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15 recordsLinked to original sources
USGS1996

Embryotoxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD): Theembryonic vasculature is a physiological target for TCDD-induced DNA damage and apoptotic cell death in medaka (Orizias latipes)

Vertebrate embryos are extremely sensitive to environmental contaminants known as planar halogenated hydrocarbons (PHHs). The physiological targets that mediate PHH-induced embryotoxicity are not known. We have characterized embryotoxicity in medaka ( Orizias latipes ) caused by 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), the prototypic PHH. DNA degradation in cells of the embryonic vasculature and loss of functional integrity of the medial yolk vein were demonstrated in TCDD-exposed embryos. Pharmacological intervention with piperonyl butoxide inhibited TCDD-induced DNA degradation, restored the functional integrity of the medial yolk vein, and protected against the embryotoxicity of TCDD. Treatment of TCDD-exposed embryos with the antioxidant N -acetylcysteine also provided significant protection against the embryotoxicity of TCDD. These results demonstrate that DNA damage and consequent cell death in the embryonic vasculature are key physiological mediators of TCDD-induced embryotoxicity.

Toxicology and Applied Pharmacology↗
USGS1996

In vivo/in vitro comparison of pharmacokinetics and pharmacodynamics of 3,3',4,4'-tetrachlorobiphenyl (PCB77)

The rat hepatoma cell line, H4IIE, serves as a useful tool to assess potential biological effects such as induction of cytochrome P4501A1 expression. The objectives of this study were twofold: to investigate the kinetic time course and dosimetry of PCB77 in rat hepatoma cells dosed with PCB77 and in liver of rats given ip doses of PCB77, and to compare in vitro and in vivo P4501A1 enzyme induction responses. For the 4-day time–course study, H4IIE cells were exposed with two doses of [ 14 C]PCB77 (0.9 and 3 μg/plate) and harvested at 15 and 30 min, 1, 2, 4, 8, and 12 hr, and 1, 2, 3, and 4 days. PCB77-derived radioactivity was detected in the cells as early as 15 min postdosing. For the dose–response study, the cells were dosed with various concentrations of PCB77 (0.00316–5.37 μg/plate) and harvested on Day 3 since ethoxyresorufin O -deethylase (EROD) activity in vitro reached its maximum on the third day postdosing. Time–course and dose–response studies revealed that only 1–3% of the total delivered dose was found in the cells, with the remainder in the media and adhering to the culture plates. For the dose–response study in vivo, male Fischer rats were dosed with a single ip injection of various concentrations of PCB77 (0.1–50 mg/kg body wt) and euthanized on Day 3. PCB77-derived radioactivity and EROD induction in vivo were measured. When EROD activity and PCB77-derived radioactivity in the rat hepatoma cells and in the rat liver were compared on an equivalent weight basis, there was a significant correlation ( r 2 = 0.985) between them. Prior to this study, no information on quantitative dosimetry and EROD activities of PCB77 has been reported to validate the in vitro assay with in vivo data.

Toxicology and Applied Pharmacology↗
USGS1969

Chronic oral DDT toxicity in juvenile coho and chinook salmon

Technical and p,p′ -DDT was incorporated into test diets and fed to juvenile chinook and coho salmon for periods as long as 95 days. Pure p,p′ -DDT was slightly more toxic to young salmon than was the technical DDT mixture. Chinook salmon appeared to be 2–3 times more sensitive to a given concentration of DDT in the diet than were coho salmon. The size of the fish greatly influenced toxicity, smaller younger fish being more susceptible to a given diet than larger older fish. The dose of DDT accumulated within the median survival time ranged from 27–73 mg/kg for chinook salmon and from 56–72 mg/kg for coho salmon. The extrapolated 90-dose LD50 ( Hayes, 1967 ) for young chinook and coho salmon were 0.0275 and 0.064 mg/kg/day, respectively. Liver size decreased on prolonged feeding with DDT, and carcass lipid content was increased. A severe surface ulceration of the nose region appeared in coho salmon fed DDT over long periods. In addition, an interesting localized degeneration of the distal convoluted tubule was observed in the kidney of coho salmon receiving DDT.

