THAM (acetate)

THAM acetate is a low-toxicity amino alcohol buffer, a CO₂-consuming proton acceptor that buffers carbon dioxide and acid both in vitro and in vivo. THAM acetate binds protons to form bicarbonate, reduces PaCO₂, and induces intracellular alkalization, thereby ameliorating hypercapnia-induced elevation of pulmonary blood vessels and pulmonary arterial pressure. THAM acetate may cause PaCO₂ rebound, hypoglycemia, and respiratory depression. THAM acetate removes amniotic epithelium and preserves the basement membrane, but depletes extracellular matrix and reduces the adhesion rate of limbal epithelial cells. THAM acetate can act as a CO₂ carrier to enhance the productivity and carbon utilization rate of Scenedesmus obliquus. THAM acetate is a key component of buffer solutions used in various biological, cell culture, biochemical, and molecular biology applications^{[1][2][3][4][5]}. In Vitro:THAM (5 min) induces intracellular alkalization in human HepG2 hepatocytes perfused with acidotic artificial media, with a larger effect in the presence of low extracellular non-bicarbonate buffer compared to high extracellular non-bicarbonate buffer^[3].
THAM (110 μL) acetate induces intracellular alkalization in human HepG2 hepatocytes bathed in acidotic human blood^[3].
THAM (2-8 mmol/L; 40 min) acetate enhances CO₂ gas absorptivity and total inorganic carbon storage capacity of modified BG-11 medium, with the highest TIC absorption observed at 8 mmol·L^-1[5].
THAM (2-8 mmol/L; 8 days) acetate improves biomass productivity of Scenedesmus dimorphus in indoor shake flask culture, while also increasing polyunsaturated fatty acid content and showing no biodegradation over 8 days^[5].
THAM (6 mmol/L; 8 days) acetate increases biomass areal productivity of Scenedesmus dimorphus by 32-33% and CO₂ utilisation efficiency by 6-12% in outdoor 2 m² raceway pond culture, while also increasing polyunsaturated fatty acid content^[5]. In Vivo:THAM (weight in kg × 9.2 mEq; i.v.; 1 hour or 3 hours) acetate reduces pulmonary vascular resistance and maintains lower pulmonary arterial pressure in lung-injured piglets with hypercapnia, even after pH rebounds to control levels, while increasing base excess and inducing a post-infusion rebound in PaCO₂^[1].