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USGS1986

Effect of injected rotenone on the production and composition of urine from the rainbow trout (Salmo gairdneri)

Renal function was evaluated in adult rainbow trout (Salmo gairdneri) dosed i.a. with rotenone at 225 and 275 μg/kg. The chemical composition of urine samples and urine flow rates collected over a 5-h pretreatment period were compared with hourly urine samples collected over a 5-h posttreatment period. Significant increases in osmolality and in concentrations of sodium, potassium, chloride, glucose, and total protein were observed in the urine of treated fish. Urine solute concentrations reached maximum values within 1 to 3 h after treatment and decreased thereafter, indicating that the effects were reversible. Concentrations of sodium and chloride were highly correlated in 2-h posttreatment urine samples at the low ( r = 0.922) and high ( r = 0.981) rotenone treatments. Urine flow rates were reduced in trout at each dose of rotenone but the decrease in volume of urine voided was not dose-dependent. In a separate study, [ 14 C]polyethylene glycol was used as a filtration marker to determine the effect of rotenone treatment (225 &mu:g/kg) on urine flow rate, glomerular filtration rate, and renal water reabsorption. We showed that posttreatment urine flow rates were reduced partly by reduced glomerular filtration and partly by increased water reabsorption. Transient increases in plasma osmolality and hematocrit also were observed 0.5 h after rotenone treatment.

Aquatic Toxicology↗

USGS1986

Tissue distribution and elimination of rotenone in rainbow trout

The fate of a single i.v. dose (120 μg/kg) of the piscicide [ 14 C]rotenone was evaluated in rainbow trout for periods up to 72 h after dosing. Rotenone was rapidly cleared from the plasma; less than 2% of the dose remained in the plasma compartment after 20 min. The highest concentrations of rotenone residues (% dose/g tissue) were in the hepatobiliary system, bile, intestine, and in heart, lateral line swimming muscle, and posterior kidney; tissues that are highly dependent on oxidative metabolism. Although rotenone activity was present in all cell fractions examined, greater than 40% was associated with the mitochondrial fraction of liver, kidney, and muscle. More than 85% of the activity extracted from these tissues, except the liver, was parent rotenone. Elimination from whole body and major tissue depots conformed to simple first-order kinetics; the estimated half-life from whole body was 68.5 h. Branchial elimination accounted for 5% of the injected dose over a 4-h period, and urinary elimination was less than 2% over a 48-h period. Rotenone was eliminated essentially unchanged across the gills; however, parent rotenone was not found in either urine or bile. More than 80% of the activity in both urine and bile eluted from HPLC chromatographs as a highly polar fraction that was not hydrolyzed by incubation with either β-glucuronidase or sulfatase. The results imply that hepatobiliary excretion is the major route of elimination for rotenone residues in the trout and that metabolism to a more polar form is a prerequisite for elimination in both the bile and the urine

Aquatic Toxicology↗

USGS1987

In situ striped bass (Morone saxatilis) contaminant and water quality studies in the Potomac River

The objectives of this study were to evaluate survival of striped bass ( Morone saxatilis ) prolarvae and yearlings in the Potomac River by using in situ test chambers; correlate survival of both striped bass life stages with the presence of water quality conditions, inorganic contaminants, and organic contaminants and conduct histological examinations of surviving yearling striped bass. Survival of striped bass prolarvae ranged from 4.5–22.5% at three field locations during three 96-h experiments; control survival was ≥81%. Yearling survival ranged from 0–77.5% at three river stations during two 7-d experiments; highest mortality occurred at the upriver station. Control survival was 100%. Poor survival of striped bass prolarvae was likely related to the presence of inorganic contaminants (monomeric aluminum, cadmium, and copper) acting singly or synergistically and sudden decreases in water temperature (< 11°C). Yearling mortality at the upriver station was likely correlated with high pH conditions from a point source discharge and perhaps inorganic contaminants. Histological examinations of yearlings suggested that test organisms exposed to Potomac River water exhibited adverse changes in the kidney.

