Erythrocytes take up oxygen and release carbon dioxide in the capillaries of the lung. In other tissues of the body the reverse reaction occurs; erythrocytes take up carbon dioxide from and deliver oxygen to cells. Carbonic anhydrases (CAs) are metalloenzymes that catalyze the interconversion between carbon dioxide (CO2) and water (H2O) and the dissociated ions of carbonic acid, i.e. bicarbonate (HCO3-) and protons (H+). The active site of most CAs contains a zinc ion. CAs maintain acid-base balance and help transport carbon dioxide. Depending on the concentrations of reactants, the reaction is reversible.

Carbonic anhydrase inhibitors have been developed to treat glaucoma via their effect on reducing intraocular pressure and decreasing aqueous humor and in managing seizures in various epileptic conditions (Supuran et al. 2003). In the ocular ciliary processes, the local production of bicarbonate by CAs promotes sodium and fluid transport. CA2 is a key isoenzyme found primarily in red blood cells (RBCs) that regulates aqueous humour production (Balfour et al. 1997, Hasegawa et al. 1994). The inhibition of CA2 in the ciliary process disrupts the formation of bicarbonate ions and reduces sodium and fluid transport, which leads to decreased aqueous humour secretion and reduced intraocular pressure (Sugrue 1996, Sugrue 2000, Iester 2008). Brinzolamide, dorzolamide, diclofenamide, ethoxzolamide and methazolamide are topical carbonic anhydrase (CA) inhibitors that treats elevated intraocular pressure (IOP) associated with open-angle glaucoma and ocular hypertension (Mincione et al. 2008).

Acetazolamide, toprimate, sultiame and zonisamide are effective in the treatment of most types of seizures, including generalized tonic-clonic and focal seizures and absence seizures (Hamidi & Avoli 2015, Aggarwal et al. 2013). They are thought to reduce seizures through the inhibition of CA, thereby increasing CO2 levels in the brain.