A low concentration of atrazine does not influence the acute toxicity of the insecticide terbufos or its breakdown products to <Emphasis Type="Italic">Chironomus tepperi</Emphasis>

The acute toxicities of the insecticide terbufos and its major breakdown products individually, as binary mixtures, and in combination with the co-applied herbicide atrazine were evaluated using final instar larvae of the midge Chironomus tepperi. Terbufos, terbufos sulfoxide and terbufos sulfone were highly toxic to C. tepperi with mean 96-h EC50 values of 2.13, 3.64 and 2.59 μg/l, respectively. No interaction was observed between atrazine (25 μg/l) and terbufos or its breakdown products while the binary mixture of terbufos sulfoxide and terbufos sulfone exhibited additive toxicity. The high toxicities of terbufos and its environmentally persistent oxidation products suggest that contamination of aquatic systems with this insecticide pose a threat to aquatic organisms whether or not atrazine is also present.     

Effects of injected methylmercury on the hatching of common loon (Gavia immer) eggs

To determine the level of in ovo methylmercury (MeHg) exposure that results in detrimental effects on fitness and survival of loon embryos and hatched chicks, we conducted a field study in which we injected eggs with various doses of MeHg on day 4 of incubation. Eggs were collected following about 23 days of natural incubation and artificially incubated to observe hatching. Reduced embryo survival was evident in eggs injected at a rate of ≥1.3 μg Hg/g wet-mass. When maternally deposited Hg and injected Hg were considered together, the median lethal concentration of Hg (LC₅₀) was estimated to be 1.78 μg Hg/g wet-mass. Organ mass patterns from eggs of chicks injected at a rate of 2.9 μg Hg/g differed from that of controls and chicks from the 0.5 μg Hg/g treatment, largely related to a negative relation between yolk sac mass and egg mercury concentration. Chicks from eggs in the 2.9 μg Hg/g treatment were also less responsive to a frightening stimulus than controls and chicks from the 0.5 μg Hg/g treatment. We also found that the length of incubation period increased with increasing egg mercury concentration. Tissue Hg concentrations were strongly associated (r ² ≥ 0.80) with egg Hg concentration.     

Abamectin effects on rainbow trout (Oncorhynchus mykiss)

The effect of abamectin (ABM) on rainbow trout (Oncorhynchus mykiss) was studied. The acute toxicity of ABM on rainbow trout was established, following the target 58-h water bath exposure of ABM concentrations from 0.6 to 4.5 μg/l, on the basis of which LD₇₅ (4.0 μg/l) was calculated. The histological changes in organs showed a direct toxicity of ABM for rainbow trout since degenerative changes in brain and kidney and—to a minor extent—in liver were established. The values of the ABM residues in fish muscle tissue with skin were proportional to the exposed concentrations of ABM.     

Embryotoxic effects of nonylphenol and octylphenol in sea urchin <Emphasis Type="Italic">Arbacia lixula</Emphasis>

Nonylphenol (NP) and octylphenol (OP), both of which are biodegradation products of alkylphenols, are widely used in industrial applications and in some domestic products. These chemicals are found widely in surface water and aquatic sediments. We have carried out a comparative embryotoxicity analysis of the effects of increasing concentrations of NP (seven concentrations ranging from 0.937 to 18.74 μg/l) and OP (six concentrations ranging from 5 to 160 μg/l) on embryos of the sea urchin Arbacia lixula. The indicators evaluated were larval malformations, developmental arrest and embryonic/larval mortality. The results revealed that low concentrations of these chemicals (NP, OP) generally caused malformations in the skeletal system. High concentrations (18.74 μg NP/l, 160 μg OP/l) were found to inhibit the growth of embryos in the early life stages by preventing mitosis. We conclude that NP and OP present a major risk to the normal development of A. lixula at the low concentrations that have been recorded in the environment. These chemicals are therefore most likely to represent an ecological hazard at the population level given the cumulative effects of other environmental pollutants.     

