Disruption of Artemia Development by Metals
Development of the brine shrimp is influenced by low concentration of several metals with the extent of disruption, determined by hatching inhibition after seventy two hours of metal exposure, depending on the type of metal and its concentration. Mercury toxicity is generally enhanced by organic derivation, however larger mercury compounds such as diphenylmercury exert less effect on Artemia development. The decline of toxicity in relation to increased size of organic mercury compounds may reflect reduced movement of the toxic compounds through cell membranes. All metals examined enter the developing organisms upon rupture of the cyst shell and may, if in sufficient concentration, delay or prevent emergence and hatching. In some cases, incompletely emerged organisms hatch while still enclosed in the cyst shell, demonstrating that completion of early developmental processes is not a prerequisite for later events. The delayed reversion of metal poisoning suggests brine shrimp are able to sequester intracellular metals, perhaps by induced synthesis of metal-binding proteins such as the metallothioneins. We have tested cloned metallothionein genes from mouse, Neurospora and Drosophila for their ability to hybridize to Southern blots of restriction-digested Artemia DNA. Our preliminary results reveal that the Drosophila metallothionein gene, cDM51, binds to Artemia DNA under moderately stringent conditions. We are just beginning to clone the Artemia genes for metallothionein or other metal-binding proteins as one approach to develop a bioassay for metals in the marine environment.