beta-carotene and citral

This study was done to determine whether retinoic acid can be produced by excentric cleavage of beta-carotene in vivo. By using an inhibitor of retinaldehyde oxidation, citral, either retinaldehyde or beta-carotene was incorporated in a micellar solution and perfused through the upper portion of small intestine of ferrets. After 2 h perfusion of 1 microM retinaldehyde, retinoic acid rose in portal blood (+3.5 +/- 1.3 nmol/L) and was detected in the intestinal mucosa (30 +/- 2 pmol/g). When citral was added at 2 mM along with retinaldehyde, retinoic acid decreased in the portal blood and retinoic acid was not detected in the intestinal mucosa. With or without the presence of citral (2 mM), the perfusion of beta-carotene (10 microM) during 2 h caused a significant rise of retinoic acid in portal blood (+2.6 +/- 0.6 nmol/L and + 4.1 +/- 0.6 nmol/L, respectively) and in liver; moreover, significant amounts of retinoic acid were detected in the intestinal mucosa (19 +/- 3 pmol/g and 36 +/- pmol/g, respectively. This study demonstrates that after intestinal perfusion of beta-carotene in the ferret in vivo, a substantial amount of retinoic acid is formed via an excentric cleavage pathway.

Topics: Acyclic Monoterpenes; Animals; beta Carotene; Chromatography, High Pressure Liquid; Ferrets; Intestinal Absorption; Intestinal Mucosa; Intestine, Small; Liver; Male; Methylation; Monoterpenes; Retinaldehyde; Terpenes; Tretinoin; Vitamin A

The hypothesis that retinoic acid (RA) is produced from the excentric cleavage of beta-carotene was tested in human intestinal homogenates in vitro. Significant amounts of RA were identified by HPLC and derivatization after incubation of intestinal mucosal homogenates with retinal, beta-carotene, or beta-apocarotenals at 37 degrees C for 60 min. RA formation was inhibited, in a dose-dependent fashion, when retinal was incubated in the presence of 0.1-3.0 mM citral (3,7-dimethyl-2,6-octadienal) under identical experimental conditions. The formation of RA from both beta-carotene and beta-apocarotenals was dose and time dependent and RA was the major metabolite of both beta-apo-8'-carotenal and beta-apo-12'-carotenal after the incubation. However, citral (0.1 to 4 mM) did not inhibit the formation of beta-apocarotenals and RA from 2 microM beta-carotene (P greater than 0.05), which proves the existence of an excentric cleavage mechanism for beta-carotene conversion into retinoids. Furthermore, RA formation from both beta-apo-8'-carotenal and beta-apo-12'-carotenal in human intestinal homogenate occurred in the presence of citral, which demonstrates that RA can be produced from excentric cleavage of beta-carotene via a series of beta-apocarotenals as intermediates.

Topics: Acyclic Monoterpenes; beta Carotene; Binding, Competitive; Carotenoids; Humans; Hydrolysis; In Vitro Techniques; Intestinal Mucosa; Monoterpenes; Terpenes; Tretinoin

Topics: Acyclic Monoterpenes; Alcohol Dehydrogenase; Aldehydes; beta Carotene; Carotenoids; Daucus carota; Glycosides; Monoterpenes; Plant Roots; Terpenes