Maryland, Virginia↗

USGS1989

Disposition of pentachlorophenol in rainbow trout (Salmo gairdneri): Effect of inhibition of metabolism

The accumulation kinetics of pentachlorophenol (PCP) were investigated in rainbow trout ( Salmo gairdneri ) in the absence and presence of 25 mg/1 salicylamide, an inhibitor of PCP metabolism. After exposure to 5 μg/1 PCP over 1–96 h, the amount of PCP in the whole fish, its concentration in water and the total amount of metabolites (water, whole fish and bile) were measured. Equations for these variables, based on a two compartment pharmacokinetic model, were fitted simultaneously to the data using the computer program NONLIN, which uses an iterative nonlinear least squares technique. Salicylamide decreased the metabolic clearance of PCP, which resulted in an increase in the bioconcentration factor (BCF); this increase was partially offset by a salicylamide-induced decrease in the apparent volume of distribution of PCP. A clearance-volume compartment model permitted partitioning of the BCF in terms of the underlying physiologic and biochemical processes (uptake clearance, metabolic clearance and apparent volume of distribution). With this approach the BCF can be categorized as either dependent (e.g., PCP) or independent of uptake and metabolism (elimination) based on the relative sizes of the clearances for uptake and metabolism. Inhibition of PCP metabolism resulted in a loss of its dependence on uptake and metabolism. The BCF estimated as the apparent volume of distribution may be useful for assessment of the risk associated with exposure and bioaccumulation potential, as elimination is generally quite variable among aquatic species.

Aquatic Toxicology↗

USGS1991

Potencies of polychlorinated dibenzo-p-dioxin, dibenzofuran, and biphenyl congeners, relative to 2,3,7,8-tetrachlorodibenzo-p-dioxin, for producing early life stage mortality in rainbow trout (Oncorhynchus mykiss)

The presence of polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs) in feral lake trout eggs ( Salvelinus namaycush ) may increase the risk of lake trout early life stage mortality in the Great Lakes. To assess the combined toxicity of PCDDs, PCDFs, and PCBs to lake trout early development, toxic potencies, relative to 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD), were determined for individual PCDD, PCDF, and PCB congeners, based on rainbow trout ( Oncorhynchus mykiss ) early life stage mortality. Newly fertilized rainbow trout eggs were injected with graded doses of 2,3,7,8-TCDD, or a PCDD, PCDF, or PCB congener. LD 50 values were determined based on the egg dose that caused mortality from hatching onset to swim-up. Toxic equivalency factors (TEFs) were calculated as 2,3,7,8-TCDD LD 50 /congener LD 50 . TEFs were for PCDDs: 2,3,7,8-TCDD = 1.0; 1,2,3,7,8-PeCDD = 0.730;and 1,2,3,4,7,8-HxCDD = 0.319; for PCDFs: 2,3,4,7,8-PeCDF = 0.359; 1,2,3,4,7,8-HxCDF = 0.280; 1,2,3,7,8-PeCDF = 0.034; and 2,3,7,8-TCDF = 0.028; and for PCBs: 3,3',4,4',5-PeCB = 0.005; 3,3',4,4'-TCB = 0.00016; 2,3,3',4,4'-PeCB and 2,3',4,4',5-PeCB < 0.00007. For PCDDs, fish-specific TEFs were 10- to 100-fold higher than TEFs determined in H4IIE rat hepatoma cells, but were similar to TEFs proposed for risk assessment. For PCDFs, fish specific TEFs were similar to TEFs determined in H4IIE cells and TEFs proposed for risk assessment. However, the most significant finding was that for the coplanar PCBs and mono- ortho -chlorinated analogues of the coplanar PCBs fish-specific TEFs were 1/14 to 1/80 less than both those determined in H4IIE cells and proposed for risk assessment. Using these fish-specific TEFs, the risk associated with exposure of early life stages of Sake trout to complex mixtures of PCDDs, PCDFs, and PCBs in the Great Lakes can be estimated.

