Key features and details
- Assay type: Quantitative
- Detection method: Colorimetric
- Sample type: Plasma, Serum, Urine, Whole Blood
Product nameHemoglobin Assay Kit
See all Hemoglobin kits
Sample typeUrine, Serum, Plasma, Whole Blood
Range900 µg/dl - 200000 µg/dl
Hemoglobin Assay Kit (ab272533) is a simple, direct and automation-ready procedure for measuring hemoglobin concentration. This assay is based on an improved Triton/NaOH method, in which the hemoglobin is converted into a uniform colored end product. The intensity of color, measured at 400 nm, is directly proportional to hemoglobin concentration in the sample. The optimized formulation exhibits high sensitivity and substantially reduces interference by substances in the raw samples.
Sensitive and accurate: Linear detection range 0.9 – 200 mg/dL hemoglobin in 96-well plate assay.
Simple and high-throughput: The “mix-and-read” procedure involves addition of a single working reagent and reading the optical density. Can be readily automated as a high-throughput assay in 96-well plates for thousands of samples per day.
Safety: Reagents are non-toxic.
Versatility: Assays can be executed in 96-well plate or cuvet.
Abcam has not and does not intend to apply for the REACH Authorisation of customers’ uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Tested applicationsSuitable for: Functional Studiesmore details
Storage instructionsPlease refer to protocols.
Components 250 tests Calibrator 1 x 10ml Reagent 1 x 50ml
FunctionInvolved in oxygen transport from the lung to the various peripheral tissues.
Tissue specificityRed blood cells.
Involvement in diseaseDefects in HBA1/HBA2 may be a cause of Heinz body anemias (HEIBAN) [MIM:140700]. This is a form of non-spherocytic hemolytic anemia of Dacie type 1. After splenectomy, which has little benefit, basophilic inclusions called Heinz bodies are demonstrable in the erythrocytes. Before splenectomy, diffuse or punctate basophilia may be evident. Most of these cases are probably instances of hemoglobinopathy. The hemoglobin demonstrates heat lability. Heinz bodies are observed also with the Ivemark syndrome (asplenia with cardiovascular anomalies) and with glutathione peroxidase deficiency.
Defects in HBA1/HBA2 are the cause of alpha-thalassemia (A-THAL) [MIM:604131]. The thalassemias are the most common monogenic diseases and occur mostly in Mediterranean and Southeast Asian populations. The hallmark of alpha-thalassemia is an imbalance in globin-chain production in the adult HbA molecule. The level of alpha chain production can range from none to very nearly normal levels. Deletion of both copies of each of the two alpha-globin genes causes alpha(0)-thalassemia, also known as homozygous alpha thalassemia. Due to the complete absence of alpha chains, the predominant fetal hemoglobin is a tetramer of gamma-chains (Bart hemoglobin) that has essentially no oxygen carrying capacity. This causes oxygen starvation in the fetal tissues leading to prenatal lethality or early neonatal death. The loss of three alpha genes results in high levels of a tetramer of four beta chains (hemoglobin H), causing a severe and life-threatening anemia known as hemoglobin H disease. Untreated, most patients die in childhood or early adolescence. The loss of two alpha genes results in mild alpha-thalassemia, also known as heterozygous alpha-thalassemia. Affected individuals have small red cells and a mild anemia (microcytosis). If three of the four alpha-globin genes are functional, individuals are completely asymptomatic. Some rare forms of alpha-thalassemia are due to point mutations (non-deletional alpha-thalassemia). The thalassemic phenotype is due to unstable globin alpha chains that are rapidly catabolized prior to formation of the alpha-beta heterotetramers.
Note=Alpha(0)-thalassemia is associated with non-immune hydrops fetalis, a generalized edema of the fetus with fluid accumulation in the body cavities due to non-immune causes. Non-immune hydrops fetalis is not a diagnosis in itself but a symptom, a feature of many genetic disorders, and the end-stage of a wide variety of disorders.
Sequence similaritiesBelongs to the globin family.
modificationsThe initiator Met is not cleaved in variant Thionville and is acetylated.
- Information by UniProt
- 3-prime alpha-globin gene
- A gamma globin
- Alpha 1 globin
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab272533 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use at an assay dependent concentration.
Use at an assay dependent concentration.
ab272533 has not yet been referenced specifically in any publications.