nanonug
Senior Member
- Messages
- 1,709
- Location
- Virginia, USA
Here's one reason tea and coffee (which contain benzoic acid) might be bad for masto people:
1. Clin Pharmacol Ther. 1995 Apr;57(4):441-5.
Topical benzoic acid induces the increased biosynthesis of prostaglandin D2 in
human skin in vivo.
Downard CD, Roberts LJ 2nd, Morrow JD.
Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN,
USA.
BACKGROUND: Benzoic acid is one of the most commonly used preservatives in
cosmetics, foodstuffs, and drug preparations. Nonetheless, products containing
this compound frequently induce cutaneous erythema. Previous studies have
suggested that prostaglandins may mediate the cutaneous vasodilation because
ingestion of cyclooxygenase inhibitors before the application of benzoic acid
markedly diminishes this symptom. However, the prostaglandin responsible has not
been conclusively determined. Recently we showed that cutaneous erythema similar
to that associated with application of venzoic acid is induced by the topical
administration of another preservative, sorbic acid, and is mediated by the
increased biosynthesis of prostaglandin (PG)D2 in the skin. This study was
designed to determine whether the cutaneous vasodilation induced by benzoic acid
is mediated by this prostaglandin in humans.
DESIGN: Benzoic acid (10% in petrolatum) was applied to the forearms of healthy
volunteers. Blood was obtained from the antecubital vein draining the treated
site and assayed for vasodilating prostaglandins and histamine.
RESULTS: Topical application of benzoic acid to four volunteers resulted in a 29-
to 8000-fold increase in plasma levels of PGD2 and a 72- to 370-fold increase in
levels of 9 alpha,11 beta-PGF2, the stable plasma metabolite of PGD2, in blood
drawn from the antecubital vein draining the treated sites. In contrast, there
were no changes in plasma levels of other vasodilating prostaglandins, PGE2 or
prostacyclin (PGI2). Increases in levels of PGD2 and 9 alpha,11 beta-PGF2 were
not found in blood drawn simultaneously from veins in the contralateral arm,
indicating the increased biosynthesis of PGD2 from the site of benzoic acid
application. Increased formation of PGD2 in response to topical application of
benzoic acid was dose dependent over a concentration range of 0.01% to 15%. The
increased synthesis of PGD2 was not accompanied by a release of histamine,
suggesting that PGD2 was not derived from the mast cell.
CONCLUSIONS: PGD2 mediates the vasodilation associated with topical application
of benzoic acid.
PMID: 7712673
1. Clin Pharmacol Ther. 1995 Apr;57(4):441-5.
Topical benzoic acid induces the increased biosynthesis of prostaglandin D2 in
human skin in vivo.
Downard CD, Roberts LJ 2nd, Morrow JD.
Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN,
USA.
BACKGROUND: Benzoic acid is one of the most commonly used preservatives in
cosmetics, foodstuffs, and drug preparations. Nonetheless, products containing
this compound frequently induce cutaneous erythema. Previous studies have
suggested that prostaglandins may mediate the cutaneous vasodilation because
ingestion of cyclooxygenase inhibitors before the application of benzoic acid
markedly diminishes this symptom. However, the prostaglandin responsible has not
been conclusively determined. Recently we showed that cutaneous erythema similar
to that associated with application of venzoic acid is induced by the topical
administration of another preservative, sorbic acid, and is mediated by the
increased biosynthesis of prostaglandin (PG)D2 in the skin. This study was
designed to determine whether the cutaneous vasodilation induced by benzoic acid
is mediated by this prostaglandin in humans.
DESIGN: Benzoic acid (10% in petrolatum) was applied to the forearms of healthy
volunteers. Blood was obtained from the antecubital vein draining the treated
site and assayed for vasodilating prostaglandins and histamine.
RESULTS: Topical application of benzoic acid to four volunteers resulted in a 29-
to 8000-fold increase in plasma levels of PGD2 and a 72- to 370-fold increase in
levels of 9 alpha,11 beta-PGF2, the stable plasma metabolite of PGD2, in blood
drawn from the antecubital vein draining the treated sites. In contrast, there
were no changes in plasma levels of other vasodilating prostaglandins, PGE2 or
prostacyclin (PGI2). Increases in levels of PGD2 and 9 alpha,11 beta-PGF2 were
not found in blood drawn simultaneously from veins in the contralateral arm,
indicating the increased biosynthesis of PGD2 from the site of benzoic acid
application. Increased formation of PGD2 in response to topical application of
benzoic acid was dose dependent over a concentration range of 0.01% to 15%. The
increased synthesis of PGD2 was not accompanied by a release of histamine,
suggesting that PGD2 was not derived from the mast cell.
CONCLUSIONS: PGD2 mediates the vasodilation associated with topical application
of benzoic acid.
PMID: 7712673