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Bioaccumulation and Metabolic Effects of the Endocrine Disruptor Methoprene in the Lobster, Homarus americanus1
Integrative and Comparative Biology, Feb 2005 by Walker, Anna N, Bush, Parshall, Puritz, Jonathan, Wilson, Thomas, Et al
Regarding decapod crustaceans, McKenney and Matthews (1990) showed that concentrations of 1 ppm methoprene were uniformly fatal to the larvae of Palaemonetes pugio while 0.1 ppm greatly reduced the number of larvae able to complete metamorphosis. Christiansen et al. (1977) reported that 1 ppm methoprene was acutely toxic to the larvae of Rhithropanopeus harrisii, but these investigators did not find harmful effects at 0.1 ppm methoprene under normal conditions of temperature and salinity. Other studies, however, revealed that this lower concentration did produce adverse effects if coupled with sub-optimal temperature and salinity (Payen and Costlow, 1977; McKenney and Matthews, 1990; Celestial and McKenney, 1994). Additional work by McKenney and Celestial (1993) on larval Palaemonetes pugio showed that 8 ppb methoprene affected growth and inhibited the completion of metamorphosis.
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McKenney and Celestial (1996) found that the juvenile forms of the estuarine mysid Mysidopsis bahia suffered complete mortality when exposed to methoprene concentrations of 125 ppb and exhibited diminished size and subsequent fecundity when reared in concentrations of methoprene as low as 8 ppb. Chu et al. (1997) found an LD50 of 0.34 ppm methoprene at 48 hr for the freshwater cladoceran Moina macrocopa; they also found that levels of 5-10 ppb actually stimulated reproduction. Ting et al. (2000) found thai exposure of the naupliar forms of the harpacticoid copepod Tigriopus califomicus to 10 ppb methoprene resulted in subsequent disruption of mate recognition, a process known to be under endocrine control. Studies by AhI and Brown (1990) demonstrated delayed ecdysis and molt-related mortality in brine shrimp larvae (Anemia sp.) exposed to 0.3 ppm methoprcnc.
These last investigators also found that methoprene had a stimulatory effect on Na/K ATPase activity in Artemia (AhI and Brown, 1991). They suggested that the mechanism of action involved direct binding of the pesticide to regulatory sites on the enzyme causing changes in conformation. Due to its hydrophobic structure, methoprene could also lodge in membranes and modify the lipid environment adjacent to enzymes leading to altered conformation and therefore activity. Subsequent studies by Lovett et al. (2001) in the green crab Carcinus maenas indicated that MF itself plays a role in osmoregulation.
In our studies of the blue crab (Callinectes sapidus), we found that methoprene, in keeping with its hydrophobic nature, could penetrate the investment coat of the blue crab embryo and localize in lipovitellin. Exposure of the embryos to environmental concentrations of methoprene resulted in an overall reduction in the number of successful hatchings and in lethargic swimming behavior on the part of the newly hatched survivors (zoea larvae). Moreover, in later larval forms (megalopae), methoprene delayed the molt to the first crab form and resulted in death of 80% of larvae after exposure for 10 days. It was our conclusion that blue crab larvae exposed to methoprene could either die as a direct result of metamorphic disruption or be compromised in their ability to swim such that they were vulnerable to increased predation (Horst and Walker, 1999).
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