Aquatic Toxicology↗

USGS1992

An egg injection method for assessing early life stage mortality of polychlorinated dibenzo- p -dioxins, dibenzofurans, and biphenyls in rainbow trout, (Oncorhynchus mykiss)

To characterize the risk that polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs) pose to salmonid early life stage survival, we developed a method to expose rainbow trout (Oncorhynchus mykiss) eggs to graded doses of PCDD, PCDF, and PCB congeners, using 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as a prototype. Rainbow trout eggs were injected 24–50 h post-fertilization with 0.2 μl of 50 mM phosphatidylcholine (PC) liposomes (control) or 0.2 μl of 5–7 graded doses of TCDD incorporated into 50 mM PC liposomes. Injection volume never exceeded 0.6% egg volume. Immediately following injection, the injection site was sealed with Super glue®, resulting in 92–97% of TCDD dose retained by the egg. Following both egg injection and waterborne egg exposure. TCDD toxicity in rainbow trout was manifested by half-hatching mortality but predominantly by sac fry mortality associated with hemorrhages, pericardial edema, and yolk sac edema. TCDD LD 50 s, following injection and waterborne exposure of rainbow trout eggs, were 421 (331–489) and 439 (346–519) pg TCDD/g egg (LD 50 , 95% fiducial limits), respectively. As in rainbow trout, TCDD toxicity in lake trout (Salvelinus namaycush) following the same two routes of exposure was manifested by half-hatching mortality but predominantly by sac fry mortality preceded by hemorrhages and yolk sac edema. LD 50 s, based on the dose of TCDD in lake trout eggs, were 47 (21–65) and 65 (60–71) pg/g following injection and waterborne exposure, respectively. The egg injection method is ideal for assessing the relationship between early life stage mortality in rainbow trout and graded egg doses of individual PCDD, PCDF, or PCB congeners.

Aquatic Toxicology↗

USGS1992

Effects of chronic exposure to soft, acidic water on gill development and chloride cell numbers in embryo-larval brook trout, Salvelinus fontinalis

Recruitment failure is considered to be a major factor contributing to the decline of fish populations in soft, acidic waters; direct mortality of embryo-larval fishes has been postulated as a major cause of the decline. Little is understood of the physiological consequences to embryo-larval fishes of prolonged exposure to soft, acidic waters; however, dysfunction of respiratory and ionoregulatory processes is suspected. In order to evaluate the effects of acid exposure on the respiratory and ionoregulatory systems of developing brook trout, Salvelinus fontinalis, differences in gill morphology and numbers of chloride cells were compared between groups cf developing embryo-larval fish continuously exposed to moderately hard well water (130.0 mg.l -1 as CaCO 3 , pH 7.94) or to reconstituted soft, acidic water (4.4 mg.l -1 as CaCO 3 , pH 5.25) designed to mimic acidic waters of northern Wisconsin acidified lakes. Exposures were maintained for up to 48 days (82 days after fertilization) during critical periods of growth and differentiation of branchial structures. The second right gill arch of each fish was examined for changes in the development of filaments and lamellae and for differences in numbers of chloride cells. Gills of fish that developed in soft, acidic water contained greater numbers of normal and degenerating chloride cells, exhibited hyperplasia of primary epithelium and multiple fusions of adjacent filaments and lamellar epithelium than the gills of control fish. Filament and lamellar lengths and numbers of lamellae per filament were significantly less ( P < 0.05) in fish that developed in soft, acidic water than in fish exposed to well water.

Wisconsin↗

USGS1993

Assimilation efficiency for sediment-sorbed benzo(a)pyrene by Diporeia spp.

Two methods are currently available for determining contaminant assimilation efficiencies (AE) from ingested material in benthic invertebrates. These methods were compared using the Great Lakes amphipod Diporeia spp. and [ 14 C]benzo(a)pyrene (BaP) sorbed to Florissant sediment (< 63 µ m). The first approach, the direct measurement method, uses total organic carbon as a tracer and yielded AE values ranging from 45.9~50.4%. The second approach, the dual-labeled method, uses 51 Cr as a non-assimilated tracer and did not yield AE values for our data. The inability of the dual-labeled approach to estimate AEs was due, in part, to the selective feeding by Diporeia resulting in a failure of the non-assimilated tracer ( 51 Cr) to track with the assimilated tracer ([ 14 C]BaP). The failure of the dual-labeled approach was not a result of an uneven distribution of the labels among particle size classes, but more likely resulted from differential sorption of the two isotopically labeled materials to particles of differing composition. The [ 14 C]BaP apparently sorbs to organic particles that are selectively ingested, while the 51 Cr apparently sorbs to particles which are selectively excluded by Diporeia. The dual-labeled approach would be a viable and easier experimental approach for determining AE values if the characteristics that govern selective feeding can be determined.

