Female fathead minnows (Pimephales promelas) exposed to copper (Cu) maternally transfer Cu tolerance to their larval offspring. Larvae produced after female parents received a sublethal 5-d, 100 µg/L Cu exposure had significantly greater survivorship in potentially lethal Cu solutions than larvae produced before those females were exposed to Cu.

Swim performances of male and female fathead minnows (Pimephales promelas) from three different suppliers were determined before and after an 8- to 9-d exposure to 175 microg/L copper (Cu). The reduction in swim performance (delta) due to the Cu exposure varied widely among individual fish, but was surprisingly consistent from one supplier to the next and between males and females. Genetic analysis of the individuals revealed significant correlations between delta and genotypic variation at the glucosephosphate isomerase-1, phosphoglucomutase-1, and lactate dehydrogenase-2 enzyme loci. Based upon delta, the most Cu-resistant fathead minnows were bred together, as were the most Cu-susceptible individuals and two groups of unselected minnows. Larvae produced by each group of adults were subjected to a survival test. The median lethal concentration (LC50) for larvae produced by Cu-resistant adults was significantly greater than the LC50s for the control groups. Surprisingly, the LC50 for the larvae produced by Cu-susceptible adults was also significantly greater than the LC50s for the control groups, but not significantly different from the larvae produced by Cu-resistant parents. While Cu tolerance has a genetic component in fathead minnows, the Cu tolerance of larval fish appears to be influenced by nongenetic as well as genetic factors.