bluuebunny/crossref_metadata_2025_split huggingface dataset:
In vitro embryotoxic effects of ethylene glycol in rats
Authors: Grafton Thomas F. , Hansen Deborah K. 
Published: February 2006

AbstractRat embryos of the CD strain were treated in a whole embryo culture system with either 30 or 40 μ1 of ethylene glycol (EG) per milliliter of culture medium for the first 8 (0–8 hr) or second 8 (8–16 hr) hr of a 48‐hr culture period. The compound was not embryolethal under these conditions but did alter growth and development. EG at 40 μ1/m1 of culture medium at 8–16 hr decreased morphological score, somite number, crown‐rump and head lengths, as well as DNA and protein contents. The most frequent abnormality induced by the compound was absence of yolk sac circulation; absent hindlimb bud, hypoplastic telencephalon, and lack of development of the otic and optic systems were also seen in EG‐exposed embryos. Since it has been reported that rodent embryos cultured in vitro lack alcohol and aldehyde dehydrogenases that metabolize EG, present results suggest that the parent compound is capable of altering normal embryonic development when administered during a brief period or organogenesis.
Prenatal and postnatal antimony exposure in rats: Effect on vasomotor reactivity development of pups
Authors: Rossi F. , Acampora R. , Vacca C. , Maione S. , Matera M. G. , Servodio R. , Marmo E. 
Published: February 2006

AbstractPregnant female rats were exposed to antimony trichloride (0.1 and 1 mg/dl in their drinking water ad libitum) from the first day of pregnancy until weaning (22nd day after delivery). Pups were exposed to antimony trichloride (0.1 and 1 mg/dl in their drinking water ad libitum) from 22nd until 60th day of age. Antimony exposure did not significantly affect maternal and pup systolic arterial blood pressure, length of gestation, and number of newborn per litter. Antimony exposure decreased maternal and pup body weight. No macroscopic teratogenic effects have been observed. Whether or not pups were exposed to antimony trichloride, pressor responses to carotid occlusion and 1‐noradrenaline and hypotensive responses to 1‐isoprenaline and acetylcholine were significantly higher on the 60th than on the 30th day of age. In pups, prenatal and postnatal antimony exposure did not affect pressor response to carotidal occlusion, while it decreased pressor response to 1‐noradrenaline and hypotensive response to 1‐isoprenaline on the 60th day after birth. At last, antimony exposure at higher concentration decreased pup hypotensive response to acetylcholine on the 60th day.
Studies on the ability of hypotonic solutions to induce chromosomal aberrations in V 79 cell
Authors: Nowak C. 
Published: February 2006

AbstractV 79 hamster cells were exposed to hypotonic culture medium or to hypotonic solutions of ammonium sulfate, sodium chloride, or trishydroxymethylaminomethane. Hypotonic treatment led in all experiments to a clear increase of chromosomal aberrations. Reasons for the aberrations observed may be directly induced DNA damage such as double strand breaks or a release of DNase after lysosomal damage because of the hypotonic treatment. Other reasons involved in the aberration production may be changes of the internal pH or damage of the chromosomal proteins.
Leukemias and blood dyscrasias following exposure to chlordane and heptachlor
Authors: Epstein Samuel S. , Ozonoff David 
Published: February 2006

AbstractWe present 25 new cases of blood dyscrasia, including leukemias, production defects, and thrombocytopenic purpura, generally following home termite treatment with the chlorinated hydrocarbon pesticides chlordane and heptachlor (C/H). These newly reported cases are consistent with 34 previously published case reports associating blood dyscrasias with C/H exposure. Additionally, the newly reported leukemias are consistent with epidemiologic evidence of excess risk of leukemia and other cancers in C/H‐exposed populations and with the carcinogenic action of C/H in animals. The importance of case reports in warning of the association of blood dyscrasias to C/H exposure is emphasized. Until the voluntary halt in production in July 1987, millions of homes in the United States were treated with chlordane and heptachlor for termites even though their agricultural uses were phased out in 1978, largely on the grounds of “imminent hazard” because of carcinogenicity. In view of the recognized myelotoxicity, carcinogenicity, and other chronic toxic effects of these pesticides, a national program for monitoring all homes treated is urgently needed to detect persistent contamination.
Teratogenicity of N‐(4‐hydroxyphenyl) ‐all‐trans‐retinamide in rats and rabbits
Authors: Kenel Michael F. , Krayer John H. , Merz Eileen A. , Fred Pritchard J. 
Published: February 2006