Reproduction in mallards exposed to dietary concentrations of methylmercury

The purpose of this experiment was to use mallards (Anas platyrhynchos) tested under controlled conditions to determine how much harm to reproduction resulted from various concentrations of mercury in eggs. Breeding pairs of mallards were fed a control diet or diets containing 1, 2, 4, or 8 μg/g mercury, as methylmercury chloride. Mean concentrations of mercury in eggs laid by parents fed 0, 1, 2, 4, or 8 μg/g mercury were 0.0, 1.6, 3.7, 5.9, and 14 μg/g mercury on a wet-weight basis. There were no signs of mercury poisoning in the adults, and fertility and hatching success of eggs were not affected by mercury. Survival of ducklings and the number of ducklings produced per female were reduced by the 4 and 8-μg/g dietary mercury treatments (that resulted in 5.9 and 14 μg/g mercury in their eggs, respectively). Ducklings from parents fed the various mercury diets were just as heavy as controls at hatching, but by 6 days of age ducklings whose parents had been fed 4 or 8 μg/g mercury weighed less than controls. Because we do not know if absorption of mercury from our diets would be the same as absorption from natural foods, the mercury concentrations we report in eggs may be more useful in extrapolating to possible harmful effects in nature than are the dietary levels we fed. We conclude that mallard reproduction does not appear to be particularly sensitive to methylmercury.     

Comparison of the interaction of methyl mercury and mercuric chloride with murine macrophages

The toxicity of organic methyl mercury was studied on murine macrophages in cell culture and compared to that of inorganic mercuric chloride. Long-term treatment of macrophage cultures with methyl mercury resulted in decreased cell viability in a concentration-dependent fashion. Experiments showed that 20 M methyl mercury was highly toxic, causing cell death within a few days, while cultures exposed to lower levels were less severely affected. Comparison of the toxicity of organic and inorganic mercury by cell viability showed no difference between equimolar concentrations of methyl mercury and mercuric chloride. Furthermore, protein synthesis (interferon-/ß) was reduced in a concentration dependent manner and had the same reduced magnitude in cells treated with either methyl mercury or mercuric chloride. However, impairment of random migration and phagocytosis of macrophages appeared at lower concentrations in cells exposed to methyl mercury than in cells exposed to mercuric chloride. Electron microscopy of cells exposed to methyl mercury revealed mercury deposits in lysosomes and dispersed in the cytoplasm and nuclei. The present study shows that methyl mercury and mercuric chloride impair cell viability and protein production in cell cultures at equimolar concentrations, while methyl mercury inhibits macrophage functions such as migration and phagocytosis at lower concentrations than mercuric chloride.     

Expression of HSP70 in Mytilus californianus following exposure to caffeine

Caffeine, a biologically active drug with many known molecular targets, is recognized as a contaminant of marine systems. Although the concentrations of caffeine reported from aquatic systems are low (ng/l–μg/l), harmful ecological effects not detected by traditional toxicity tests could occur as a result of caffeine contamination. We used Hsp70, a molecular biomarker of cellular stress, to investigate the sub-lethal cellular toxicity of environmentally relevant concentrations of caffeine on the mussel Mytilus californianus, a dominant species in the rocky intertidal zone along the Oregon Coast. Hsp70 concentrations in the gill and mantle tissue of mussels exposed to 0.05, 0.2, and 0.5 μg/l of caffeine for 10, 20, and 30 days were compared to basal levels in control mussels. Hsp70 in the gill tissue of M. californianus had an initial attenuation of the stress protein followed by a significant up-regulation relative to controls in all but the 0.5 μg/l treatment. Hsp70 in the mantle tissue of mussels exposed to caffeine did not differ from control mussels. This study provides laboratory evidence that environmentally relevant concentrations of caffeine can exert an effect on M. californianus gill tissue at the molecular-level.     