Toxicology and Applied Pharmacology↗
USGS1970

Toxicity of DDT to Japanese quail as influenced by body weight, breeding condition, and sex

Controlled experiments were utilized to simulate the stresses on wild birds of breeding condition and of weight loss due to migration. Light conditions in the laboratory were manipulated to produce Japanese quail ( Coturnix coturnix japonica ) in breeding condition and not in breeding condition. Within each of these groups, some birds were partially starved before dosage and some were fully fed. Birds were then fed dietary levels of 0, 700, 922, 1214, or 1600 ppm dry weight of p,p′ -DDT for a period of 20 days or until death. Birds partially starved before dosage were more susceptible to DDT intoxication than nonstarved ones, and birds not in breeding condition were slightly more so than birds in breeding condition. Similarly, males died earlier than females, and the birds of the lighter weight strain used in the second half of the study died earlier than the birds of the heavier strain used in the first half. The heavier birds of each sex not only survived longer than lighter individuals receiving the same treatments, but they also lost a greater proportion of their weight before death. During the early portion of the dosage period, females in breeding condition were less sensitive to DDT than were females not in breeding condition and males. After 10 days on dosage, however, the cumulative mortality of females in breeding condition rapidly approached that of males and of females not in breeding condition. Food restriction prior to dosage, strains of quail, breeding conditions, and sexes resulted in weight differences and a corresponding accentuation or delay of the effects of the different levels of DDT.

Toxicology and Applied Pharmacology↗
USGS1971

Comparative acute oral toxicity of pesticides to six species of birds

Acute oral LD50 values were determined for 16 common pesticides on mallard ducks ( Anas platyrhynchos ), ring-necked pheasants ( Phasianus colchicus ), chukar partridges ( Alectoris graeca ), coturnix quail ( Coturnix coturnix japonica ), common pigeons ( Columba livia ), and house sparrows ( Passer domesticus ). Analyses of the data revealed that (1) the average sensitivity of any one species to the 16 pesticides did not differ statistically from that of any other species, and (2) at the same time, the species varied widely in their sensitivity to any given compound. The average range of the LD50 values for single chemicals in the 6 species was nearly 10-fold. With differences of this magnitude, it is recommended that extrapolation of toxicity data from one species to another be avoided.

Toxicology and Applied Pharmacology↗
USGS1972

The acute oral toxicity of 369 pesticidal, pharmaceutical and other chemicals to wild birds

The acute po toxicity of 369 chemicals was determined for 1 or more species of wild birds, always including either red-winged blackbirds or starlings. Of these, 180 chemicals were toxic to 1 or more species at 100 mg/kg or less. Statistical comparison of redwing, starling and rat data indicated that redwings were more sensitive to chemicals than starlings, and both were more sensitive than rats.

Toxicology and Applied Pharmacology↗
USGS1974

Plasma enzyme activities in coturnix quail fed graded doses of DDE, polychlorinated biphenyl, malathion, and mercuric chloride

Male Coturnix quail (Coturnix coturnix japonica) were fed diets for 12 weeks containing graded levels of DDE, polychlorinated biphenyl (Aroclor 1254), malathion, and mercuric chloride. Birds were bled prior to exposure and at 2, 4 and 12 weeks, and the plasma used to measure the activities of creatine kinase, aspartate aminotransferase, cholinesterase, fructose-diphosphate aldolase, and lactate dehydrogenase. Abnormal activity of certain plasma enzymes was noted in birds after 2 and 4 weeks, but these changes were not proportional to dose or exposure time. At 12 weeks increases in each of the activities of plasma enzymes of birds fed organochlorines, and decreases in cholinesterase activity of birds fed malathion or mercuric chloride, were proportional to the log dose of the respective agents. In addition, the pattern of enzyme responses in the 4 experimental groups had changed, and was illustrative of the specific type of substance that had been fed. The data suggest that qualitative and quantitative identification of environmental contaminants in birds, and perhaps a variety of wild animals, may be possible by utilization of multiple plasma enzyme assays. Residue analyses after 12 weeks of feeding showed that DDE accumulated in carcasses and livers at concentrations up to 4-fold higher than those in the diets. In contrast residues of Aroclor 1254 attained in carcasses were identical to, and in livers one-half of, the concentration in the feed. Mercury did not accumulate as much in the tissues; residues attained were one-twentieth or less of those in the feed.