AbstractN‐(4‐hydroxyphenyl)‐all‐trans‐retinamide (HPR) has potential efficacy in the treatment of dermatologic, arthritic, and neoplastic disorders. The teratogenicity of such a compound is of special concern in light of the known adverse effects of retinoids, in general, on the developing conceptus. In these studies, Sprague‐Dawley rats and New Zealand White rabbits were treated orally from gestation days 6 to 15 and 6 to 18, respectively, with 0, 20, 125, or 800 mg/kg/day of HPR.In rat fetuses, low incidences of hydrocephaly (mid‐ and high‐dosage groups) were observed. Fetal tissue (ng/g) and maternal plasma (ng/ml) concentrations of HPR, its major metabolite (N‐[4‐methoxyphenyl] retinamide [MPR]) and retinol were determined in separate groups of similarly‐treated rats 3 h following the last dose on gestation day 15. Fetal tissue concentrations of HPR and MPR were approximately one‐half maternal plasma concentrations. A dose related reduction in maternal plasma and fetal tissue concentrations of retinol were also observed.In mid‐ and high‐dosage rabbit fetuses, a dose‐related increase in the incidence of dome‐shaped head was observed. Subsequent skeletal evaluation revealed delays in skull bone ossification and a widening of the frontal and frontoparietal sutures. Microphthalmia was also observed in two high‐dosage fetuses. A dose‐dependent and statistically significant reduction in maternal plasma retinol levels was observed across all dosage groups.
Prenatal and postnatal thallium exposure in rats: Effect on development of vasomotor reactivity in pups
Authors: Rossi F. , Marrazzo R. , Berrino L. , De Santis D , Lisa M. , Susanna V. , Montanaro C. , Fici F. , Marmo E. 
Published: February 2006

AbstractVasomotor reactivity has been evaluated in rats exposed perinatally and postnatally to thallium sulphate (1 mg/dl in their drinking water ad libitum).Prenatal and postnatal exposure to thallium did not modify the values of the systolic arterial blood pressure on the 30th and 60th day in pups of normotensive and DOCA‐hypertensive rats. The hypertensive responses induced by endosinusal carotid hypotension and by 1‐noradrenaline in pups of normotensive and DOCA‐hypertensive rats, exposed or not exposed to thallium sulphate, were more intensive on the 60th than on the 30th day. Similar effects were observed for the hypotensive responses induced by 1‐isoprenaline and acetylcholine. Prenatal exposure to thallium did not modify hypertensive responses induced by endosinusal carotid hypotension on the 30th and 60th days, but it caused a decrease of hypertensive responses induced by 1‐noradrenaline on the 30th and 60th days and hypotensive responses induced by 1‐isoprenaline and acetylcholine exclusively on the 60th day.Postnatal exposure to thallium did not modify hypertensive responses induced by endosinusal carotid hypotension and hypotensive responses induced by acetylcholine, but it caused a decrease of hypertensive responses induced by 1‐noradrenaline on the 30th and 60th days in pups of normotensive rats and exclusively on the 60th day in pups of DOCA‐hypertensive rats. Moreover, postnatal exposure to thallium caused a decrease of the hypotensive response induced by 1‐isoprenaline exclusively on the 60th day.Our findings show that prenatal and postnatal exposure to thallium sulphate modifies the rat's developing vascular autonomic nervous system with a reduction of the α, β‐adrenergic and muscarinic vasomotor reactivity.
Mutagenicity and carcinogenicity studies of homemade “rust‐proof cutting fluid”
Authors: Wang Da , Huang Wei‐Qun , Wang Heng‐Wen 
Published: February 2006

AbstractA homemade rust‐proof cutting fluid (RPCF) used in China was tested for carcinogenicity by an in vivo chronic experiment and for mutagenicity by the Ames Salmonella microsomal assay. Undiluted and threefold water‐diluted fluid were given as drinking water to groups of young adult Wistar rats for 2 years. The treatment induced 11/40 malignant tumors with 9/40 acinar adenocarcinomas of the pancreas in the high‐dose group. Simultaneous administration of ascorbic acid dissolved in the undiluted fluid at 2 g acid per 1 g sodium nitrite resulted in 1/40 pancreatic carcinoma. The results of the Ames test showed that the technical RPCF was mutagenic to TA100 with or without metabolic activation. It was concluded that the homemade RPCF, which is comprised of sodium nitrite, triethanolamine, and polyethylene glycol, may form direct‐acting mutagen(s) upon storage and form, in vivo, e.g., nitrosamines that caused acinar pancreatic carcinoma in Wistar rats. Simultaneous administration of ascorbic acid is suggested for the protection of workers exposed to the rust‐proof cutting fluid.
Qualitative analysis of chromosomal evolution in a colcemid‐treated chinese hamster population
Authors: Simi S. , Colella C. M. , Mariani T. , Piras A. , Rainaldi G. 
Published: February 2006

