The primary objective of this study was to determine whether cadmium (Cd) exposures alter reproduction in fathead minnows (Pimephales promelas). Pairs of sexually mature minnows were exposed to waterborne Cd at 0, 12.5, 25, or 50 μg/L for 21 days. During this exposure period, the reproductive success of pairs was assessed. Following the exposure, gonadosomatic index (GSI), male secondary sexual characteristics, male plasma 11-ketotestosterone (11-KT) concentrations, and female plasma estradiol (E 2 ) concentrations were determined. Results of this study show that Cd exposures impair reproduction in fathead minnows. Pairs exposed to 50 μg/L experienced a significant decline in spawning frequency and fecundity relative to unexposed minnows. Cd exposures also caused alterations in male secondary sexual characteristics, as males exposed to 25 μg/L had significantly fewer nuptial tubercles than controls. Furthermore, males exposed to 12.5 μg/L Cd experienced a significant increase in plasma 11-KT concentrations relative to controls. No alterations in GSI or female plasma E 2 concentrations were observed.Cadmium (Cd) is a common environmental pollutant that poses a significant threat to the health of aquatic ecosystems due to its persistent release through anthropogenic activities such as mining and smelting operations (Henson and Chedrese 2004). Cd concentrations in the water range from background levels of 1 μg/L to 400 μg/L in contaminated sites (Tilton et al. 2003). Like many heavy metals, Cd has a long half-life and can bioaccumulate over time in various organs including the liver, kidneys, testes, and ovaries (Henson and Chedrese 2004). The effects of Cd on the health of freshwater fish have been well studied especially with regard to survival (Benoit et al. 1976;Middaugh and Dean 1977;Hwang et al. 1995), calcium ionoregulation (Roch and Maly 1979;Wendelaar Bonga and Lock 1992), and skeletal development (Muramoto 1981;Cheng et al. 2000). However, fewer studies have investigated the effects of Cd exposure on the reproductive success of fishes despite evidence that Cd can act as a reproductive toxin (Signhal et al. 1985) and endocrine disruptor (Henson and Chedrese 2004).Studies have shown that exposure to Cd damages gonads and impairs gametogenesis. The testes appear to be particularly sensitive to Cd exposures. Several studies have shown that Cd causes testicular apoptosis and necrosis (Singhal et al. 1985;Das 1988). Exposure to 10 mg/ L Cd increases capsase 3 gene expression, an indicator of apoptosis, in the testes of black gobies (Gobius niger) (Migliarini et al. 2005). Male and female Asian cyprinids (Labeo bata) exposed to a range of Cd concentrations (1-15 mg/L) for four months experienced reductions in gonadosomatic index (GSI) relative to unexposed fish (Das 1988). In addition, the testes of exposed males lacked spermatids and spermatozoa, while the ovaries of exposed females In addition to alterations in gametogenesis, exposure to Cd has been shown to alter steroidogenesis. For example, female ...