Evaluation of the use of salivary lead levels as a surrogate of blood lead or plasma lead levels in lead exposed subjects

We conducted a study to evaluate the use of parotid salivary lead (Pb-saliva) levels as a surrogate of the blood lead (Pb-B) or plasma lead levels (Pb-P) to diagnose lead exposure. The relationship between these biomarkers was assessed in a lead exposed population. Pb-saliva and Pb-P were determined by inductively coupled plasma mass spectrometry, while in whole blood lead was determined by graphite furnace atomic absorption spectrometry. We studied 88 adults (31 men and 57 women) from 18 to 60 years old. Pb-saliva levels varied from 0.05 to 4.4 μg/l, with a mean of 0.85 μg/l. Blood lead levels varied from 32.0 to 428.0 μg/l in men (mean 112.3 μg/l) and from 25.0 to 263.0 μg/l (mean 63.5 μg/l) in women. Corresponding Pb-Ps were 0.02–2.50 μg/l (mean 0.77 μg/l) and 0.03–1.6 μg/l (mean 0.42 μg/l) in men and women, respectively. A weak correlation was found between Log Pb-saliva and Log Pb-B (r=0.277, P<0.008), and between Log Pb-saliva and Log Pb-P (r=0.280, P=0.006). The Pb-saliva/Pb-P ratio ranged from 0.20 to 18.0. Age or gender does not affect Pb-saliva levels or Pb-saliva/Pb-P ratio. Taken together, these results suggest that salivary lead may not be used as a biomarker to diagnose lead exposure nor as a surrogate of plasma lead levels at least for low to moderately lead exposed population.     

Acute toxicity of nonylphenols and bisphenol A to the embryonic development of the abalone <Emphasis Type="Italic">Haliotis diversicolor supertexta</Emphasis>

Acute toxic effects and mechanisms of two typical endocrine disrupting chemicals, nonylphenols (NPs) and bisphenol A (BPA), to the embryonic development of the abalone Haliotis diversicolor supertexta, were investigated by the two-stage embryo toxicity test. The 12-h median effective concentrations (EC₅₀) of NPs and BPA to the trochophore development were 1016.22 and 30.72 μg L⁻¹, respectively, and the respective 96-h EC₅₀ values based on the completion of metamorphosis (another experimental endpoint) were reduced to 11.65 and 1.02 μg L⁻¹. Longer exposure time and magnified exposure concentrations in the benthic diatom, that serves as both food source and settlement substrate during the metamorphosis, via bioaccumulation, led to the higher sensitivity of metamorphosis to target EDCs compared with the trochophore development. The hazard concentrations for 5% of the species (HC₅) could be employed as the safety thresholds for the embryonic development of the abalone. The 12-h HC₅ values of NPs and BPA were 318.68 and 13.93 μg L⁻¹, respectively, and the respective 96-h HC₅ values were 0.99 and 0.18 μg L⁻¹, which were at environmentally relevant levels. Results of proteomic responses revealed that NPs and BPA altered various functional proteins in the abalone larvae with slight differences between each chemical and affected various physiological functions, such as energy and substance metabolism, cell signalling, formation of cytoskeleton and cilium, immune and stress responses at the same time, leading to the failure of metamorphosis.     

Erratum to: Use of two validated in vitro tests to assess the embryotoxic potential of mycophenolic acid

Mycophenolate mofetil is a widely used immunosuppressive drug that recently has been categorized as a human teratogen. Animal experiments indicate a teratogenic potential of the drug, but so far, it has not been studied in embryotoxicity in vitro assays. The aim of this study was to evaluate the in vitro embryotoxic potential of mycophenolic acid and investigate the ability of such tests to detect its embryotoxic potential. We used two validated assays: the rat whole embryo culture and the murine embryonic stem cell test. Rat embryos cultured from gestational day 9.5 for 48 h with the drug showed dysmorphogenic development already at a concentration of 250 μg mycophenolic acid/l medium. At concentrations of 750 μg/l and more, all rat embryos exhibited malformations. The main effects were defective yolk sac blood circulation, neural tube defects (open cranial neural pore), malformations of the head with missing eye anlagen and heart anomalies. Moreover, the exposed embryos showed a concentration-dependent decrease in protein content, crown-rump length, number of somites and morphological score. The murine embryonic stem cell test was slightly more sensitive. Proliferation and differentiation of the ES-D3-cells were significantly impaired at concentrations of 31 and 125 μg mycophenolic acid/l medium, respectively. In the differentiation assay, at a concentration of 125 μg mycophenolic acid/l medium and more, the number of wells with differentiated cardiomyocytes significantly decreased. Additionally, a cytotoxicity assay with balb/c 3T3 mouse fibroblasts was used to compare the proliferation and vitality of embryonic cells with adult cells. In the balb/c 3T3 cytotoxicity assay, the number of vital mouse fibroblasts significantly decreased at a mycophenolic acid concentration of 62 μg/l and more. In conclusion, by using the two validated in vitro tests, we showed that mycophenolic acid exhibits a pronounced embryotoxic potential at cytotoxic concentrations. This result from validated in vitro tests is of special interest, because it supports the use of the tests to detect human teratogens.     

