5. Parietal cells of the stomach release hydrochloric acid (HCl) to aid in digestion.
Why are parietal cells themselves not digested by HCl?
a. They contain inhibitory enzymes that inactivate the HCl
b. They are protected by mucous secreted by cells in the gastric pit
c. HCl has to be activated by pepsinogen which is released by peptic cells
d. Bicarbonate ions inside the parietal cells neutralize HCl
Parietal cells in the stomach secrete hydrochloric acid (HCl) essential for digestion, yet remain undigested due to protective mechanisms. The correct answer to the MCQ is option b: parietal cells are protected by mucous secreted by cells in the gastric pit. This mucus forms a barrier preventing HCl from damaging the gastric mucosa, including parietal cells.
Option Analysis
a. Inhibitory enzymes inactivate HCl
Parietal cells lack enzymes that neutralize HCl; instead, HCl secretion occurs via H+/K+-ATPase pumps into canaliculi, maintaining neutral intracellular pH through bicarbonate exchange. This option is incorrect as no such inhibitory enzymes exist in parietal cells.
b. Mucous from gastric pit cells
Surface mucous cells (foveolar) and mucous neck cells in gastric pits secrete a viscous mucus layer trapping bicarbonate, creating a pH gradient (luminal pH 1-2 to near-neutral at epithelium). This shields parietal cells and mucosa from HCl diffusion.
c. HCl activation by pepsinogen
Pepsinogen from chief (peptic) cells activates to pepsin in acidic conditions, but HCl functions independently without needing activation; it directly denatures proteins. This reverses the process, making the option incorrect.
d. Bicarbonate neutralizes HCl inside cells
Parietal cells generate bicarbonate intracellularly via carbonic anhydrase, exchanging it basolaterally for chloride to maintain neutral pH during secretion, but HCl forms in the lumen post-pumping. Neutralization occurs in mucus, not directly inside cells against secreted HCl.
Gastric Protection Mechanism
Parietal cells pump H+ into canaliculi (pH ~0.8) while exporting bicarbonate, causing an “alkaline tide” in blood. The overlying mucus-bicarbonate barrier from pit cells prevents back-diffusion of luminal HCl. Disruptions lead to ulcers, highlighting mucus as primary defense. For CSIR NET aspirants, focus on this multilayer protection: intracellular pH homeostasis plus extracellular mucus shield.
