Influence of nutrient enrichment on temporal and spatial dynamics of dissolved oxygen within northern temperate estuaries.

In temperate estuaries of the southern Gulf of St. Lawrence, intermittent seasonal anoxia coupled with phytoplankton blooms is a regular occurrence in watersheds dominated by agricultural land use. To examine the spatial relationship between dissolved oxygen and phytoplankton throughout the estuary to assist in designing monitoring programs, oxygen depth profiles and chlorophyll measurements were taken bi-weekly from May to December in 18 estuaries. In five of those estuaries, dissolved oxygen data loggers were set to measure oxygen at hourly intervals and at multiple locations within the estuary the subsequent year. The primary hypothesis was that dissolved oxygen in the upper estuary (first 10% of estuary area) is predictive of dissolved oxygen mid-estuary (50% of estuary area). The second hypothesis was that hypoxia/superoxia in the estuary is influenced by temperature and tidal flushing. Oxygen depth profiles conducted in the first year of study provided preliminary support that dissolved oxygen in the upper estuary was related to dissolved oxygen throughout the estuary. However, dissolved oxygen from loggers deployed at 10% and 50% of estuary area did not show as strong a correlation as expected (less than half the variance explained). The strength of the correlation declined towards the end of summer. Spatial decoupling of oxygen within the estuary suggested influence of local conditions. Chlorophyll concentration seemed also to be dependent on local conditions as it appeared to be coupled with the presence of sustained anoxia in the upper estuary with blooms typically occurring within 7 to 14 days of anoxia. The practical implication for oxygen monitoring is that one location within the most severely impacted part of the estuary is not sufficient to fully evaluate the severity of eutrophication effects.

Glutathione S-transferase activities in African catfish injected with ß-naphthoflavone: effects of ploidy, gender, dose, and sampling time.

Glutathione S-transferases (GST) are considered among the most controversial biomarkers of water pollutants in fish with little known about factors influencing their activities. The objective of this study was to investigate how gender, dose, ploidy, and sampling time alter hepatic GST activities in African catfish (Clarias gariepinus) following ß-naphthoflavone (ß-NF) injection. Newly matured male and female diploid and triploid fish were intraperitoneally (i.p.) injected with 0, 15, or 75 mg/kg of ß-NF, and livers were excised 24, 48, and 72 h post-injection. Results showed that hepatic GST activities were significantly inhibited by both doses of ß-NF. Inhibition was greater in females than males, but no significant differences were observed between diploid and triploid fish. Enzymatic activities differed over time with lowest levels 72 h post-injection. These results extend our understanding of GST activity in fish and highlight the necessity of considering confounding factors when comparing different studies.

Co-exposure to metals modulates CYP1A mRNA inducibility in Atlantic tomcod Microgadus tomcod from two populations.

Populations from urbanized and industrialized sites are often exposed to mixtures of chemical contaminants including aromatic hydrocarbons (AHs) and heavy metals. The effects of mixtures of these contaminants on these populations are largely unknown. The Hudson River Estuary is highly contaminated with a variety of AHs including, PCBs and PAHs, and metals, and its population of Atlantic tomcod Microgadus tomcod bioaccumulates those which are persistent. The Hudson River's tomcod population exhibits resistance to persistent AHs as exemplified by significantly decreased inducibility of hepatic cytochrome P4501A (CYP1A) mRNA. We used hepatic CYP1A mRNA inducibility in tomcod from the Hudson River and a sensitive population to investigate the effects of acute co-exposure to metals on aryl hydrocarbon receptor (AHR)-mediated gene expression. Adult tomcod from the Hudson River and the cleaner Miramichi River were i.p. injected with one dose of benzo[a]pyrene (B[a]P) or coplanar PCB77 and graded doses of four metals, As, Cd, Cr, and Ni, and levels of hepatic CYP1A mRNA and protein were assayed. We observed no effects of metals treatment on basal levels of hepatic CYP1A mRNA expression, but all four metals significantly reduced CYP1A mRNA inducibility in tomcod from one or both populations. The magnitude of the inhibition of CYP1A mRNA inducibility differed among the metals and fish from the two populations. Also, the profile of the metals modulation of induced CYP1A mRNA showed differences that depended on the time after treatment of sacrifice. Our results demonstrate that co-exposure to several metals can impact inducible, but not basal levels of CYP1A expression and perhaps other toxicities mediated by the AHR.

B[a]P-DNA binding in early life-stages of Atlantic tomcod: population differences and chromium modulation.

Atlantic tomcod (Microgadus tomcod) from the Hudson River (HR) are resistant at the molecular and organismic levels to the effects of exposure to dioxin-like aromatic hydrocarbon (AH) compounds, but much less so to benzo[a]pyrene (B[a]P). The aims of this study were to determine in early life-stages of tomcod exposed to B[a]P: (1) if DNA binding levels differed between fish from the HR and Miramichi River (MR), and (2) if co-exposure to chromium could modulate this genotoxic effect. After exposure to [(3)H]B[a]P alone, DNA-bound radioactivity was 5-10-fold higher in embryos and larvae of MR than HR descent. Co-exposure to chromium modulated DNA binding levels in offspring of both populations. In MR embryos, co-exposure to chromium inhibited B[a]P uptake. These results demonstrated resistance to the genotoxic effects of B[a]P in early life stages of HR tomcod at an ecologically important endpoint and suggest the ability of chromium to modulate AH-induced genotoxicity.

Morphological and neurotoxicological findings in tropical freshwater fish (Astyanax sp.) after waterborne and acute exposure to water soluble fraction (WSF) of crude oil.

The water-soluble fraction (WSF) of crude oil is a complex highly volatile and toxic mixture of hydrocarbon chains (polyaromatics, heterocyclics), phenols, and heterocyclic compounds containing nitrogen and sulfur. To evaluate the toxic effects of WSF in tropical freshwater teleosts and to develop methodologies that could investigate the toxic mechanisms of WSF in tropical organisms, an acute toxicity experiment was conducted with Astyanax sp. Three dilutions (15%, 33%, and 50%) of WSF obtained from Campos Bay's crude oil (Brazil) were used to study morphological and biochemical responses of the fish. Prior to exposure, the distribution and rate of volatilization of the WSF into each aquarium for the same exposure period was quantified by spectrofluorimetry. Five individuals of Astyvanax sp. were exposed to duplicate WSF of 0, 15, 33, and 50% for each of 12-, 24-, and 96-h exposures for a total of 120 individuals. Liver and gills were sampled from five fish from each treatment and were analyzed by histology, scanning and transmission electron microscopy. A fragment of muscle was also collected from each fish to measure acetylcholinesterase activity. Water analysis showed that only 4 h after dilution, an important loss of hydrocarbons in 33% and 50% of WSF was observed. In addition, 50% of hydrocarbon mass was lost in all tested dilutions after 24 h with significant difference for the 50% WSF at all measured times, demonstrating the high volatility of WSF in freshwater. Damage in the liver and the gills included the presence of necrosis, loss of hepatocytes limit, inflammation areas, cellular proliferation, aneurysms, and disorganization of the second lamellae. The 33% WSF significantly reduced acetylcholinesterase activity in fish. Our study demonstrated that the WSF of crude oil caused damage in organs and tissues of tropical freshwater Astyanax sp. and provided also the basis for a better understanding of the toxic mechanisms of WSF in freshwater fishes.