Aquatic Toxicology↗

USGS1993

Toxicity and bioaccumulation of waterborne and dietary selenium in juvenile bluegill ( Lepomis macrochirus )

Juvenile bluegill ( Lepomis macrochirus ) were exposed to waterborne selenium as a 6:1 mixture of selenate to selenite (as Se) for 60 d and to dietary seleno- l -methionine for 90 d. Measured concentrations of total selenium in the waterborne exposure ranged from 0.16 to 2.8 mg/l, and concentrations of seleno- l -methionine in the test diet ranged from 2.3 to 25.0 mg/kg wet weight. Mortality, body weight, condition factor, swimming and feeding behavior, aggression, and selenium tissue residues were monitored during the tests. Increased mortality at measured concentrations of 0.64 mg Se/l and greater was the primary adverse effect of waterborne selenium on the juvenile bluegill. Bluegill exposed to 2.8 mg/l of waterborne Se for 30 d exhibited a significant reduction in condition factor ( K ), whereas dietary exposure of bluegill to 25 mg Se/kg for 30 d and 13 mg Se/kg or greater for 90 d elicited significant reductions in K . Mortality and swimming activity of bluegill were not affected in the dietary exposure. Net accumulation of Se from both water and diet was directly related to exposure concentration. Bioconcentration factors ranged from 5 to 7 for bluegill exposed to waterborne Se and from 0.5 to 1.0 for fish exposed to dietary Se. Results of these laboratory tests indicate that survival of bluegill may be impaired in natural waters with elevated Se concentrations.

Aquatic Toxicology↗

USGS1994

Effects of the planar PCB 3,3′,4,4′-tetrachlorobiphenyl (TCB) on ovarian development, plasma levels of sex steroid hormones and vitellogenin, and progeny survival in the white perch (Morone americana)

Adult white perch were given three intraperitoneal injections of 3,3′,4,4′-tetrachlorobiphenyl (TCB) at one of three different doses (0.2–5.0 mg TCB/kg body weight). The TCB injections were initiated approx. 3 months prior to the spawning season and given at 3-week intervals. Fewer females matured in the group receiving the highest dose of TCB. Those fish that did mature had a gonadal somatic index approximately half that of control females. Circulating levels of the sex steroid hormones, estradiol-17β and testosterone, and of the egg yolk precursor, vitellogenin, were not significantly altered by TCB exposure. By 7 days post-hatch survival of larvac produced from females exposed to 1.0 and 5.0 mg/kg TCB was reduced as compared to controls (0, 1 and 54%, respectively). These results show that: (1) TCB impairs both maturation of adult females and survival of their offspring, and (2) decreased larval survival may occur at TCB doses less than those required to decrease ovarian growth, oocyte maturation, or circulating sex steroid hormone and vitellogenin concentrations in the adult fish.

Aquatic Toxicology↗

USGS2004

Roles of uptake, biotransformation, and target site sensitivity in determining the differential toxicity of chlorpyrifos to second to fourth instar Chironomous riparius (Meigen)