AbstractColcemid is known to inhibit the spindle formation and to induce polyploidy and chromosomal nondisjunction. Using a V79 Chinese hamster cell line, we have shown that colcemid is able to induce the formation of cells that are numerically diploid but whose karyotype, when analyzed with the G‐banding technique, differs from that of the untreated ones. Even though these cells have a normal chromosomal constitution, they carry alterations in the chromosomal balance and, consequently, in gene dosage. This could result in an abnormal expression of cellular genes or in the expression of new or preexisting recessive mutations, even in a diploid chromosomal constitution.
Dominant lethality in mice—a test for mutagenicity of influenza X‐31 virus
Authors: Pathki Vandana K. , Polasa H. 
Published: February 2006

AbstractThe induction of dominant lethal mutation in germ cells is the cause of embryonic death resulting in the reduction of litter size in the F1 progeny. Dominant lethal mutations were induced when male mice were infected with live A2 influenza virus. The chromosomal aberrations induced in the germ cells were shown to be responsible for the dominant lethality. Killed influenza virus was also potent in inducing chromosomal aberrations in spermatocytes of mice. In light of these observations, the UV‐inactivated virus was tested for its potency in induction of dominant lethality in both female and male germ cells. The virus‐inoculated females were mated with uninjected males and vice versa. Both the inactivated and live virus were found to induce dominant lethality in both female and male mice, indicating that not only the live virus but also the inactivated virus is capable of bringing about chromosomal damage resulting in dominant lethality.
Effects of N‐acetylcysteine on fetal development and on phenytoin teratogenicity in mice
Authors: Wong Mayme , Wells Peter G. 
Published: February 2006

AbstractThe teratogenicity of phenytoin may result from its enzymatic bioactivation to a reactive intermediate, which interacts irreversibly with fetal tissues. Since glutathione (GSH) is involved in the detoxification of many reactive intermediates, N‐acetylcysteine (NAC), a glutathione precursor, was evaluated for its effects on murine fetal development and phenytoin teratogenicity. NAC, 100 to 275 mg/kg, was given intraperitoneally (ip) or per os (po), or as 266 to 410 mg/kg in the drinking water, at various times before or after phenytoin, 65 to 75 mg/kg ip, on gestational days 12 and 13. Dams were killed on gestational day 19, fetal resorptions were noted, and fetuses were examined for anomalies. Significant reductions in phenytoin‐induced fetal weight loss and cleft palates were observed when NAC was given by gavage 6 hours after phenytoin or in the drinking water with the lower dose of phenytoin. NAC administered in the drinking water also reduced the incidence of resorptions produced by the higher dose of phenytoin and enhanced postpartum survival in fetuses exposed to 65 or 75 mg/kg phenytoin (P < .05). Conversely, the incidence of resorptions increased when NAC was given by gavage at other times before or after phenytoin, by single or repetitive ip injections, or in high concentrations in the drinking water (P < .05). When given with the higher dose of phenytoin, NAC administered via the drinking water significantly increased the incidence of phenytoin‐induced cleft palates and fetal weight loss (P < .05). Similar results were obtained with a single ip injection of NAC and a lower dose of phenytoin. Thus, when given orally, NAC can partially reduce phenytoin teratogenicity and embryopathy. However, altering the route of NAC administration, or increasing the dose of phenytoin and/or NAC, enhanced phenytoin embryotoxicity, and NAC alone at higher doses had embryopathic effects.
Effect of smokeless tobacco on the development of the cd‐1 mouse fetus
Authors: Paulson Ruth , Shanfeld Joseph , Sachs Larry , Ismail Mounira , Paulson John 
Published: February 2006

