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International Journal on Algae
SJR: 0.219 SNIP: 0.261 CiteScore™: 0.24

ISSN Imprimir: 1521-9429
ISSN En Línea: 1940-4328

International Journal on Algae

DOI: 10.1615/InterJAlgae.v16.i1.70
pages 95-105

The Growth Response of Prorocentrum minimum Pavill. (Dinophyta) to Karlotoxin Exposure

G. Ozbay
Delaware State University, Department of Agriculture and Natural Resources, 1200 North Dupont Highway, Dover, Delaware 19901, USA
Sh. S. Chambliss
Delaware State University, Department of Agriculture and Natural Resources, 1200 North Dupont Highway, Dover, Delaware 19901, USA
G. H. Wikfors
National Oceanic and Atmospheric Administrations (NOAA), National Marine Fisheries Service Center, Milford Laboratory, Milford, Connecticut 06460, USA
J. E. Adolf
University of Hawaii Hilo, Hilo, Hawaii 96729, USA
L. K. Chintapenta
Delaware State University, Department of Agriculture and Natural Resources, 1200 North Dupont Highway, Dover, Delaware 19901, USA
A. R. Place
University of Maryland Biotechnology Institute, Institute of Marine and Environmental Technology, Columbus Center, Baltimore, MD 21202, USA

SINOPSIS

Extracellular metabolites produced by harmful algae can act as growth-inhibiting agents for other phytoplankton species, influencing species competition and succession and hence affecting structure of the plankton community. Karlodinium veneficum Ballant., a cosmopolitan estuarine dinoflagellate, produces toxic compounds known as karlotoxins that exhibit sterol-dependent, cytotoxic activity and are frequently associated with fish kills. Karlotoxin-sensitive cells tend to have desmethyl sterols as predominant cellular sterols, and karlotoxin-resistant cells have 4-methyl sterols as dominant sterols. The allelopathic effects of karlotoxins on other algae have been described, but the question of whether or not K. veneficum is allelopathic against Prorocentrum minimum, a common co-occurring dinoflagellate, is unknown. We determined the sterol profiles of two different Chesapeake Bay strains (RR4B1 and IB) of P. minimum and also exposed them to different concentrations of karlotoxin extracted from K. veneficum cells. The strains, RR4B1 and IB, experienced mortality at high toxin concentrations, i.e., 256 ng mL−1. After 24 hours of exposure, cell counts declined resulting in calculated "negative growth rates" of −1.17 (d−1) for RR4B1 and −0.45 (d−1) for strain IB. This shows that karlotoxin is lethal to P. minimum at high concentrations irrespective of sterol profiles that include substantial quantities of 4-methyl sterols.


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