Mercury and other heavy metals in free-ranging mink of the lower Great Lakes basin, Canada, 1998–2006

Mercury concentrations were examined in livers of free-ranging mink (Neovison vison) trapped in the lower Great Lakes basin from 1998 to 2006. Significant geographic variation in total mercury levels was found in mink from 13 Great Lakes locations, many of which are within Great Lakes Areas of Concern (AOCs). Total mercury levels in mink from these locations were generally low to moderate, with means (±SE) ranging from 0.99 (±0.36) μg/g dry weight in mink from inland Lake Erie to 7.31 (±1.52) μg/g in mink from Walpole Island in the St. Clair River AOC. Overall, mercury exposure was highest in mink trapped in locations associated with large riverine wetlands. Total mercury concentrations were negatively related to the percentage of mercury present as methylmercury and positively related to selenium concentrations, consistent with increasing demethylation of methylmercury with increasing total mercury concentrations. One-year old mink had significantly higher levels of mercury and selenium than mink under 1 year but similar to mink 2 years of age and older. Mercury levels were below those associated with mercury toxicity. Concentrations of cadmium, lead and arsenic were low and largely associated with environmental background levels. Significant age and sex effects were found for cadmium. Lead levels were significantly lower in mink infected by the lung nematode parasite compared to uninfected animals. Further studies of biomagnification of methylmercury in wetland environments, where top predators such as mink may be an increased risk of exposure, are warranted.     

Effects of sublethal copper exposure on two gammarid species: which is the best competitor?

Biomarker responses in organisms exposed to copper were examined by comparing two gammarid species, Gammarus roeseli and Dikerogammarus villosus, based on gender. G. roeseli specimens were exposed to 20 μg/L of copper for 6, 12, 24 and 48-h periods, while D. villosus were exposed to 20 and 30 μg/L of copper for 12, 48 and 72 h. Males and females of each species were exposed separately and biomarker measurements were performed for each species and gender. The selected biomarkers were antioxidant enzymes as total glutathione peroxidase (GPxtot), selenium-dependent glutathione peroxidase (SeGPx), and catalase activities. Malondialdehyde level (MDA) was measured as a biomarker of toxic effect. Energy reserves were evaluated by means of lipid, glycogen and protein levels. For both species and gender, antioxidant enzyme activities were weakly modified by copper exposure and differences were transient. MDA levels were increased in both species and genders in exposed animals compared to controls, when energy reserves were decreased. G. roeseli was more rapidly overwhelmed by copper toxicity while the first response of D. villosus was the mobilization of its energetic content. D. Villosus probably has specific physiological properties that enable it to cope with copper toxicity and thus become the best competitor.     

Low exposure levels of urban metals induce heterotrophic community tolerance: a microcosm validation

The biological response of periphyton chronically exposed to metals of urban origin (Cd, Ni and Zn) was investigated with a Pollution-Induced Community Tolerance (PICT) approach using a previously developed short-term toxicity test based on β-glucosidase (heterotrophic) activity. Periphyton was grown on plastic membranes immersed in indoor aquaria contaminated with metals at realistic contamination levels (0.3, 3 μg/l for Cd, 5, 50 μg/l for Ni, 20, 200 μg/l for Zn). After 3 weeks of exposure, biofilms’ parameters (dry-weight, chlorophyll a concentration, heterotrophic activity) were analyzed and tolerance acquisition of the heterotrophic communities was assessed using the toxicity test. Modifications of bacterial and eukaryotic community structure were assessed with Automated Ribosomal Intergenic Spacer Analysis (ARISA). Effects of metal exposure were observed on biofilms parameters in the Cd and Zn experiments. Tolerance levels increased for both Cd-exposed biofilms, and for the high metal treatment biofilms in the Ni and Zn experiments. Analysis of the ARISA profiles showed that metal exposure affected the structure of both bacterial and eukaryotic communities. Moreover, Cd tolerance of the Zn-exposed heterotrophic communities was evaluated, which showed that the Zn-tolerant community (high metal treatment in the Zn experiment) also became tolerant to Cd (co-tolerance). The study shows that tolerance acquisition can be detected after exposure to environmental metal concentrations using β-glucosidase activity as an endpoint in short-term toxicity tests.     

