The Challenges of Characterizing the Zooplankton Community Response Following Simulated Spills of Diluted Bitumen into Boreal Lake Limnocorrals.

We attempted to characterize zooplankton community response following spills of the unconventional crude oil, diluted bitumen (dilbit), into 10-m diameter, ~ 100 m3, ~ 1.5-m deep boreal lake limnocorrals, including two controls and seven dilbit treatments ranging from 1.5 to 180 L (1:100,000 to 1:1,000 v/v, dilbit:water). Community composition and abundances were monitored weekly to bi-weekly over three months. Total zooplankton biomass and abundance seemingly collapsed in all limnocorrals, regardless of treatment, though some rotifer species persisted. As a result, it was not possible to determine the impacts of dilbit. We theorize several potential non-oil-related reasons for the sudden community collapse - including elevated zinc levels, fish grazing pressures, and sampling biases - and provide guidance for future work using in-lake enclosures.

Simulating diluted bitumen spills in boreal lake limnocorrals - part 2: Factors affecting the physical characteristics and submergence of diluted bitumen.

We examined the fate and behaviour of diluted bitumen (dilbit) as it weathered for 70 days in freshwater limnocorrals (10 m diameter × 1.5 m depth) installed in a boreal lake to simulate dilbit spills in a natural aquatic environment. We added seven different dilbit spill volumes, ranging from 1.5 to 180 L, resulting in oil-to-water ratios between 1:71,000 (v/v, %) and 1:500 (v/v, %). Volatile hydrocarbons in the dilbit slick decreased rapidly after the dilbit was spilled on the water's surface, and dilbit density and viscosity significantly increased (>1 g mL-1 and >5,000,000 mPa s, respectively). Dilbit sank to the bottom sediments in all treatments, and the time to sinking was positively correlated with spill volume. The lowest dilbit treatment began to sink on day 12, whereas the highest dilbit treatment sank on day 31. Dilbit submerged when its density surpassed the density of freshwater (>0.999 g mL-1), with wind, rain, and other factors contributing to dilbit sinking by promoting the break-up of the surface slick. This experiment improves our ability to predict dilbit's aquatic fate and behaviour, and its tendency to sink in a boreal lake. Our findings should be considered in future pipeline risk assessments to ensure the protection of these important aquatic systems.

Selenium bioaccumulation in stocked fish as an indicator of fishery potential in pit lakes on reclaimed coal mines in Alberta, Canada.

Pit lakes are a common reclamation strategy for open pit mines; however, there is a concern about their water quality and suitability as fish habitat because they are often contaminated by metals or metalloids. This study assessed the exposure of fish and invertebrates to selenium (Se) and other metals and metalloids in pit lakes formed by open pit coal mining in Tertiary (thermal coal) and in Cretaceous (metallurgical coal) bedrock. Juvenile hatchery rainbow trout, Oncorhynchus mykiss, and brook trout, Salvelinus fontinalis, were stocked into two thermal coal pit lakes (water Se < 2 µg/L, low water Se) and two metallurgical coal pit lakes (water Se > 15 µg/L, high water Se). Se accumulation in stocked fish and concentrations in invertebrates were characterized over a period of 2 years. In the metallurgical pits, invertebrates had higher Se concentrations and fish accumulated Se to higher levels (exceeding USEPA tissue Se guidelines) than biota in the thermal pits. Rainbow and brook trout accumulated similar concentrations of Se in their muscle and exhibited a similar relationship between whole-body and muscle Se concentrations. These results may be used by resource managers to assess compliance with whole-body tissue Se guidelines and to determine if pit lakes in coal mining areas pose a significant Se risk to wildlife or human health. The high Se exposure in metallurgical coal pits indicates that under the current mining and reclamation strategy, these lakes are not suitable for management as recreational "put and take" fisheries.

The physiological stress response and oxidative stress biomarkers in rainbow trout and brook trout from selenium-impacted streams in a coal mining region.

Selenium (Se) is an essential element that can be toxic at concentrations slightly greater than those required for homeostasis. The main chronic toxic effects of Se in fish are teratogenic deformities, but Se can also activate the physiological stress response and redox cycle with reduced glutathione causing oxidative damage. Rainbow trout, Oncorhynchus mykiss, appear to be more sensitive to Se than brook trout, Salvelinus fontinalis. The objective of this study was to compare the physiological stress response (plasma cortisol, glucose, triiodothyronine, thyroxine, gill Na+/K+ ATPase, cortisol secretory capacity, K and liver somatic index) and oxidative stress biomarkers (liver GSH, GPx, lipid peroxidation, vitamin A and vitamin E) in rainbow trout (RNTR) and brook trout (BKTR) collected from reference and Se-exposed streams. The physiological stress response was not impaired (cortisol secretory capacity unchanged); although there were species differences in plasma cortisol and plasma glucose levels. Liver GSH, GPx and vitamin levels were higher in RNTR than BKTR, but lipid peroxidation levels were not different. The elevated GSH reserves may make RNTR more sensitive to Se-induced lipid peroxidation, but this may be offset by the RNTR's higher antioxidant (GPx and vitamin) levels. Species-specific biochemical differences may mediate differences in Se sensitivity and be used in aquatic Se risk assessments.

Physiological stress response in white suckers from agricultural drain waters containing pesticides and selenium.