Early life stages of aquatic organisms tend to be more sensitive to various chemical contaminants than later life stages. This research attempted to identify the key biological factors that determined sensitivity differences among life stages of the aquatic insect Chironomous riparius. Specifically, second to fourth instar larvae were exposed in vivo to both low and high waterborne concentrations of chlorpyrifos to examine differences in accumulation rates, chlorpyrifos biotransformation, and overall sensitivity among instars. In vitro acetylcholinesterase (AChE) assays were performed with chlorpyrifos and the metabolite, chlorpyrifos-oxon, to investigate potential target site sensitivity differences among instars. Earlier instars accumulated chlorpyrifos more rapidly than later instars. There were no major differences among instars in the biotransformation rates of chlorpyrifos to the more polar metabolites, chlorpyrifos-oxon, and chlorpyridinol (TCP). Homogenate AChE activities from second to fourth instar larvae were refractory to chlorpyrifos, even at high concentrations. In contrast, homogenate AChE activities were responsive in a dose-dependent manner to chlorpyrifos-oxon. In general, it appeared that chlorpyrifos sensitivity differences among second to fourth instar C. riparius were largely determined by differences in uptake rates. In terms of AChE depression, fourth instar homogenates were more sensitive to chlorpyrifos and chlorpyrifos-oxon than earlier instars. However, basal AChE activity in fourth instar larvae was significantly higher than basal AChE activity in second to third instar larvae, which could potentially offset the apparent increased sensitivity to the oxon. ?? 2003 Elsevier B.V. All rights reserved.

Aquatic Toxicology↗

USGS2005

Aqueous exposure to Aroclor 1254 modulates the mitogenic response of Atlantic salmon anterior kidney T-cells: Indications of short- and long-term immunomodulation

Polychlorinated biphenyls (PCBs) exist as persistent organic pollutants in numerous river systems in the United States. Unfortunately, some of these rivers are sites of active Atlantic salmon restoration programs, and polychlorinated biphenyls have been implicated as ancillary factors contributing to failed salmon restoration. Here, we investigate the immediate and chronic effects of intermediate duration aqueous PCB exposure (1 or 10 ??g L-1 Aroclor 1254) on the mitogen-stimulated lymphoproliferative response of Atlantic salmon anterior kidney leukocytes (AKLs). A short-term study was designed to examine immunomodulation in Atlantic salmon smolts immediately following 21 days of aqueous exposure, while a long-term study evaluated chronic impacts in the mitogen response in parr 15 months post-exposure as larvae. The proliferative response of AKLs to the mitogens concanavalin A (CON A), phytohemaglutinnin-P (PHA-P), pokeweed mitogen (PWM), and lipopolysaccharide were used as an indice of immunomodulation. The proliferative response to the T-cell mitogens CON A and PHA-P was significantly increased in the 10 ??g L-1 group (n = 10; P = 0.043 and 0.002, respectively) immediately following exposure of smolts. Additionally, The PHA-P response was significantly increased in the 1 ??g L-1 exposure group (n = 10, P = 0.036). In fish treated as larvae and tested 15 months later, the PHA-P sensitive populations exhibited elevated proliferation in the 1 and 10 ??g L-1 groups (n = 12, P < 0.04) relative to the vehicle control while the PWM response was significantly increased (n = 12, P = 0.036) only in the 10 ??g L-1 treated groups. These results demonstrate an immunomodulatory effect of PCBs on T-cell mitogen sensitive populations of lymphocytes in Atlantic salmon as well as long-term immunomodulation in PHA-P and PWM sensitive populations. ?? 2005 Elsevier B.V. All rights reserved.

Aquatic Toxicology↗

USGS2005

Individual variability in esterase activity and CYP1A levels in Chinook salmon (Oncorhynchus tshawytscha) exposed to esfenvalerate and chlorpyrifos