Toxicology and Applied Pharmacology↗
USGS1977

Responsiveness of 6 to 14 generations of birds to dietary dieldrin toxicity

The lethal dietary toxicity of dieldrin was estimated repeatedly during 8 years of testing young bobwhites (Colinus virginianus), Japanese quail (Coturnix c. japonica), ring-necked pheasants (Phasianus colchicus), and mallards (Anas platyrhynchos). Toxicities, quantified as 8-day LC50 values (5 days on toxic diet, followed by 3 days of untreated feed), were estimated at least 18 times per species. Average dietary LC50 values (ppm) and their 95% confidence limits for 14-day-old quail and 10-day-old pheasants and mallards were: bobwhite, 38 (34?42); Japanese quail, 61 (58?64); ring-necked pheasant, 56 (53?59); and mallard, 179 (163?195). No time-related changes were detected in LC50 values for any of the species.

Toxicology and Applied Pharmacology↗
USGS1978

Embryotoxic effects of crude oil in mallard ducks and chicks

Recent studies in this laboratory have revealed that surface applications of microliter amounts of some crude and fuel oils that coat less than 10% of the egg surface reduce hatching considerably in different avian species. Applications of paraffin compounds that coat equal areas of the egg surface do not reduce hatching suggesting that toxicity is due to causes other than asphyxia. In the present study, 1–10 μl of South Louisiana crude oil, an API reference oil, were applied to the surface of fertile mallard ( Anas platyrhynchos ) and chicken ( Gallus gallus ) eggs. Early embryolethality was greater in mallard embryos than in chick embryos, but later embryolethality that coincided with the time of rapid outgrowth of the chorioallantoic membrane was more prevalent in chick embryos. The overall incidence of embryolethality was similar in both species. Retardation of growth as reflected by embryonic body weight, crown-rump length, beak length, and general appearance was more pronounced in chick than mallard embryos. Teratogenic defects were more frequent in chick embryos, and incomplete or abnormal ossification of the skull was the most common. External application of equivalent amounts of a mixture of paraffin compounds present in crude oil had virtually no embryotoxic effects in either species, suggesting that other components including aromatic hydrocarbons and organometallics may cause the embryotoxicity.

Toxicology and Applied Pharmacology↗
USGS1979

Acute oral and percutaneous toxicity of pesticides to mallards: Correlations with mammalian toxicity data

Acute oral (po) and 24-hr percutaneous (perc) LD50 values for 21 common pesticides (19 anticholinesterases, of which 18 were organophosphates, and one was a carbamate; one was an organochlorine central nervous system stimulant; and one was an organonitrogen pneumotoxicant) were determined in mallards ( Anas platyrhynchos ). Three of the pesticides tested were more toxic percutaneously than orally. An index to the percutaneous hazard of a pesticide, the dermal toxicity index (DTI = po LD50/perc LD50 × 100), was also calculated for each pesticide. These toxicity values in mallards were compared with toxicity data for rats from the literature. Significant positive correlations were found between log po and log percutaneous LD50 values in mallards ( r = 0.65, p < 0.01), between log po LD50 values in mallards and in rats ( r = 0.71, p < 0.01), and between log DTI values in mallards and in rats ( r = 0.52, p < 0.05). Percutaneous toxicity values were not significantly correlated between mallards and rats ( r = 0.36, p > 0.10). Variations in percutaneous methodologies are discussed with reference to interspecies variation in toxicity values. It is recommended that a mammalian DTI value approaching 30 be used as a guideline for the initiation of percutaneous toxicity studies in birds, when the po LD50 and/or projected percutaneous LD50 are less than expected field exposure levels.

