MAK126
Bilirubin Assay Kit
sufficient for 180 colorimetric tests
Synonym(s):
Hematoidin Assay Kit
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About This Item
UNSPSC Code:
12161503
NACRES:
NA.84
usage
sufficient for 180 colorimetric tests
detection method
colorimetric
relevant disease(s)
hematological disorder; gastrointestinal diseases
storage temp.
2-8°C
Related Categories
General description
Bilirubin, also known as hematoidin, is a degradation product formed as a result of heme catabolism in the liver. Bilirubin circulates in the blood stream as either the unconjugated insoluble form (indirect bilirubin) or the soluble glucuronide-conjugated form (direct bilirubin). Conjugated bilirubin moves from the bile canaliculi of the liver to the gall bladder where it is excreted into the small intestine during digestion. High levels of bilirubin can result in jaundice and may indicate liver disease, blood disorders, or blockage of the bile ducts.
Application
Bilirubin Assay Kit has been used to measure the total bilirubin concentration in samples.
Suitable for the detection of total and conjugated bilirubin in serum samples.
Not suitable for plasma samples. Anticoagulants in plasma interfere with the assay
Not suitable for plasma samples. Anticoagulants in plasma interfere with the assay
Biochem/physiol Actions
The assay, based on the improved Jendrassik-Grof method, utilizes the reaction of bilirubin with diazotized sulfanilic acid resulting in a colorimetric product measured at 530 nm, proportionate to the bilirubin present in the sample. This assay kit measures both total and conjugated bilirubin. Total bilirubin is assessed using caffeine benzoate to split bilirubin from the unconjugated bilirubin protein complex.
Features and Benefits
Compatible with high-throughput handling systems. Can be adapted for use with cuvettes.
Storage Class Code
12 - Non Combustible Liquids
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
监管及禁止进口产品
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Chengyou Jia et al.
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Liver kinase B 1 (LKB1 or STK11) and PTEN (phosphatase and tensin homologue deleted on chromosome 10) are two tumor suppressors that regulate the mTOR signaling pathway. Deletion studies show that loss of either Lkb1 (Lkb+/- ) or Pten (PtenloxP/loxP;
Regulation of lipid metabolism by obeticholic acid in hyperlipidemic hamsters.
Dong B,et al.
Journal of Lipid Research, 58(2), 350-363 (2017)
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Cancer cachexia is a debilitating metabolic syndrome contributing to cancer death. Organs other than the muscle may contribute to the pathogenesis of cancer cachexia. This work explores new mechanisms underlying hepatic alterations in cancer cachexia. We used transcriptomics to reveal
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Progression and regression of hepatic lesions in a mouse model of NASH induced by dietary intervention and its implications in pharmacotherapy.
Ding ZM, et al.
Frontiers in Pharmacology, 9, 410-410 (2018)
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