Cholera toxin's mechanism of action results in the characteristic 'rice-water' diarrhoea. The toxin activates adenylate cyclase by ADP-ribosylation of which G-protein subunit?
- A Gαs (stimulatory), causing persistent increase in cAMP ✓
- B Gαi (inhibitory), causing decreased cAMP
- C Gβγ subunit, directly opening chloride channels
- D Gq, activating phospholipase C and IP3 cascade
Explanation
Cholera toxin (CT) B subunit binds GM1 ganglioside; the A1 subunit enters the cell and ADP-ribosylates the Gαs protein, permanently activating adenylate cyclase. This causes a sustained rise in intracellular cAMP, which activates protein kinase A, phosphorylates CFTR (cystic fibrosis transmembrane conductance regulator) and other channels, resulting in massive Cl− secretion with accompanying Na+ and H2O — producing profuse watery diarrhoea (10–20 L/day). Pertussis toxin ADP-ribosylates Gαi; cholera toxin targets Gαs.
Reference: Park's Textbook of Preventive and Social Medicine, 27th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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