Haptoglobin Typing ELISA Assay
The Haptoglobin Typing ELISA Assay is For Research Use Only
Size: 1×96 wells
Sensitivity: See Package Insert
Incubation Time: 1.5 hours
Sample Type: Serum, plasma
Sample Size: 15 µL
Alternative Names: Hp Typing ELISA
Haptoglobin (Hp) is a normally occurring acute phase serum protein whose primary physiological role is to scavenge free hemoglobin (Hb), a potent oxidizing agent, from the circulation. Free Hb, released during hemolysis of red blood cells, promotes the accumulation of hydroxyl free radicals which can cause oxidative damage to tissues. Hp acts as an antioxidant by first forming complexes with Hb and then clearing the complexes from the circulation by uptake via the CD163 macrophage receptor.
Hp is polymorphic in man and occurs as either one of three phenotypes, Hp 1-1, Hp 2-1, or Hp 2-2. The prevalence of the three phenotypes of Hp is 16% Hp 1-1, 48% Hp 2-1, and 36% Hp 2-2. Substantial evidence supports the pathogenetic role for the Hp 2-2 phenotype. First, the clearance of the Hb/Hp complex is Hp phenotype dependent with Hp 1-1/Hb complexes being cleared more efficiently than Hp 2- 2/Hb complexes. Second, the Hp 2-2/Hb complex is an inferior antioxidant compared to the Hp 1-1/Hb complex in studies measuring conjugated diene formation of linolenic acid or TBARS formation by oxidized LDL. Third, Hp 1-1 is more efficient in preventing heme release from Hp/Hb complexes than Hp 2-2, a finding that may help explain differences in antioxidant capabilities between the different Hp types. Finally, recent studies show impaired reverse cholesterol transport in diabetics carrying the Hp 2-2 genotype, presumably due to the binding of Hp 2-2/Hb complexes to HDL followed by subsequent iron-mediated oxidative damage. The presence of the Hp 2-2 phenotype in diabetic individuals predicts cardiovascular risk. Several longitudinal studies have established that the Hp 2-2 phenotype is an independent risk factor for cardiovascular disease in type 1 and in type 2 diabetics. Although the distribution of Hp phenotypes is not different in individuals with or without diabetes, the Hp 2-2 phenotype was shown to be a risk factor only in patients with diabetes. This may occur because in a diabetic patient, glycosylation of hemoglobin and the reduction of macrophages expressing the CD163 receptor may contribute to the increase in oxidative stress and tissue damage. It has been shown that the oxidation of LDL by glycosylated hemoglobin is not completely blocked by binding to Hp and the impaired removal of the complexes results in their localization in HDL particles. This increased oxidation of lipoproteins by the Hp 2- 2/Hb complexes likely contributes to the development of vascular complications in diabetics.
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