AbstractThe objective of this study was to examine the effect of smokeless tobacco (ST) on the development of the CD‐1 mouse fetus. ST was administered continuously via Alzet osmotic minipumps during the critical gestational days 7–14 and 6–13. Two ST dosages were administered, 3.2 mg/ml (Dosage I) and 6.4 mg/ml (Dosage II), which yielded plasma nicotine levels within the range comparable to those of an average ST user or smoker (36.0 ng/ml).Plasma nicotine levels were maintained in the range of 29.4 ± 4.8 ng/ml to 44.3 ± 16.0 ng/ml for the Dosage I group of dams, and in the range of 34.6 ± 10.9 ng/ml of 75.5 ± 19.9 ng/ml for the Dosage II group of dams. The main effect on the fetus was weight reduction, with Dosage I producing a tendency toward weight reduction (p = .08). Dosage II produced a significant 8.6% weight reduction from normal (p < .0001) and an increase in fetal deaths (p < .03). Dosage I produced an increase in the incidence of hemorrhages and supernumerary ribs, and a significant delay (p < .05) in ossification of the supraoccipital bone, the sacrococcygeal vertebrae, and the bones of the forefoot and hindfoot. There were no significant differences between placental weights. Weights of dams were significantly reduced only at the higher ST exposure levels.We conclude that at plasma nicotine levels comparable to those of an average ST user, ST produces weight reduction, delayed ossification, and increase in hemorrhages and fetolethality in the CD‐1 mouse fetus.
Stage‐related induction of chromosomal aberrations and SCE in mouse embryos treated transplacentally during organogenesis with MMC and DMBA
Authors: Müller Lutz 
Published: February 2006

AbstractDuring organogenesis, mouse embryos were treated transplacentally with MMC and DMBA. The clastogenic and SCE‐inducing effects of MMC and the clastogenic effects of DMBA were analyzed in metaphases from whole embryo suspensions. Positive effects were observed on all the days of pregnancy on which the embryos were analyzed, i.e., on days 10, 11, 12, and 13. Whereas the MMC‐induced SCE‐frequencies did not change significantly during the tested period, the clastogenic effects of MMC and DMBA varied drastically. Extremely high aberration rates were observed in embryos on day 11; on the other days the aberration rates were much lower. Factors that might have given rise to these stage‐related effects are discussed.
Effect of nitrous oxide on embryonic macromolecular synthesis and purine levels
Authors: Hansen Deborah K. , Grafton Thomas F. 
Published: February 2006

AbstractNitrous oxide (N2O), an anesthetic gas, has been implicated as a human teratogen. The mechanism for its developmental toxicant effects is not known but may involve depression of embryonic macromolecular synthesis caused by alterations in precursor concentrations. Such changes might be caused by decreased folate levels. Pregnant rats were exposed to 50% N2O for 24 hours on day 10 of gestation; this is not an anesthetic dose. Embryos were removed immediately after exposure and grown in a rodent whole embryo culture system for 4 hours in medium containing radiolabeled precursors for RNA or protein. Exposure to N2O decreased embryonic DNA and RNA contents but did not alter number of somite pairs or protein content. Such treatment also decreased incorporation of radiolabeled uridine into acid‐precipitable RNA. There was no difference between control and treated embryos in the incorporation of radiolabeled leucine into protein. There were also no differences between control and exposed embryos in the level of acid‐soluble purines. The lower DNA and RNA contents in N2O‐treated embryos are apparently not the result of decreased levels of adenine or guanine.
Comparison of behaviors for detection of heritable mutations
Authors: Ficsor Gyula , Goldner Lee , Panda Brahma B. 
Published: February 2006

AbstractGroups of five male HA (ICR) mice were injected intraperitoneally with 60, 150, 300, or 600 mg/kg body weight of ethyl methanesulfonate (EMS) or with saline vehicle. Each male was mated to two untreated females at 2 and 5 weeks after treatment. The two successive matings utilized sperm derived from post‐ and premeiotic germ cells, respectively. Progeny were evaluated for litter size, body weight, negative geotactic response, swimming patterns, limb use while swimming, water escape time, and open‐field motor coordination activity. Body weight, geotactic response, limb use, and open‐field behavior test results demonstrated that EMS causes heritable behavior mutations in both post‐ and pre‐meiotic germ cells. Among the tests that showed inherited differences between control and treated groups, the computer‐monitored open‐field behavior test was the most definitive.
Effect of heat shock on the mutagenicity of mutagens and carcinogens in Euglena gracilis
Authors: Chreč Ondrej , Krajčvič Juraj , Ebringer Libor , Polónyi Jozef 
Published: February 2006

AbstractThe effect of heat‐shock treatment (42°C for 15 min) on the ability of four mutagens and carcinogens to induce hereditary bleaching in Euglena gracilis cells was investigated. All four mutagens (treatment time: 1–24 h) tested after heat shock increased the frequency of bleached mutants of Euglena gracilis.
Somatic mutation induced by heliotrine in Drosophila
Authors: Sivlingham R. , Brink N. G. 
Published: February 2006

