We offer the following assays:


2,3 DPG

Hemoglobin, the protein in the blood that carries oxygen, uses 2,3-DPG to control how much oxygen is released once blood gets out into the tissues. The more 2,3-DPG in the cell, the more oxygen is delivered to body tissues. Conversely, the less 2,3-DPG in the cell, the less oxygen is delivered. Increasing the amount of 2,3-DPG is the body’s primary way of responding to a lack of oxygen. Anemia, obstructive lung disease, cystic fibrosis, and congenital heart disease are all accompanied by increases in 2,3-DPG. When more oxygen is required because of increased metabolism, such as in hyperthyroidism, more 2,3-DPG is produced. Decreased 2,3-DPG results from an inherited lack of the red blood cell enzymes 2,3-DPG mutase and 2,3-DPG phosphatase. These enzymes are needed to make 2,3-DPG. Without 2,3-DPG to control the movement of oxygen to its tissues, the body responds by making more red blood cells, a condition called erythrocytosis. The outside membrane of the cell is weakened, causing it to have an irregular shape and burst, or hemolyze, easily. This condition is called nonspherocytic hemolytic anemia. 2,3-DPG levels are important in large blood transfusions, because stored blood quickly loses 2,3-DPG and its ability to deliver oxygen. After transfusion, the red cells rebuild the 2,3-DPG, but it takes about 24 hours to regain a normal level of 2,3-DPG and hemoglobin function.



Several assays for the determination of hemoglobin (HGB) are in use today. The direct optical method of Harboe is known as a sensitive and reproducible assay. In this assay HGB is quantified by measuring the oxyhemoglobin absorbance peak at 415 nm. The assay is suited to measure free HGB in plasma and total HGB in whole blood.



Lactic acid (lactate) is an intermediate in carbohydrate metabolism. Lactic acidosis, which is determined in blood, occurs in two different clinical settings. Type A (hypoxic) is associated with decreased tissue oxygenation such as shock and heart failure. Type B (metabolic) is associated with disease (diabetes, neoplasia, liver disease), intake of drugs and toxins, or inborn errors of metabolism. Type A is a common form of lactic acidosis. Lactate levels in cerebro-spinal fluid (CSF) normally parallel blood levels. However, biochemical alterations in the central nervous system can result in changes in CSF lactate concentrations independent of blood values.

Lactate is determined first by oxidation with lactate oxidase, which result in the generation of H2O2. H2O2 is then detected with reagents that result in the development of a red dye. Because lactate is rapidly metabolized by red blood cells, blood samples have to be carefully collected and treated to prevent this.