Abstract
Treatment of the microalga Porphyridium cruentum with salicylhydroxamic acid (SHAM) inhibited growth and affected fatty acid composition. At a relatively low concentration (40 μM) SHAM predominantly inhibits Δ6 desaturation. The effect of the inhibitor was most intense in phosphatidylcholine (PC) and phosphatidylethanolamine, in which the proportions of the downstream products of the Δ6 desaturase were reduced, whereas that of the substrate, 18:2, increased. As a result of the availability of 18:2, 18:3ω3, which under normal conditions is not observed, appeared predominantly in chloroplastic lipids. Pulse labeling with linoleic acid has shown that SHAM inhibits Δ6 desaturation almost immediately, suggesting an apparent inhibition of the activity of the desaturase, rather than its synthesis or that of its cofactors. Furthermore, the addition of γ-linolenic acid to SHAM-inhibited cultures relieved the inhibition. Following exposure to the inhibitor, 18:3ω3 appeared first in chloroplastic glycolipids and only later in PC, indicating that the former are the substrates for the first dedicated step of the proposed ω3 pathway in this alga.
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