Toxicology and Applied Pharmacology↗
USGS1980

Dopamine and norepinephrine depletion in ring doves fed DDE, dieldrin, and Aroclor 1254

The levels of dopamine and norepinephrine were measured in one-half of the brain of ring doves fed a control diet or a diet containing 2, 20, or 200 ppm DDE; 1, 4, or 16 ppm dieldrin; or 1, 10, or 100 ppm Aroclor 1254. Levels of DDE, dieldrin, or Aroclor 1254 were determined in the other half of each brain. The intermediate and high levels of each chemical caused depletions in both neurotransmitters, and brain residues of each chemical were negatively correlated with levels of neurotransmitters. The highest concentrations of DDE, dieldrin, and Aroclor 1254 depressed averages of dopamine to 42.4, 41.4, and 45.2% of the control level and norepinephrine to 61.6, 62.0, and 56.9% of controls, respectively. Depletions of dopamine and norepinephrine could result in abnormal behavior of contaminated birds in the wild, and the detection of such depletions could become an important tool in assessing contaminant-induced behavioral aberrations in birds.

Toxicology and Applied Pharmacology↗
USGS1982

Embryotoxic and biochemical effects of waste crankcase oil on birds' eggs

Waste crankcase oil (WCO) is a major source of oil pollution in both the aquatic and terrestrial environment and has been implicated in the poisoning of mammals and fish. It is also mutagenic. Since birds' eggs are highly sensitive to external microliter applications of environmentally polluting oils, we examined the developmental effects of external applications of WCO on eggs of the mallard duck (Anas platyrhynchos) and the bobwhite quail (Colinus virginianus). At 48 hr of development, mallard eggs were exposed externally to 2, 5, or 15 :l of WCO or 15 :l of clean crankcase oil (CCO) while bobwhite eggs received proportional doses of 0.5, 1, or 3 :l of WCO and 3 :l of CCO in a similar manner. WCO was highly embryotoxic to both species compared to CCO and resulted in dose-dependent mortality, reduced growth, and abnormal survivors. Application of 15 :l WCO resulted in 84% mortality in mallards and 3 :l WCO resulted in 88% mortality in bobwhites. Abnormal survivors included embryos with subcutaneous edema, incomplete ossification, and eye and brain defects. Red blood cell *-aminolevulinic acid dehydratase (ALAD) activity, liver ALAD activity, and hemoglobin concentration were significantly lower after treatment with WCO in embryos and hatchlings of both species. Plasma uric acid, plasma alanine aminotransferase (ALT), and plasma aspartate aminotransferese (AST) were significantly elevated in WCO-treated mallards after hatching. Biochemical effects, growth retardation, and mortality at proportionally lower dose levels were more pronounced in mallards than in bobwhites. Chemical analysis of the WCO and CCO revealed a considerably higher content of aromatic hydrocarbons in WCO than in CCO. Lead levels were highly elevated in WCO (4600 ppm) compared to CCO (2 ppm).

Toxicology and Applied Pharmacology↗
USGS1984

Subchronic organophosphorus ester-induced delayed neurotoxicity in mallards

Eighteenweek-old mallard hens received 0, 10, 30, 90, or 270 ppm technical grade EPN (phenylphosphonothioic acid O -ethyl- O -4-nitrophenyl ester) in the diet for 90 days. Ataxia was first observed in the 270-ppm group after 16 days, in the 90-ppm group after 20 days, in the 30-ppm group after 38 days; 10 ppm failed to produce ataxia. By the end of 90 days all 6 birds in the 270-ppm group exhibited ataxia or paralysis whereas 5 of 6 birds in the 90-ppm group and 2 of 6 birds in the 30-ppm group were visibly affected. Treatment with 30 ppm or more resulted in a significant reduction in body weight. Brain neurotoxic esterase activity was inhibited by averages of 16, 69, 73, and 74% in the 10-, 30-, 90-, and 270-ppm groups, respectively. Brain acetylcholinesterase, plasma cholinesterase, and plasma alkaline phosphatase were significantly inhibited as well. Distinct histopathological effects were seen in the 30-, 90-, and 270-ppm groups which included demyelination and degeneration of axons of the spinal cord. Additional ducks were exposed in a similar manner to 60-, 270-, or 540-ppm leptophos (phosphonothioic acid O -4-bromo-2,5-dichlorophenyl- O -methylphenyl ester) which resulted in similar behavioral, biochemical, and histopathological alterations. these findings indicate that adult mallards are probably somewhat less sensitive than chickens to subchronic dietary exposure to organophosphorus insecticides that induce delayed neurotoxicity.

