COMAT Foundational Biomedical Science (FBS) Practicce Exam

Cholera toxin exerts its effects by overactivating adenylate cyclase, leading to an increase in cyclic AMP (cAMP) levels within the cell. This process begins when cholera toxin binds to the GM1 ganglioside receptor on the surface of intestinal epithelial cells. The toxin then undergoes endocytosis and ultimately activates a G protein, specifically the Gs protein.

Upon activation, Gs stimulates adenylate cyclase, which catalyzes the conversion of ATP to cAMP. The resultant rise in cAMP activates protein kinase A (PKA), which in turn phosphorylates various target proteins that disrupt normal cellular processes. This dysregulation leads to the characteristic symptoms of cholera, such as severe watery diarrhea, because it causes the intestines to secrete excessive amounts of water and electrolytes.

The implications of increased cAMP levels have wide-reaching effects on electrolyte balance and fluid transport in the intestinal lumen, ultimately resulting in dehydration and electrolyte imbalances in patients affected by cholera. Understanding this mechanism is critical to grasping how cholera manifests its symptoms at the cellular level.