THAM

THAM (Tris) is a low-toxicity amino alcohol buffer, a specific CO₂-consuming proton acceptor that buffers carbon dioxide and acid both in vitro and in vivo. THAM 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 may cause PaCO₂ rebound, hypoglycemia, and respiratory depression. THAM removes amniotic epithelium and preserves the basement membrane, but depletes extracellular matrix and reduces the adhesion rate of limbal epithelial cells. THAM can act as a CO₂ carrier to enhance the productivity and carbon utilization rate of Scenedesmus obliquus. THAM 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) induces intracellular alkalization in human HepG2 hepatocytes bathed in acidotic human blood^[3].
THAM (2-8 mmol/L; 40 min) 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) 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) 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) 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].