Concept:
Aspirin thins the blood by stopping platelets from making the chemical (thromboxane A2) that makes them clump together. The key is how aspirin chemically alters the enzyme involved.
Step 1: Platelets use the enzyme cyclooxygenase-1 (COX-1) to produce thromboxane A2, a strong promoter of platelet aggregation.
Step 2: Aspirin transfers its acetyl group onto a serine residue in COX-1, acetylating the enzyme. This block is irreversible — and since platelets have no nucleus to make new enzyme, the effect lasts the platelet's whole lifespan (about 7–10 days).
Why the others are wrong: Salicylic acid, acetic acid and gentisic acid are just breakdown/metabolic products of aspirin; they are not the cause of the antiplatelet action. The antiplatelet effect comes specifically from acetylation of COX-1.
Answer: Option (3) — Acetylates of COX-1 enzyme.