Biochemistry—Cyclooxygenase-1 (COX-1) and Physiology How is the enzyme COX-1 important for human health under normal conditions?

Introduction / Context:
Cyclooxygenases (COX-1 and COX-2) convert arachidonic acid into prostaglandin H2, the precursor of diverse prostanoids. COX-1 is constitutively expressed in many tissues and supports homeostatic functions, including gastric mucosal protection. Understanding COX-1 roles explains both therapeutic benefits and side effects of nonsteroidal anti-inflammatory drugs (NSAIDs).

Given Data / Assumptions:

• COX-1 is a constitutive cyclooxygenase active under basal conditions.
• Prostanoids derived from COX-1 support mucus and bicarbonate secretion and regulate gastric blood flow.
• Aspirin and many NSAIDs inhibit COX activity, reducing prostaglandin synthesis.

Concept / Approach:
Identify the specific physiological function linked to COX-1 rather than general cellular processes. The maintenance of gastric mucosa via prostaglandins is the classical COX-1 function; blocking COX-1 may compromise the stomach lining and increase ulcer risk, particularly with chronic NSAID use.

Step-by-Step Solution:

Verification / Alternative check:
Clinical observations: nonselective NSAIDs that inhibit COX-1 and COX-2 can cause gastric irritation and ulcers, consistent with loss of COX-1-derived protective prostaglandins.

Why Other Options Are Wrong:

• CO2 transport is mediated by carbonic anhydrase and hemoglobin buffering, not COX-1.
• DNA synthesis involves polymerases and nucleotide metabolism, not COX-1.
• Aspirin is an acetylating inhibitor of COX; COX-1 is not a derivative of aspirin.
• Heme catabolism to biliverdin involves heme oxygenase, not COX-1.

Common Pitfalls:
Conflating COX-1 and COX-2 roles; assuming all eicosanoid pathways are interchangeable without tissue-specific functions.

Final Answer:
It catalyzes formation of prostaglandins that help maintain the stomach lining