Sublethal effects of esfenvalerate pulse-exposure on spawning and non-spawning Australian crimson-spotted rainbowfish (Melanotaenia fluviatilis)
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The spawning activity of the Australian crimson-spotted rainbowfish (Melanotaenia fluviatilis) was monitored over a period of nine days. After the first three days, groups of rainbowfish were pulse-exposed with the pyrethroid insecticide esfenvalerate at one of six nominal concentrations (0, 1, 3.2, 10.0, 32.0, or 100 μ/L). The effects of esfenvalerate on fecundity, total hatch, hatchability of eggs, frequency of hatch defects, and the survival and growth of subsequent larvae were monitored. Hepatic cytochrome P-450 activity (ECOD, EROD, EFCOD) was measured six days post-exposure in controls and fish exposed to 32 μg/L esfenvalerate. Cytochrome P-450 activity was also measured in single sex populations of male and female rainbowfish similarly exposed. The effects of esfenvalerate pulse-exposure on the lymphoproliferation of immune cells isolated from spawning and non-spawning groups of rainbowfish were examined in a second experiment.
Over 75% of fish pulse-exposed to 100 μg/L esfenvalerate died, and males in all treatments were more strongly affected than females. There was a negative correlation between pesticide concentration, fecundity, and total hatch. All eggs laid in the first three days post-exposure failed to hatch in some treatments, although esfenvalerate pulse-exposure did not increase the prevalence of deformed larvae. Esfenvalerate pulse-exposure significantly increased hepatic ECOD activity in male rainbowfish but had no effect on male EROD or EFCOD activities. There was no significant effect of esfenvalerate pulse-exposure on hepatic EROD, ECOD, or EFCOD activities of female rainbowfish. Unstimulated lymphocyte proliferation was lower in treated female rainbowfish than non-exposed female fish, and there was some evidence of an interaction with spawning activity.
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