To assess the effect of agriculture drain water, a complex mixture containing pesticides and selenium (Se), on the physiological stress response, white suckers were collected from irrigation return flows in the summer and the fall and subjected to a stress challenge. Water (0.40-26.71microg/L) and muscle Se (0.37-1.52microg/g ww) levels were elevated at two sites and plasma acetylcholinesterase (AChE) activity (a marker of pesticide exposure) was lower in the fall (5.97+/-0.45micromol/min/mL) than the summer (10.73+/-0.73micromol/min/mL). Fish raised plasma cortisol levels in response to the stress challenge 11.8 times above basal levels (12.8+/-4.9ng/mL). Multivariate statistics linked Se exposure to elevated plasma glucose levels, and pesticide exposure to elevated liver glycogen levels generating hypotheses for further testing. This study showed that white suckers accumulated Se from agricultural drain water and the complex mixtures present in the drain water influenced the physiological stress response.

Assessment of selenium effects in lotic ecosystems.

The selenium literature has grown substantially in recent years to encompass new information in a variety of areas. Correspondingly, several different approaches to establishing a new water quality criterion for selenium have been proposed since establishment of the national water quality criterion in 1987. Diverging viewpoints and interpretations of the selenium literature have lead to opposing perspectives on issues such as establishing a national criterion based on a sediment-based model, using hydrologic units to set criteria for stream reaches, and applying lentic-derived effects to lotic environments. This Commentary presents information on the lotic verse lentic controversy. Recently, an article was published that concluded that no adverse effects were occurring in a cutthroat trout population in a coldwater river with elevated selenium concentrations (C. J. Kennedy, L. E. McDonald, R. Loveridge, and M. M. Strosher, 2000, Arch. Environ. Contam. Toxicol. 39, 46-52). This article has added to the controversy rather than provided further insight into selenium toxicology. Information, or rather missing information, in the article has been critically reviewed and problems in the interpretations are discussed.

Antioxidant potentials of vitamin A and carotenoids and their relevance to heart disease.

Despite being one of the first vitamins to be discovered, the full range of biological activities for vitamin A remains to be defined. Structurally similar to vitamin A, carotenoids are a group of nearly 600 compounds. Only about 50 of these have provitamin A activity. Recent evidence has shown vitamin A, carotenoids and provitamin A carotenoids can be effective antioxidants for inhibiting the development of heart disease. Vitamin A must be obtained from the diet: green and yellow vegetables, dairy products, fruits and organ meats are some of the richest sources. Within the body, vitamin A can be found as retinol, retinal and retinoic acid. Because all of these forms are toxic at high concentrations, they are bound to proteins in the extracellular fluids and inside cells. Vitamin A is stored primarily as long chain fatty esters and as provitamin carotenoids in the liver, kidney and adipose tissue. The antioxidant activity of vitamin A and carotenoids is conferred by the hydrophobic chain of polyene units that can quench singlet oxygen , neutralize thiyl radicals and combine with and stabilize peroxyl radicals. In general, the longer the polyene chain, the greater the peroxyl radical stabilizing ability. Because of their structures, vitamin A and carotenoids can autoxidize when O2 tension increases, and thus are most effective antioxidants at low oxygen tensions that are typical of physiological levels found in tissues. Overall, the epidemiological evidence suggests that vitamin A and carotenoids are important dietary factors for reducing the incidence of heart disease. Although there is considerable discrepancy in the results from studies in humans regarding this relationship, carefully controlled experimental studies continue to indicate that these compounds are effective for mitigating and defending against many forms of cardiovascular disease. More work, especially concerning the relevance of how tissue concentrations, rather than plasma levels, relate to the progression of tissue damage in heart disease is required. This review assembles information regarding the basic structure and metabolism of vitamin A and carotenoids as related to their antioxidant activities. Epidemiological, intervention trials and experimental evidence about the effectiveness of vitamin A and carotenoids for reducing cardiovascular disease is also reviewed.

Mobilization of antioxidant vitamin pools and hemodynamic function after myocardial infarction.

BACKGROUND: Although most previous studies have attempted to correlate plasma concentrations of vitamins with specific cardiovascular end points, metabolic considerations suggest that changes in myocardial tissue and storage organs may be better indicators of myocardial oxidative stress. METHODS AND RESULTS: Rats fed commercial chow or a diet enriched with vitamin E for 2 weeks were subjected to either a surgical myocardial infarction (MI) or a sham procedure. Rats were hemodynamically assessed 16 weeks after surgery, and their heart, liver, kidney, and plasma were analyzed for antioxidant vitamins E (tocopherol) and A (retinol and total retinyl esters). At 16 weeks, MI rats on a control diet showed depressed peak systolic and elevated diastolic pressures in both right and left ventricles compared with their sham controls. Plasma concentrations of vitamins E and A in MI rats were not different from sham controls fed the same diet. However, concentrations of vitamin E in left ventricle and liver and of vitamin A in liver (retinol) and kidney (retinyl esters) were decreased in rats with MI compared with the sham controls. Vitamin E supplementation improved hemodynamic function in rats with MI and increased plasma, myocardial, liver, and kidney concentrations of vitamin E. The vitamin E diet also prevented the loss of total retinyl esters from the kidney but not of retinol from the liver in MI rats. CONCLUSIONS: Dietary supplements of vitamin E can sustain better cardiac function subsequent to MI. Antioxidant vitamin levels in the myocardium or in storage organs and not in plasma may be better indicators of myocardial oxidative stress.