Toxicology and Applied Pharmacology↗
USGS1984

Neurotoxic and teratogenic effects of an organophosphorus insecticide (phenyl phosphonothioic acid- O -ethyl- O -[4-nitrophenyl] ester) on mallard development

Phenyl phosphonothioic acid- O -ethyl- O -[4-nitrophenyl] ester (EPN) is one of the 10 most frequently used organophosphorus insecticides and caused delayed neurotoxicity in adult chickens and mallards. Small amounts of organophosphorus insecticides placed on birds' eggs are embryotoxic and teratogenic. For this reason, the effects of topical egg application on EPN were examined on mallard ( Anas platyrhynchos ) embryo development. Mallard eggs were treated topically at 72 hr of incubation with 25 μl of a nontoxic oil vehicle or with EPN in the vehicle at concentrations of approximately 12, 36, or 108 μg/g egg, equivalent to one, three, and nine times the agricultural level of application used to spray crops. Treatment with EPN resulted in 22 to 44% mortality over this dose range by 18 days of development compared with 4 and 5% for untreated and vehicle-treated controls. EPN impaired embryonic growth and was highly teratogenic: 37–42% of the surviving embryos at 18 days were abnormal with cervical and axial scoliosis as well as severe edema. Brain weights were significantly lower in EPN-treated groups at different stages of development including hatchlings. Brain neurotoxic esterase (NTE) activity was inhibited by as much as 91% at 11 days, 81% at 18 days, and 79% in hatchlings. Examination of brain NTE activity during the course of normal development revealed an increase of nearly sixfold from Day 11 through hatching. The most rapid increase occurred between Day 20 and hatching. Brain acetylcholinesterase (AChE) activity was inhibited by as much as 41% at 11 days, 47% at 18 days, and 20% in hatchlings. Plasma cholinesterase and alkaline phosphatase activities were inhibited and plasma aspartate aminotransferase activity was increased at one or more stages of development. Hatchlings from EPN-treated eggs were weaker and slower to right themselves. Histopathological examination did not reveal demyelination and axonopathy of the spinal cord that was characteristic of delayed neurotoxicity in adult birds.

Toxicology and Applied Pharmacology↗
USGS2005

A non-lethal method to estimate CYP1A expression in laboratory and wild Atlantic salmon ( Salmo salar )

Expression of cytochrome P4501A (CYP1A) has been used as a biomarker for possible exposure to contaminants such as PCBs and dioxins in teleost fish. Using a quantitative reverse transcription-polymerase chain reaction (Q-RT-PCR) and a non-lethal gill biopsy, we estimated levels of CYP1A mRNA expression in Atlantic salmon ( Salmo salar ). Groups of ten Atlantic salmon juveniles (48–76 g) received an intraperitoneal injection of 50 μg g − 1 β-naphthoflavone (BNF) or vehicle. Their gill tissues were repeatedly sampled by non-lethal biopsies on day 0, 1, 2 and 7. Control fish expressed basal levels of CYP1A over the duration of sampling. BNF-treated salmon demonstrated similar levels of CYP1A to control fish at day 0 and higher levels over the course of each additional sampling point. Gill biopsies from wild salmon sampled from Millers River (South Royalston, Worcester County, MA, USA), known to contain PCBs, showed significantly higher CYP1A levels over an uncontaminated reference stream, Fourmile Brook (Northfield, Franklin County, MA, USA). We conclude that gill biopsies coupled with Q-RT-PCR analysis is a valuable tool in environmental assessment of wild Atlantic salmon populations and has the potential to be applied to other populations of fish as well.

Comparative Biochemistry and Physiology, Part C: T↗