Aluminum toxicity perturbs long bone calcification in the embryonic chick

Long bone calcification in chick embryos acutely- or chronically-treated with aluminum (Al) citrate was investigated. Acutely treated embryos received 100 μl of 60 mM Al citrate, 60 mM sodium (Na) citrate, or 0.7% sodium chloride on day 8 of incubation. Chronically treated embryos received a daily 25 μl dose of the above solutions beginning on day 8. Following 2–8 days of additional incubation, blood was collected, embryos killed, hind limbs radiographed, and tibias collected. Radiography indicated that Al administration resulted in a persistent angulation in the mid-diaphysis of tibias and femurs and a transient mineralization defect during the 10- to 12-day period of incubation. Tibias from 10- to 12-day embryos which were administered Al contained significantly less (P < 0.005) bone calcium (Ca) compared with tibias from NaCl-treated embryos. By day 14 there were no significant differences among the Ca content of tibias from embryos acutely treated with Al citrate, Na citrate or NaCl. Similarly, the rate of ⁴⁵Ca uptake by tibias of embryos treated with Al was significantly lower on days 10 (acute) and 12 (chronic) with no significant differences in Ca uptake rate among the three treatment groups by day 16. In each treatment group bone alkaline phosphatase (ALPase) activity increased approximately tenfold between days 10 and 16. At all stages, bone ALPase activity was consistently higher and significantly different (chronic) compared with levels in NaCl-treated embryos. In contrast, Al had no significant effect on the rate of tibia collagen and noncollagenous protein synthesis or serum levels of procollagen carboxy-terminal propeptide (PICP), osteocalcin, and parathyroid hormone (PTH). Received: 22 March 1999 / Accepted: 27 July 1999     

The sensitivity of grass shrimp, Palaemonetes pugio, embryos to organophosphate pesticide induced acetylcholinesterase inhibition

Grass shrimp, Palaemonetes pugio, are common inhabitants of salt marshes along the Atlantic and Gulf coasts of North America. Grass shrimp embryos are brooded externally on the abdomen of adult females for about 2 weeks prior to hatching. In South Carolina, the spring spawning period for grass shrimp coincides with the period of peak pesticide application on crops grown along the South Carolina coast. Thus, grass shrimp of all developmental stages are at risk of exposure to pesticides present in nonpoint source agricultural runoff. Organophosphate (OP) insecticides are commonly applied agricultural chemicals which produce toxicity by inhibiting the nervous system enzyme, acetylcholinesterase (AChE). The purpose of this study was to examine the development of AChE activity in grass shrimp embryos and to assess their sensitivity to OP-induced AChE inhibition. Embryos were exposed for 24 h to either chlorpyrifos or malathion. All exposure concentrations were nominal and ranged from 0 to 2.00 μg l(-1) for chlorpyrifos and from 0 to 120.00 μg l(-1) for malathion. Quantifiable levels of AChE activity first appeared at Stage V of development and increased as embryonic development progressed. AChE inhibition by the OPs was assessed in Stage VI and Stage VII embryos. Both stages of embryos were more sensitive to chlorpyrifos than malathion. The 24-h Effective Concentration (EC(50)) values for chlorpyrifos were 0.49 μg l(-1) (95% C.I.=0.33-0.77 μg l(-1)) and 0.36 μg l(-1) (95% C.I.=0.33-0.38 μg l(-1)) for Stage VI and Stage VII embryos, respectively. In comparison, malathion 24-h EC(50) values were 55.53 μg l(-1) (95% C.I.=22.08-80.73 μg l(-1)) for Stage VI embryos and 29.93 μg l(-1) (95% C.I.=25.22-44.22 μg l(-1)) for Stage VII embryos. For both OPs, there were no significant differences in the EC(50) values calculated for Stage VI and Stage VII embryos; however, AChE inhibition was significantly (P相似文献   

