Airborne Compositae dermatitis: monoterpenes and no parthenolide are released from flowering Tanacetum parthenium (feverfew) plants.

The air around intact feverfew (Tanacetum parthenium) plants was examined for the presence of airborne parthenolide and other potential allergens using a high-volume air sampler and a dynamic headspace technique. No particle-bound parthenolide was detected in the former. Among volatiles emitted from the aerial parts of feverfew plants and collected by the dynamic headspace technique a total of 41 compounds, mainly monoterpenes, were identified and quantified by GC and GC-MS. Alpha-Pinene, camphene, limonene, gamma-terpinene, (E)-beta-ocimene, linalool, p-cymene, (E)-chrysanthenol, camphor and (E)-chrysanthenyl acetate were the predominant monoterpenes accounting for nearly 88% of the total volatiles emitted. The average total yield of volatiles emitted over 24 h was 18,160 ng/g fresh weight of leaves and flowers, corresponding to the emission of approximately 8 mg volatiles per day from one full-grown feverfew plant. No parthenolide or other sesquiterpene lactones were detected. The present investigation does not support the theory of airborne sesquiterpene lactone-containing plant parts or of direct release of sesquiterpene lactones from living plants as the only explanations for airborne Compositae dermatitis. Potential allergens were found among the emitted monoterpenes and their importance in airborne Compositae dermatitis is discussed.

DNA methylation is involved in maintenance of an unusual expression pattern of an introduced gene.

In one of 30 transgenic tobacco (Nicotiana tabacum) plants, the expression of an introduced beta-glucuronidase (GUS) gene driven by the cauliflower mosaic virus 35S promoter, was found to be repressed as the plant matured, whereas the endogenous GUS activity was unaffected. Plants grown from seeds or regenerated from leaf discs derived from this plant showed a similar temporal pattern of expression. Suspension-cultured cells established from nonexpressing leaves did not express the introduced gene. In these cells, the silent gene could be reactivated by treatment for 5 or 10 days with 5-azacytidine. Overall, demethylation of the genome preceded recovery of the enzyme activity. The increase in the fraction of reactivated cells progressed in two phases. Up to 8 weeks after starting the 5-azacytidine treatment, approximately 2 to 4% of the cells were expressing GUS, followed by a dramatic increase of GUS-expressing cells. Thirteen weeks after starting the 5-azacytidine treatment, the fraction of GUS-expressing cells amounted to 80%. At this time, the original overall level of DNA methylation was reestablished. The degree of DNA demethylation, as well as the magnitude of reactivation, was dependent on the duration of the 5-azacytidine treatment. These results demonstrate that DNA methylation appears to be involved in the regulation of the introduced GUS gene and that this development-dependent pattern of expression can be inherited.