Selenium (Se), an essential element, can bioaccumulate and become toxic. The main toxicity symptom in fish, teratogenicity, is mediated by oxidative stress; however, little is known about the effect of Se on the physiological stress response (PSR). The effects of Se on the PSR and oxidative stress parameters were investigated in rainbow trout, brook trout, and white suckers. The PSR was activated by acute and sub-chronic laboratory exposures to NaSeO3, but not exposure to environmental levels of Se. Species-specific sensitivity to Se may be explained by biochemical differences. Rainbow trout (exhibit oxidative damage with Se exposure) have greater GSH reserves (cycles with Se causing oxidative stress) than brook trout. Selenium in agricultural drain water did not accumulate to dangerous levels in white suckers, but additional stressors (e.g. pesticides) were present. Differences in sensitivity to Se may alter competitive interactions between species, changing community compositions and putting additional pressure on threatened species. / xiii, 150 leaves ; 29 cm.

Fish are exposed to multiple stressors in their environment. The interactive effects of pesticide exposure and increased temperature on the physiological stress response were investigated in a comparative field study with cold-water (whitefish, Prosopium williamsoni) and cool-water (sucker, Catostomus) fish from the Oldman River, Alberta, Canada, and in a laboratory study with rainbow trout, Oncorhynchus mykiss. Physiogical stress indicators were measured, and exposure to pesticides was estimated using acetylcholinesterase (AChE) inhibition. Species-specific differences in AChE activities and responses of the physiological stress axis were detected in whitefish and suckers, suggesting that whitefish are a more sensitive species to temperature and pesticide stress. In vivo Dimethoate exposure inhibited AChE activity in various tissues and disrupted the physiogical stress response. Commercial Dimethoate, in vitro, caused a decrease in viability and cortisol secretion while pure grade Dimethoate did not. The results from this study can be used in predictions of fish vulnerability to stress. / ix, 137 leaves : ill. ; 29 cm.

This dissertation examines the ability of in vitro biotransformation assays to provide an indication of metabolic potential. The potential for xenobiotic compounds to bioconcentrate in aquatic organisms is expressed through the bioconcentration factor (BCF). The metabolic loss of ibuprofen, norethindrone and propranolol was measured using rainbow trout (Oncorhynchus mykiss) and channel catfish (Ictalurus punctatus) gill and liver S9 fractions, microsomes and cell suspensions. Metabolic transformation rates (kM) were extrapolated from in vitro intrinsic clearance of parent compound (CLm) and integrated into a refined BCF model. In general, CLm of test compounds was greater in liver S9 fractions and hepatocytes. However, the influence of hepatic metabolism on kM and BCF was limited by hepatic blood flow (20-25%) compared to gill blood flow (~100%). A significant difference was noted between BCF solely based on KOW and BCF including kM. These studies indicate that the inclusion of kM in BCF models can bring predicted bioconcentration estimates closer to in vivo values. Primary cell suspensions are preferred over subcellular fractions as cell suspensions possess both phase I and phase II enzyme activity. Further study was conducted on ibuprofen biotransformation pathways. As fish do not contain the same cytochrome P450 (CYP) 2C homologs known to metabolize ibuprofen in mammals, it cannot be assumed that piscine biotransformation is similar. Metabolite analysis found 2-hydroxy-ibuprofen as the major metabolite in S9 and microsomal fractions. Additional assays involving the induction and inhibition of specific CYP isozymes support CYP1A2 as an alternative metabolic pathway.

This study evaluated the effects of a major chlorine disturbance on fish communities in Pecan creek by the City of Denton's Pecan Creek Water Reclamation Plant. Fish communities in Pecan Creek were sampled using a depletion methodology during February, April, July, and November, 1999. February and April sampling events showed that the fish communities were severely impacted by the chlorine. Sampling during July and November showed fish communities recovered in Pecan Creek. The first-twenty minutes of shocking and seining data were analyzed to mirror an equal effort methodology. This methodology was compared to the depletion methodology to see if the equal effort methodology could adequately monitor the recovery of Pecan Creek after the chlorine disturbance. It was determined that the equal effort methodology was capable of monitoring the recovery of Pecan Creek, but could not accurately represent the fisheries community as well as the depletion method. These data using the twenty-minute study were compared to a previous study. Results of this study were similar to those found in a previous study, although fish communities were more severely impacted and took longer to recover.

This study evaluated the effects of chlorinated effluent discharged from the City of Denton, Texas' wastewater treatment plant on Pecan Creek's fish and macroinvertebrate assemblages, and their recovery upon dechlorination. A baseline of ecological conditions was established while chlorine was present in the effluent (June 1993- October 1993), and was evaluated again after dechlorination with sulfur dioxide (October 1993-August 1994). In situ Asiatic clam and fathead minnow ambient toxicity tests, and fish and macroinvertebrate collections were used to establish this baseline for comparison to post-dechlorination results.