15-Hydroperoxyabietic acid (15-HPA) has been isolated from Portuguese colophony of the gum rosin type and identified as its methyl ester. The structure of the compound was elucidated using UV, IR, NMR and mass spectrometry. 15-HPA methyl ester was found to be an elicitor when tested in colophony-sensitized guinea-pigs. The sensitizing capacity was verified in the same species and 15-HPA methyl ester was considered to be a strong allergen. The eliciting potential was also verified in patients with known allergy to colophony. The Portuguese gum rosin investigated contained approximately 1% of 15-HPA. Based on its allergenicity and the amounts isolated, we conclude that 15-HPA is a main contact allergen in Portuguese gum rosin.

In order to investigate whether abietic acid itself is the allergenic component of colophony, 2 commercial samples were extensively purified and tested in guinea pigs and in colophony-sensitive patients. In the modified FCAT method, sensitization was obtained with Portuguese colophony and when challenged with purified abietic acid, the animals showed no reaction. In the GMPT method, the animals were exposed to purified abietic acid. Challenging with 2 different samples of it gave no significant reaction. When patch tested, patients sensitive to colophony showed no reactions to abietic acid which had been purified immediately before the test. It is concluded that abietic acid itself is not a contact allergen.

Membrane lipids of green plants digalactosyldiacylglycerol (DGalDG) and monogalactosyldiacylglycerol (MGalDG) are hydrolyzed in vitro by human duodenal contents, pancreatic juice and bile salt stimulated lipase and guinea pig and rat pancreatic lipase-related protein 2 to free fatty acids, di- and monogalactosylmonoacylglycerols and water soluble galactose-containing compounds. The fate of intermediate products is unknown. We have investigated the digestion and absorption of DGalDG in rats. [3H]- and [14C]-labeled DGalDG in galactolipid dispersions, and 200 g/L soybean triacylglycerol (TG) oil-galactolipid emulsions of different concentrations were fed orally to intact and lymphatic duct cannulated rats. Chyle, gastrointestinal tract, liver and plasma were analyzed for radioactivity in different lipid classes. Recovery of [3H] also was determined in feces. Comparison was made with an emulsion of [14C]dipalmitoyl-phosphatidylcholine ([14C]DPPC), soybean TG oil and soybean phosphatidylcholine (PC). Less than 2% of the radioactivity in chyle was found in DGalDG, >70% of the radioactivity in triacylglycerol (TG), and the remaining part in glycerophospholipids. In intact rats, <1.5% of radioactivity in liver and plasma was identified as DGalDG. In experiments where 120 mg galactolipid-phospholipid mixture or 120 mg PC were given in a soybean TG oil-emulsion, the absorption of galactolipid fatty acids was less complete than PC-fatty acids, as indicated by analysis of feces and intestinal contents. Galactolipids are not absorbed intact or as reacylated monoacyl compounds by rats.

Pretreatment of human leukocytes with the new xanthine compound, 3,7-dihydro-1,8-dimethyl-3-phenyl-1H-purine-2,6-dione (D 4026), induced a dose-dependent and statistically significant inhibition of immunoglobulin E-mediated histamine release in the concentration interval 0.1-1000 microM. Histamine release elicited with suboptimum amounts of the triggering agent (anti-IgE or antigen) was inhibited to a greater extent than a release initiated with optimum amounts. At a concentration of 10 microM, D 4026 had at least the same inhibitory effect as 100 microM theophylline. When leukocytes were incubated simultaneously with D 4026 and a histamine H-2 receptor-stimulating drug (histamine or clonidine), the two drugs combined induced an inhibition significantly greater than the sum of their individual inhibitory effects. Only pure additive inhibitory effects were, however, obtained during simultaneous treatment of leukocytes with theophylline and histamine.

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