Acetylcholinesterase (AChE) activity has traditionally been monitored as a biomarker of organophosphate (OP) and/or carbamate exposure. However, AChE activity may not be the most sensitive endpoint for these agrochemicals, because OPs can cause adverse physiological effects at concentrations that do not affect AChE activity. Carboxylesterases are a related family of enzymes that have higher affinity than AChE for some OPs and carbamates and may be more sensitive indicators of environmental exposure to these pesticides. In this study, carboxylesterase and AChE activity, cytochrome P4501A (CYP1A) protein levels, and mortality were measured in individual juvenile Chinook salmon (Oncorhynchus tshawytscha) following exposure to an OP (chlorpyrifos) and a pyrethroid (esfenvalerate). As expected, high doses of chlorpyrifos and esfenvalerate were acutely toxic, with nominal concentrations (100 and 1 ??g/l, respectively) causing 100% mortality within 96 h. Exposure to chlorpyrifos at a high dose (7.3 ??g/l), but not a low dose (1.2 ??g/l), significantly inhibited AChE activity in both brain and muscle tissue (85% and 92% inhibition, respectively), while esfenvalerate exposure had no effect. In contrast, liver carboxylesterase activity was significantly inhibited at both the low and high chlorpyrifos dose exposure (56% and 79% inhibition, respectively), while esfenvalerate exposure still had little effect. The inhibition of carboxylesterase activity at levels of chlorpyrifos that did not affect AChE activity suggests that some salmon carboxylesterase isozymes may be more sensitive than AChE to inhibition by OPs. CYP1A protein levels were ???30% suppressed by chlorpyrifos exposure at the high dose, but esfenvalerate had no effect. Three teleost species, Chinook salmon, medaka (Oryzias latipes) and Sacramento splittail (Pogonichthys macrolepidotus), were examined for their ability to hydrolyze a series of pyrethroid surrogate substrates and in all cases hydrolysis activity was undetectable. Together these data suggest that (1) carboxylesterase activity inhibition may be a more sensitive biomarker for OP exposure than AChE activity, (2) neither AChE nor carboxylesterase activity are biomarkers for pyrethroid exposure, (3) CYP1A protein is not a sensitive marker for these agrochemicals and (4) slow hydrolysis rates may be partly responsible for acute pyrethroid toxicity in fish. ?? 2005 Elsevier B.V. All rights reserved.

Aquatic Toxicology↗

USGS2006

The chlorinated AHR ligand 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) promotes reactive oxygen species (ROS) production during embryonic development in the killifish ( Fundulus heteroclitus )

Exposure to dioxin-like chemicals that activate the aryl hydrocarbon receptor (AHR) can result in increased cellular and tissue production of reactive oxygen species (ROS). Little is known of these effects during early fish development. We used the fish model, Fundulus heteroclitus , to determine if the AHR ligand and pro-oxidant 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) can increase ROS production during killifish development, and to test a novel method for measuring ROS non-invasively in a living organism. The superoxide-sensitive fluorescent dye, dihydroethidium (DHE), was used to detect in ovo ROS production microscopically in developing killifish exposed to PCB126 or vehicle. Both in ovo CYP1A activity (ethoxyresorufin- o -deethylase, EROD) and in ovo ROS were induced by PCB126. In ovo CYP1A activity was inducible by PCB126 concentrations as low as 0.003 nM, with maximal induction occurring at 0.3 nM PCB126. These PCB126 concentrations also significantly increased in ovo ROS production in embryonic liver, ROS being detectable as early as 5 days post-fertilization. These data demonstrate that the pro-oxidant and CYP1A inducer, PCB126, increases both CYP1A activity and ROS production in developing killifish embryos. The superoxide detection assay (SoDA) described in this paper provides a semi-quantitative, easily measured, early indicator of altered ROS production that can be used in conjunction with simultaneous in ovo measurements of CYP1A activity and embryo development to explore functional relationships among biochemical, physiological and developmental responses to AHR ligands.

Aquatic Toxicology↗

USGS2006

The effect of chronic chromium exposure on the health of Chinook salmon (Oncorhynchus tshawytscha)

