Organic and aqueous extraction of lipids from birch pollen grains exposed to gaseous pollutants.

Abstract

The lipid fraction of birch pollen grains (BPGs) is not yet fully described, although pollen lipid molecules may play a role in the allergic immune response. The mechanisms by which atmospheric pollutants modify allergenic pollen grains (PGs) are also far from being elucidated despite high potential effects on allergic sensitization. This work is a contribution to a better description of the lipid profile (both external and cytoplasmic) of BPGs and of alterations induced by gaseous air pollutants. Several lipid extractions were performed using organic and aqueous solvents on BPGs following exposure to ozone and/or nitrogen dioxide and under conditions favoring the release of internal lipids. Ozone reacted with alkenes to produce aldehydes and saturated fatty acids, while nitrogen dioxide was shown to be unreactive with lipids. NO2 exhibited a protective effect against the reactivity of alkenes with ozone, probably by competition for adsorption sites. The decreased reactivity of ozone during simultaneous exposure to NO2/O3 raised the possibility of a Langmuir-Hinshelwood mechanism. Oxidation reactions induced by exposure of BPGs to ozone did not substantially modify the extraction of lipids by aqueous solvent, suggesting that the bioaccessibility of lipids was not modified by oxidation. On the contrary, the rupture of PGs appeared to be a key factor in enhancing the bioaccessibility of bioactive lipid mediators (linoleic and α-linolenic acids) in an aqueous solution. The internal lipid fraction of BPGs has specific characteristics compared with external lipids, with more abundant hexadecanoic acid, tricosanol, and particularly unsaturated fatty acids (linoleic and α-linolenic acids). Several mechanisms of action of gaseous pollutants on allergenic pollen were identified in this study: gaseous air pollutants can (i) modify the external lipid fraction by reactivity of alkenes, (ii) adsorb on the surface of PGs and be a source of oxidative stress after inhalation of PGs, and (iii) promote the release of cytoplasmic bioactive lipids by facilitating pollen rupture.