Toxicity of seven phthalate esters to embryonic development of the abalone Haliotis diversicolor supertexta

The toxicity of seven phthalate esters (PAEs), dimethyl phthalate (DMP), diethyl phthalate (DEP), dibutyl phthalate (DBP), butylbenzyl phthalate (BBP), di-n-hexyl phthalate (DnHP), di-(2-ethylhexyl) phthalate (DEHP) and di-n-octyl phthalate (DOP) to embryogenesis and larval development of the marine univalve Haliotis diversicolor supertexta was examined by means of two-stage embryo toxicity test. At the blastula stage, the normal embryonic development of H. diversicolor supertexta showed a good dose-response decrease when exposed to DMP, DEP, DBP, BBP, and DnHP. 9-h EC₅₀ values of DMP, DEP, DBP, BBP, and DnHP were 55.71, 39.13, 8.37, 2.65, and 3.32 mg/l, respectively. 9-h EC₅₀ values of DEHP and DOP were not available due to their low solubility. The toxicity order of seven tested PAEs was BBP>DnHP>DBP>DEP>DMP>DOP>DEHP. With the completion of metamorphosis as an experimental endpoint, the 96-h no-observed effect concentration values of DBP, DEHP and the other five tested PAEs were 0.022, 0.021, and 0.020 mg/l, respectively. Due to simple obtainment, convenient stimulation to spawn in the lab, greater sensitivity than mature species, and short culture time, the embryos of H. diversicolor supertexta have the potential to be utilized in acute toxicity test for at least PAEs.     

The mysid <Emphasis Type="Italic">Siriella armata</Emphasis> as a model organism in marine ecotoxicology: comparative acute toxicity sensitivity with <Emphasis Type="Italic">Daphnia magna</Emphasis>

Siriella armata (Crustacea, Mysidacea) is a component of the coastal zooplankton that lives in swarms in the shallow waters of the European neritic zone, from the North Sea to the Mediterranean. Juveniles of this species were examined as standard test organisms for use in marine acute toxicity tests. The effects of reference toxicants, three trace metals (Copper, Cadmium and Zinc), and one surfactant, sodium dodecyl sulfate (SDS) were studied on S. armata neonates (<24 h) reared in the laboratory. Acute toxicity tests were carried out with filtered sea water on individual chambers (microplate wells for metals or glass vials for SDS) incubated in an isothermal room at 20°C, with 16 h light: 8 h dark photoperiod for 96 h. Each neonate was fed daily with 10–15 nauplii of Artemia salina. Acute (96 h) LC₅₀ values, in increasing order, were 46.9 μg/L for Cu, 99.3 μg/L for Cd, 466.7 μg/L for Zn and 8.5 mg/L for SDS. The LC₁₀, NOEC and LOEC values were also calculated. Results were compared with Daphnia magna, a freshwater cladoceran widely used as a standard ecotoxicological test organism. Acute (48 h) LC₅₀ values were 56.2 μg/L for Cu, 571.5 μg/L for Cd, 1.3 mg/L for Zn and 27.3 mg/L for SDS. For all the reference toxicants studied, the marine mysid Siriella armata showed higher sensitivity than the freshwater model organism Daphnia magna, validating the use of Siriella mysids as model organisms in marine acute toxicity tests.     

Toxicity of β-blockers in a rat whole embryo culture: concentration-response relationships and tissue concentrations

