Selenium (Se) is an essential trace element to most living organisms, however when compared to other ingested essential trace elements Se has the lowest margin of safety between essential and toxic concentrations. Oviparous vertebrates, especially fishes, are highly susceptible to dietary Se toxicity. Greater incidences of deformities and/or mortalities have been observed in F1 generation larval fishes whose parents were exposed to excess dietary Se in the form of selenomethionine (SeMet), however little information is available on effects of chronic dietary SeMet exposure to adult fish and persistent effects of in ovo SeMet exposure to F1 generation fish. This thesis investigated effects of chronic dietary exposure of excess Se in the form of SeMet on swimming performance (Ucrit), oxygen consumption (MO2), stored energy (triglycerides and glycogen), and the physiological stress response (cortisol production) in adult zebrafish (Danio rerio), as well as immediate (incidence of deformities and mortality) and persistent (e.g. changes in Ucrit, MO2, bioenergetics, the physiological stress response and reproduction) effects of in ovo exposure to SeMet in F1 generation zebrafish. In addition, the study investigated potential underlying mechanisms of SeMet-induced developmental toxicities in early life stages of zebrafish using embryo microinjection. Two separate dietary SeMet exposure studies in adult zebrafish and two in ovo SeMet maternal transfer studies in F1 generation zebrafish were conducted. The first dietary or in ovo exposure study explored effects of excess SeMet exposure on adult zebrafish or the entire life cycle of F1 generation zebrafish. The second study investigated mechanisms of observed SeMet-induced effects on adult or F1 generation zebrafish. In the first feeding study, a significant reduction in Ucrit and greater accumulation of stored energy were observed in the excess dietary SeMet exposed groups when compared to the Se-sufficient dietary control group. The second feeding study showed a greater metabolic rate, and impaired aerobic energy metabolism and triglyceride homeostasis in adult fish fed excess dietary SeMet, which was associated with a reduction in swimming performance and accumulation of triglycerides. Embryos collected from adult zebrafish in both dietary SeMet exposure studies were used to investigate effects of in ovo SeMet exposure on the entire life cycle of F1 generation fish. The first study showed a greater incidence of mortality, an increasing trend for deformities in F1 generation larval zebrafish, and reduced Ucrit in F1 generation adult fish exposed to excess SeMet via in ovo maternal transfer. However, concentrations of stored energy, cortisol and reproduction were unaltered. The second study found that impaired aerobic performance might have been responsible for the reduction in Ucrit of F1 generation adult zebrafish exposed to excess SeMet. Since there is a high variability in Se deposition among eggs via natural maternal transfer, SeMet embryo microinjection was adopted to mimic maternal transfer and to investigate potential mechanisms of SeMet-induced developmental toxicities in early life stages of zebrafish. Greater gene expression of oxidant-inducible transcription factors and impairment in gene expression of an enzyme involved in methionine catabolism were observed in early life stages of zebrafish exposed to excess SeMet via in ovo microinjection. The research presented in this thesis suggests that environmentally relevant dietary SeMet exposure can alter physiological responses in adult fishes and reduce survivability of F1generation fishes, which could impact fitness and recruitment of wild fishes inhabiting Se-contaminated aquatic ecosystems. In addition, the study suggests that SeMet-induced developmental toxicities in early life stages of fishes might be related to oxidative stress or impaired methylation, or a combination of these mechanisms.