Arachidonic Acid
Also written as COX, LOX.
(c) Arachidonic acid is a relatively non essential fatty acid
What our notes say
- (c) Arachidonic acid is a relatively non essential fatty acid (bchem EOY 2014 (2) — Past Paper Questions & Answers)
- Arachidonic acid metabolites — prostaglandins (via cyclo-oxygenase: vasodilatation, pain, fever), leukotrienes (via lipoxygenase: LTB4 is chemotactic, LTC4/D4/E4 cause bronchoconstriction and permeability). (General & Systemic Pathology SAQ Paper II — 15 July 2025 (MBPA 3500, MKU Year 3,)
- Eicosanoids are lipid mediators derived from arachidonic acid and include prostaglandins, leukotrienes, and thromboxanes. (Endocrine LAqs and SAqs)
- Eicosanoids are derived from arachidonic acid (a polyunsaturated fatty acid, 20:4), which is the primary precursor for this hormone class. (LECTURE 1: Principles of Endocrinology)
- | Aspirin / NSAIDs | COX blocked → arachidonic acid shunted to lipoxygenase → ↑ leukotrienes → bronchoconstriction and inflammation | (Bronchial Asthma: Pathophysiology, Diagnosis and GINA Stepwise Management)
- Prostaglandins (from arachidonic acid via COX pathway) — cause vasodilation and potentiate pain/fever (Pathology Mechanisms: Inflammation, PE, & Impaired Healing)
Study material on Arachidonic Acid
- Pharmacology CRASH Course
- ONCOPATHOLOGY - 30 KEY SHORT ANSWER QUESTIONS Hallmarks 1,2 & 3
- Cat. Pathology: Acute Inflammation, Mediators & Pulmonary Embolism
- Hallmarks of Cancer: Molecular Basis, Cell Cycle & Oncogenes
- Platelet Disorders
- LECTURE 1: Principles of Endocrinology
- Inflammation and Tissue Repair - MCQs
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Practice questions on Arachidonic Acid
In studying arachidonic acid metabolism, a researcher finds that alternatively activated (M2) macrophages produce different lipid mediators than classically activated (M1) macrophages. What explains the transition from pro-inflammatory to anti-inflammatory lipid mediators?
- Increased COX-1 expression replacing COX-2
- Switch from leukotriene to lipoxin production
- Enhanced thromboxane synthesis
- Reduced phospholipase A2 activity
- Increased 5-lipoxygenase activity
Answer: B. The switch from leukotrienes (pro-inflammatory) to lipoxins (anti-inflammatory) is a key mechanism for terminating inflammation. Lipoxins are generated from arachidonic acid by the lipoxygenase pathway (like leukotrienes) but have opposite effects - they inhibit neutrophil chemotaxis and adhesion. This represents an active termination mechanism. Lipoxins require transcellular biosynthesis - neutrophils make precursor
Which enzyme releases arachidonic acid from cell membrane phospholipids, initiating eicosanoid synthesis?
- Cyclooxygenase (COX)
- Phospholipase A2
- Lipoxygenase
- Thromboxane synthase
Answer: B. Phospholipase A2 is the enzyme that cleaves arachidonic acid from membrane phospholipids. This is the first and crucial step in eicosanoid biosynthesis, occurring during inflammation, allergy, and cell injury. The released arachidonic acid is then metabolized by COX or lipoxygenase pathways. ---
The conversion of arachidonic acid to prostagladins and thromboxanes is mediated by? ---
- Lipoxygenase
- Cyclooxgenase(s)
- Phospholipase A2
- Diacylglycerollipase(s)
- Cytochrome P450
Answer: A.