Tartrazine and the prostaglandin system.

Area of Science:

• Biochemistry
• Pharmacology
• Immunology

Background:

• Aspirin-sensitive asthma is a condition where nonsteroidal anti-inflammatory drugs (NSAIDs) trigger asthma symptoms.
• Tartrazine, a common food dye, has been anecdotally linked to asthma exacerbations in sensitive individuals.
• The mechanism underlying potential tartrazine sensitivity in asthma remains unclear.

Purpose of the Study:

• To investigate the effect of tartrazine on prostaglandin production.
• To determine if tartrazine inhibits cyclooxygenase (COX) activity, a key enzyme in prostaglandin synthesis.
• To elucidate the potential mechanism of cross-sensitivity between tartrazine and aspirin in aspirin-sensitive asthma.

Main Methods:

• In vitro evaluation of tartrazine's effect on prostaglandin production.
• Assays using sheep seminal vesicles, guinea pig lung microsomes, and human platelets to measure cyclooxygenase activity.
• Assessment of tartrazine's impact on acyl hydrolase activation, the rate-limiting step in prostaglandin synthesis.
• Analysis of the effect of sulfanilic acid, a major tartrazine metabolite, on cyclooxygenase.

Main Results:

• Tartrazine did not inhibit cyclooxygenase activity in any of the tested in vitro systems.
• Tartrazine did not affect the activation of acyl hydrolase.
• Sulfanilic acid, the primary metabolite of tartrazine, also showed no inhibitory effect on cyclooxygenase.

Conclusions:

• Tartrazine does not appear to inhibit prostaglandin production via cyclooxygenase inhibition.
• The findings suggest that prostaglandin inhibition is unlikely to be the mechanism for any cross-sensitivity between tartrazine and aspirin in aspirin-sensitive asthmatics.