This study was designed to determine fish health impairment of Chinook salmon ( Oncorhynchus tshawytscha ) exposed to chromium. Juvenile Chinook salmon were exposed to aqueous chromium concentrations (0–266 μg l −1 ) that have been documented in porewater from bottom sediments and in well waters near salmon spawning areas in the Columbia River in the northwestern United States. After Chinook salmon parr were exposed to 24 and 54 μg Cr l −1 for 105 days, neither growth nor survival of parr was affected. On day 105, concentrations were increased from 24 to 120 μg Cr l −1 and from 54 to 266 μg Cr l −1 until the end of the experiment on day 134. Weight of parr was decreased in the 24/120 μg Cr l −1 treatment, and survival was decreased in the 54/266 μg Cr l −1 treatment. Fish health was significantly impaired in both the 24/120 and 54/266 μg Cr l −1 treatments. The kidney is the target organ during chromium exposures through the water column. The kidneys of fish exposed to the greatest concentrations of chromium had gross and microscopic lesions (e.g. necrosis of cells lining kidney tububules) and products of lipid peroxidation were elevated. These changes were associated with elevated concentrations of chromium in the kidney, and reduced growth and survival. Also, variations in DNA in the blood were associated with pathological changes in the kidney and spleen. These changes suggest that chromium accumulates and enters the lipid peroxidation pathway where fatty acid damage and DNA damage (expressed as chromosome changes) occur to cause cell death and tissue damage. While most of the physiological malfunctions occurred following parr exposures to concentrations ≥120 μg Cr l −1 , nuclear DNA damage followed exposures to 24 μg Cr l −1 , which was the smallest concentration tested. The abnormalities measured during this study are particularly important because they are associated with impaired growth and reduced survival at concentrations ≥120 μg Cr l −1 . Therefore, these changes can be used to investigate the health of resident fish in natural waters with high chromium concentrations as well as provide insight into the mechanisms of chromium toxicity.

Aquatic Toxicology↗

USGS2006

Dietary exposure of largemouth bass to OCPs changes expression of genes important for reproduction

Dieldrin and p,p???-DDE are ubiquitous contaminants known to act as endocrine disruptors, causing impaired development and reproduction in fish and wildlife. In order to elucidate the mechanisms by which dieldrin and p,p???-DDE cause endocrine disruption in largemouth bass (Micropterus salmoides), fish were exposed subchronically through the diet to both contaminants. Following 120 days of exposure, p,p???-DDE decreased estradiol in females, but increased 11-ketotestosterone in both sexes. Dieldrin on the other hand, decreased estradiol and 11-ketotestosterone in both sexes. Both pesticides also altered steady state mRNA expression levels of a set of genes chosen to represent three possible mechanisms of endocrine disruption: (1) direct interaction with soluble sex steroid receptors, (2) biosynthesis of endogenous sex hormones, and (3) metabolism of endogenous hormones. p,p???-DDE acted as a weak estrogen, increasing the expression of vitellogenin and estrogen receptor ?? in the liver. p,p???-DDE also altered the expression of genes involved in the synthesis of endogenous hormones as well as their metabolism. Dieldrin, on the other hand, only altered expression of vitellogenin and not estrogen receptor ??. Dieldrin also altered the expression of genes involved in hormone synthesis and metabolism, and it dramatically lowered plasma hormone levels. Both pesticides targeted expression of genes involved in all three modes of action, suggesting that they each have multiple modes of action. ?? 2006 Elsevier B.V. All rights reserved.

Aquatic Toxicology↗

USGS2006

Larval exposure to environmentally relevant mixtures of alkylphenolethoxylates reduces reproductive competence in male fathead minnows

