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Bicarbonate is a fundamental inorganic anion that serves as the primary extracellular buffer in the human body, essential for maintaining acid-base homeostasis and physiological pH. It is produced endogenously through the hydration of carbon dioxide, a reaction mediated by carbonic anhydrase enzymes, and is regulated primarily by the kidneys and lungs. In clinical medicine, exogenous bicarbonate (typically as sodium bicarbonate) is used to treat metabolic acidosis associated with conditions like renal failure, shock, or severe dehydration. Furthermore, it is a critical agent in toxicology for enhancing the renal clearance of acidic drugs like salicylates and for mitigating the cardiotoxicity of sodium channel-blocking agents such as tricyclic antidepressants. While it is not a protein target like a receptor or enzyme, its concentration and transport are the focal points of numerous therapeutic interventions aiming to stabilize systemic pH or modulate the acidic microenvironment of tumors.
Bicarbonate acts as a physiological buffering agent that neutralizes hydrogen ions to form carbonic acid, which subsequently dissociates into water and carbon dioxide, raising the pH of extracellular fluids [1, 7]. In toxicological contexts, it facilitates the alkalinization of urine, which shifts the equilibrium of weak acids toward their ionized form, preventing renal reabsorption and enhancing excretion [7, 8]. It also increases serum sodium and alkalinity to reverse drug-induced sodium channel blockade [4, 15].
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