Beta-adrenoceptor blockers are widely used drugs for the treatment of cardiovascular diseases. Since β-blockers cross the placenta, it is essential to consider possible adverse effects on the embryo. Six β-adrenoceptor blockers were tested at various concentrations (10 – 5000 μM) in a rat whole embryo culture. Although inducing a very similar pattern of dysmorphogenetic effects (incomplete flexure, disturbed development of the neural tube, the head, the heart and the tail bud), the compounds exhibited a wide range of embryotoxic potency. Estimation of the EC₅₀ (median-concentration producing dysmorphogenesis in 50% of the embryos) for the six compounds revealed differences of more than two orders of magnitude: propranolol 25 μM, alprenolol 30 μM, metoprolol 100 μM, pindolol 150 μM, acebutolol 500 μM, atenolol 4000 μM. Measurements of the concentrations of the various drugs in the cultured embryos at corresponding EC₅₀ levels showed differing values: metoprolol 4.5 μM, propranolol 5.2 μM, alprenolol 8.4 μM, pindolol 9.0 μM, acebutolol 12.5 μM and atenolol 77.0 μM. With regard to the EC₅₀ and the degree of substance transfer to the embryo it can be stated that propranolol and metoprolol show a much higher intrinsic potency to interfere with normal in vitro embryonic development than, e.g. atenolol. Received: 1 September 1993 / Accepted: 16 February 1994     

Effects of copper on development of the fathead minnow,Pimephales promelas Rafinesque

Embryos of the fathead minnow, Pimephales promelas Rafinesque, were exposed to total copper concentrations (Cu_T) of 0.6, 61, 113, 204, 338 and 621 μg/l from 5 to 10 h post-fertilization through 2 days post-hatch. A decrease in hatching time was observed with increasing total copper concentration but there was no decrease in embryonic developmental rate. Therefore, embryos hatched at earlier stages of development. Significant (P ≤ 0.05) declines in percent survival and percent total hatch were observed at 621 μg/l Cu_T) but not at 338 μg/l Cu_T or lower concentrations. The percentage of embryos with abnormalities was greater at 338 and 621 μg/l Cu_T than at 204 μg/l Cu_T and lower concentrations.Individuals exposed to copper during early development were then exposed to the same test concentrations for 28 days post-hatch. Survivors at 113 through 338 μg/l Cu_T were at earlier stages of development than were control fish. The percentage of fish surviving decreased with increasing copper concentration over the range 61 through 204 μg/l Cu_T. The percentage of fish surviving at 204 μg/l Cu_T was not significantly different from that at 338 μg/l Cu_T, and there were no survivors at 621 μg/l Cu_T. Surviving larvae at all copper concentrations from 61 through 621 μg/l Cu_T showed decreased length, weight and coefficient of condition compared to controls. The percentage of larvae with abnormalities increased significantly with increasing copper concentration. The calculated 96-h LC₅₀ (larval stage) was 250 μg/l Cu_T and the 28-day LC₅₀ (larval stage) was approximately 123 μg/l Cu_T.     

Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin on benzo(a)pyrene hydroxylase activity in embryos of the Japanese medaka (Oryzias latipes)

When Japanese medaka embryos were exposed to 12 ng/l 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) beginning on the day of fertilization (day 0), benzo(a)pyrene hydroxylase (B(a)PH) activity was induced in the whole embryo 105000g fraction by day 5 of development, which coincided with liver development. The induction of B(a)PH activity also coincided with the appearance of 2,3,7,8-TCDD induced hemorrhagic and edematous lesions. B(A)PH induction only occurred in embryos exposed to toxic concentrations (greater than 10 ng/l) of 2,3,7,8-TCDD. B(a)PH induction also occurred in embryos after exposure to 10 ng/l 2,3,7,8-tetrachlorodibenzofuran (TCDF) and 50 g/l 1,2,7,8-TCDD. Both 2,3,7,8-TCDF and 1,2,7,8-TCDD are toxic to Japanese medaka embryos at concentrations that resulted in the induction of B(a)PH activity. B(a)PH activity was not induced by the non-toxic congener 1,3,6,8-TCDD at concentrations as high as 50 g/l. The structure activity relationship for B(a)PH induction in Japanese medaka embryos was similar to that which is observed in other species and biological systems, suggesting that the biological activities of these compounds may also be mediated through the putativeAh receptor in these fish embryos. At 50 g/l, -naphthoflavone (BNF) induced B(a)PH activity in Japanese medaka embryos to similar levels as 2,3,7,8-TCDD did at toxic concentrations. However, at 50 g/l, BNF was not toxic to Japanese medaka embryos. Therefore, the induction of B(a)PH activity probably did not directly result in the toxicity observed in these fish embryos after exposure to 2,3,7,8-TCDD.Presented in part at the 28th Annual Meeting of the Society of Toxicology, Atlanta, GA, 1989.