Effects of salinity and two coastal waters on the growth and toxin content of the dinoflagellate Alexandrium minutum

Author: Grzebyk Daniel  

Publisher: Oxford University Press

ISSN: 1464-3774

Source: Journal of Plankton Research, Vol.25, Iss.10, 2003-10, pp. : 1185-1199

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Abstract

The dinoflagellate Alexandrium minutum strain AM89BM was studied to investigate its capacity to adapt to different salinities and the influence of salinity on cellular content of paralytic shellfish toxins (PST), in batch culture in enriched offshore seawater media. The strain shows optimal growth (average rate ≥0.5 div day−1) at salinities between 20 and 37 p.s.u., peaking at 25 p.s.u. (0.63 ± 0.07 div day−1). Under a high NO3:PO43– mole ratio (76), cell PST content increased during growth phase, peaking toward the end of growth phase or in the early stationary phase. The PST content was low (∼10 fmol PST cell−1) from 30 to 37 p.s.u., but it increased at lower salinities, with the maximum value (∼50 fmol PST cell−1) recorded at 15 p.s.u. We then compared growth rate and toxin content of A. minutum cells grown in 3- and 0.2-m filtered estuarine water (27 p.s.u.), and a similarly filtered seawater collected from an oyster farming area (36 p.s.u.), with a N- and P-enriched offshore seawater (37 p.s.u.). In both estuarine water treatments, growth was fast (≥0.8 div day−1) and the cell PST content increased only in the early growth phase, peaking in mid-growth phase at 9.56 ± 1.06 and 7.63 ± 0.44 fmol PST cell−1 in the 3- and 0.2-m filtered waters, respectively. In the 3-m filtered oyster farm water, although inorganic nutrient concentrations were very low, A. minutum grew well (0.68 ± 0.06 div day−1), suggesting mixotrophic nutrition; as PST production was nearly zero, the cell toxin content decreasing to 1.11 fmol PST cell−1, we hypothesize that toxin biosynthesis was greatly weakened due to the lack of amino acid precursors in prey material. In the offshore seawater, A. minutum grew slowly (0.18 ± 0.04 div day−1) and cells lost toxins down to 1.08 fmol PST cell−1, suggesting that growth was limited and PST production stopped due to the lack of some vitamins, and/or trace metals.