AbstractThe pyrrolizidine alkaloid heliotrine has been shown to be a powerful mutagen in Drosophila. This report has evaluated the teratogenicity of heliotrine in this organism. The alkaloid was fed to larvae and its teratogenic effects measured in various developmental stages of the insect. The pupal stage is predominantly affected. The main consequences of treatment were failed eclosions at higher alkaloid concentrations (10−4 M), while lower concentrations (10−4 M) permitted the eclosion of adults, but these showed abdominal abnormalities ranging from severe distortions to reduced numbers of tergite bristles. mei‐9 strains of Drosophila were more sensitive to the production of somatic chromosomal changes as well as the teratogenic effects of the alkaloid. These strains also showed reduced numbers of cells in histoblast nests of 6‐hour‐old prepupae. It is suggested that reduced numbers of histoblast cells in prepupae may be a consequence of genetic damage and this in turn leads to the abdominal distortions and reduced bristle numbers observed.
Comparative antimutagenicity of chlorophyllin and five other agents against aflatoxin B1‐induced reversion in Salmonella typhimurium strain TA98
Authors: Whong Wen‐Zong , Stewart John , Brockman Herman E. , Ong Tong‐man 
Published: February 2006

AbstractChlorophyllin was studied for its antimutagenic activity against aflatoxin B1 in Salmonella typhimurium strain TA98 using the plate‐incorporation test in the presence of S9 activation. Comparative antimutagenicity between chlorophyllin and certain commonly studied antimutagens (i.e., vitamins A, C, and E, retinoic acid, and β‐carotene) was also examined. A dose‐related inhibition of aflatoxin B1 mutagenicity by chlorophyllin was observed, with the mutagenicity being abolished by 860 nmole chlorophyllin per plate. The inhibitory activity of chlorophyllin occurred only when cells were treated concurrently with chlorophyllin and aflatoxin B1. The antimutagenic potency of chlorophyllin was comparable to that of vitamin A and higher than that of retinoic acid and β‐carotene. Vitamins C and E had no effect on aflatoxin B1 mutagenicity under the conditions used. The results of toxicity tests and a reconstruction experiment showed that inhibition of the mutagenicity of aflatoxin B1 by chlorophyllin and the other active agents was due to antimutagenicity.
Human embryonic cell growth assay for teratogens with or without metabolic activation system using microplate
Authors: Tsuchiya Toshie , Matuoka Atsuko , Sekita Setsuko , Hisano Takuzo , Takahashi Atsushi , Ishidate Motoi 
Published: February 2006

AbstractIn vitro microassay for the screening of teratogens was investigated on cancer chemotherapeutic agents sterigmatocystins and benzimidazoles using human embryonic palatal mesenchymal (HEPM) cells. Five thousand cells were inoculated into each well of 96‐well microtiter plates, and cultivated for 24 hr, after which the media were changed with new ones that contained various amounts of chemicals; after cultivation for an additional 72 hr, the media were discarded, and cells attached to the tissue plate were fixed and stained with Giemsa's solution; the cell number then was counted by colony counter with three readings for each well. For the metabolic activation, the liver S9 obtained from rats pretreated with phenobarbital and 5,6‐benzoflavone and cofactors (S9 mix) were added directly to the HEPM cell cultures along with chemicals. After 6 hr, the cultures were exchanged with a fresh medium and incubated for a further 72 hr. The final IC50 (the concentration that inhibits growth 50%) concentration‐finding run had 7 to 11 concentration points (mean, three to four wells).Concentrations of the cancer chemotherapeutic agents that inhibited growth by 50% ranged from 0.001 to 10 μg/ml. Sterigmatocystins indicated strong inhibition; among three derivatives, O‐acetyl sterigmatocystin was the most potent inhibitor. Benzimidazoles also exhibited an inhibitoy action on HEPM cell growth; nitro and chloro groups at the 5 position in 2‐(2‐pyridyl)benzimidazole were found to be potent substituents. As for the activation of cyclophosphamide in the HEPM cell culture, IC50 was decreased to 1.0 ug/ml by the incubation with S9 mix for 6 hr under our experimental conditions, and sterigmatocystin was found to be activated by S9 mix. This system was simple and useful for the detection of teratogens that inhibit HEPM cell growth with or without metabolic activation system.