The ubiquitous presence of nonylphenolethoxylate/octylphenolethoxylate (NPE/OPE) compounds in aquatic environments adjacent to wastewater treatment plants (WWTP) warrants an assessment of the endocrine disrupting potential of these complex mixtures on aquatic vertebrates. In this study, fathead minnow larvae were exposed for 64 days to a mixture of NPE/OPE, which closely models the NPE/OPE composition of a major metropolitan WWTP effluent. Target exposure concentrations included a total NPE/OPE mixture load of 200% of the WWTP effluent concentration (148 μg/L), 100% of the WWTP effluent concentration (74 μg/L) and 50% of the WWTP effluent concentration (38 μg/L). The NPE/OPE mixture contained 0.2% 4- t -octylphenol, 2.8% 4-nonylphenol, 5.1% 4-nonylphenolmonoethoxylate, 9.3% 4-nonylphenoldiethoxylate, 0.9% 4- t -octylphenolmonoethoxylate, 3.1% 4- t -octylphenoldiethoxylate, 33.8% 4-nonylphenolmonoethoxycarboxylate, and 44.8% 4-nonylphenoldiethoxycarboxylate. An additional exposure of 5 μg/L 4-nonylphenol (nominal) was conducted. The exposure utilized a flow-through system supplied by ground water and designed to deliver consistent concentrations of applied chemicals. Following exposure, larvae were raised to maturity. Upon sexual maturation, exposed male fish were allowed to compete with control males in a competitive spawning assay. Nest holding ability of control and exposed fish was carefully monitored for 7 days. All male fish were then sacrificed and analyzed for plasma vitellogenin, developmental changes in gonadal tissues, alterations in the development of secondary sexual characters, morphometric changes, and changes to reproductive behavior. When exposed to the 200% NPE/OPE treatment most larvae died within the first 4 weeks of exposure. Both the 100% and 50% NPE/OPE exposures caused a significant decrease in reproductive behavior, as indicated by an inability of many of the previously exposed males to acquire and hold a nest site required for reproduction. In contrast, the 5 μg/L 4-nonylphenol exposure resulted in significantly enhanced reproductive behavior compared to that of control males and a majority of the nesting sites were held by previously exposed males. No significant change in the development of gonadal tissues was observed. The 100% NPE/OPE exposure resulted in a significant reduction in the gonadal somatic index and in the prominence of secondary sexual characteristics of exposed larvae. This study indicates that NPE/OPE mixtures have an effect on the reproductive competence of previously exposed male fathead minnows. In addition, 4-nonylphenol concentrations utilized in all exposures were below regulatory guidelines, suggesting that evaluation of 4-nonylphenol alone may not be sufficient for identifying potentially adverse effects of this suite of compounds usually found as mixtures in the aquatic environment.

Aquatic Toxicology↗

USGS2007

Effects of aqueous exposure to polychlorinated biphenyls (Aroclor 1254) on physiology and behavior of smolt development of Atlantic salmon

Polychlorinated biphenyls (PCBs) are a widespread aquatic contaminant and are present in both wild and hatchery raised Atlantic salmon, Salmo salar. The possible sub-lethal alterations in smolt physiology and behavior due to PCB exposure of salmon have not been widely examined. In this study, we examined the effects of the PCB mixture Aroclor 1254 on survival and smolt development of Atlantic salmon. In separate experiments, fish were exposed as yolk-sac larvae or as juveniles just prior to the parr-smolt transformation in April to 1 ??g l-1 (PCB-1) or 10 ??g l-1 (PCB-10) aqueous Aroclor 1254 (A1254), or vehicle for 21 days. After exposure, yolk-sac larvae were reared at ambient conditions for 1 year, until the peak of smolting the following May. Juveniles were sampled immediately after exposure. Both groups were assessed for behavioral, osmoregulatory, and endocrine disruption of smolt development at the peak of smolting. PCB-1 and PCB-10 treated yolk-sac larvae exhibited significant increases in the rate of opercular movement after 14 and 21 days of exposure. At the peak of smolting, prior exposure as yolk-sac larvae to PCB-1 did not affect behavior, while PCB-10 dramatically decreased volitional preference for seawater. Neither concentration of A1254 had long-term effects on the osmoregulatory or endocrine parameters measured in animals exposed as yolk-sac larvae. Juvenile fish exposed to PCB-1 or PCB-10 during smolting exhibited a dose-dependent reduction in preference for seawater. Fish treated with the higher dose of A1254 also exhibited a 50% decrease in gill Na+,K+-ATPase activity and a 10% decrease in plasma chloride levels in freshwater. In addition, plasma triiodothyronine was reduced 35-50% and plasma cortisol 58% in response to exposure to either concentration; whereas plasma thyroxine, growth hormone, and insulin-like growth factor I levels were unaffected. These results indicate that the effects of exposure to A1254 may vary according to developmental stage. Exposure to A1254 in the freshwater environment can inhibit preparatory adaptations that occur during smolting, thereby reducing marine survival and sustainability of salmon populations. ?? 2007 Elsevier B.V. All rights reserved.

Aquatic Toxicology↗