaction due to the addition of diazo reagent: one is the direct type, which is positive without the addition of alcohol, and the other is the indirect type, which is colored after the addition of alcohol. The first type is mono - or diglucuronic acid (ester), and the second type is free type. It is a normal metabolite of hemoglobin and can be formed by the reduction of biliverdin. If further reduced, the vinyl group will be changed into ethyl group of bilirubin c30h40o6n. The methylene group is saturated with hydrogen to form mesobilirubin (urobilinogen).

Bilirubin is a pigment produced by hemoglobin in red blood cells. Red blood cells have a fixed life span (the average life span of normal red blood cells is about 120 days). They are destroyed every day. At this time, hemoglobin will be decomposed into heme (haem) and heme. Heme generates biliverdin, trivalent Fe ion and CO under the action of NADPH and H ion, and biliverdin generates bilirubin under the action of NADPH and H ion. Heme is then reconstituted into tissue proteins.

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