bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reproductive toxicology of inhaled styrene oxide in rats and rabbits
Authors: Sikov Melvin R. , Cannon William C. , Carr Daniel B. , Miller Rodney A. , Niemeier Richard W. , Hardin Bryan D. 
Published: October 2006

AbstractExperiments were performed to evalute reproductive and developmental toxicology in rats and rabbits exposed to styrene oxide by inhalation. Female rats were exposed to 100 or 300 ppm styrene oxide or to filtered air for 7 h/day, 5 days/week for 3 weeks. Extensive mortality occurred in rats that received prolonged exposure to 100 ppm styrene oxide while 300 ppm was rapidly lethal. As a result exposures were terminated in this latter group and the group was eliminated from further study. The rats of the 0 and 100 ppm groups were then mated and exposed to 0 or 100 ppm styrene oxide daily through 18 days of gestation (dg).Female rabbits were artificially inseminated and exposed for 7 h daily to 0, 15, or 50 ppm styrene oxide through 24 dg. Both of these lower concentrations used for exposure of the rabbits produced mortality of does. The rats were killed at 20 dg and the rabbits at 30 dg. Pregnant animals were examined for toxic changes including altered tissue weights and histopathologic effects. Litters were evaluated using several measures of embryotoxicity, and live fetuses were examined for external, visceral, and skeletal malformations.Exposure during gestatation appeared to increase preimplantation loss in rats, and tended to increase the incidence of resorptions in rabbits. In both species, fetal weights and crown‐rump lengths were reduced by gestational exposure. The incidences of ossification defects of the sternebrae aned occipital bones were increased by gestational exposure of rats to styrene oxide. These results indicate that inhalation exposures at these concentrations produce reproductive and development toxicity, as well as maternal toxicity.
The teratogenic potential and dose–response of dermally administered ethylene glycol monomethyl ether (EGME) estimated in rats with the chernoff–kavlock assay
Authors: Wickramaratne G. A. De S. 
Published: October 2006

AbstractThe Chernoff and Kavlock in vivo assay was used to study the teratogenic potential of ethylene glycol monomethyl ether (EGME). It was administered to pregnant rats on days 6–17 (inclusive) of gestation by the dermal route at an application rate of 10 ml kg−1 body weight of 3%, 10%, 30% and 100% EGME with physiological saline as the solvent. 100% was lethal to the pregnant rats, 30% was lethal to the fetuses, 10% produced small litter sizes with poor survival and 3% had no adverse effects. By the ‘rules’ developed to evaluate results from the assay, 10% was judged to be a potentially teratogenic dose in the rats. The study also demonstrated the usefulness of this assay for pre‐screening or additional investigations for suspected teratogens when route of exposure could be important in determining the potential hazard.
Determination of rat β2‐microglobulin in urine and in serum. I. development of an immunoassay based on latex particles agglutination
Authors: Viau C. , Bernard A. , Lauwerys R. 
Published: October 2006

AbstractRat β2‐microglobulin has been isolated from the urine of rats pretreated with sodium chromate. The purified protein was used to raise antisera in two rabbits. Treatment of the antisera with ammonium sulphate followed by gel chromatography led to an immunoglobulin fraction which was used to coat latex particles by physical adsorption. The latex suspension was used in an automated system including an optical particle counter to analyse the protein in serum, urine and cerebrospinal fluid. Serum contains 5.8 mg of β2‐microglobulin/l, of which 33% is found as a 55000 dalton complex while 66% is present as the ‘free’ protein. The daily urinary excretion of β2‐microglobulin in females is about 2 μg of which 7% is found to be a 65000‐dalton complex while 92% is the free protein. From this, it can be calculated that the fractional urinary excretion of β2‐microglobulin is about 0.03%. The cerebrospinal fluid contains about 1 mg of β2‐microglobulin/l. Preliminary tests also suggest that the method can be adapted for non‐automated turbidimetric detection. In the automated assay, the within‐ and between‐assay coefficients of variation are less than 10% for the three biological fluids tested. The analytical recovery in the urine is 93%. In urine, β2‐microglobulin undergoes proteolytic degradation at pH below 6. This does not represent a serious drawback to its use as a sensitive index of tubular function since in most experimental circumstances, rats excrete urine with a pH above this value.
Comparison of the effects of urinary flow on adjusted and non‐adjusted excretion of heavy metals and organic substances in ‘healthy’ men
Authors: Araki S. , Murata K. , Aono H. , Yanagihara S. , Niinuma Y. , Yamamoto R. , Ishihara N. 
Published: October 2006

AbstractThe effect of variation in urinary flow rate (ml urine min−1, UF) on adjusted and non‐adjusted urinary excretion of metals and organic substances was examined in ten ‘healthy’ men. The effect of UF was found to be eliminated when urinary concentrations of lead (Pb), hippuric acid (HA), delta‐aminolevulinic acid (ALA) and coproporphyrin (CP) were adjusted to urinary specific gravity and to UF. Similarly, the effect of UF on inorganic mercury (Hg) was eliminated when the concentration was adjusted to timed excretion and to UF. The effect on zinc (Zn) and copper (Cu) was eliminated when adjusted to urinary creatinine (Cn) and to UF. The difference in the effect of UF on the adjusted urinary excretion was explained by the effect of UF on timed excretion of substance, which was ranked in the following order: Pb, HA, total urinary solutes, ALA and CP; Zn; Cu; Cn; and Hg. It was concluded that ‘UF‐adjusted concentration’ is applicable to measurement of all substances in urine as a method of minimizing UF effects, while the other three adjustment methods have only limited uses.
Chelation in metal intoxication. XIX. α‐mercapto‐β‐aryl acrylic acid as antidotes to nickel and lead toxicity
Authors: Sharma B. L. , Kachru D. N. , Singh S. , Tandon S. K. 
Published: October 2006

AbstractIn view of the reported effectiveness of α‐mercapto‐β‐(2‐furyl) acrylic acid (MFA) as an effective antidote to inorganic mercury toxicity, some α‐mercapto‐β‐aryl acrylic acids were synthesized and examined for their efficacy in counteracting nickel and lead intoxication in rats. α‐mercapto‐β‐(3,4‐dimethoxyphenyl)acrylic acid (MDA) was most effective and other compounds were less but about equally effective in enhancing urinary excretion and in reducing tissue concentration of Ni. MDA was the only compound to remove Ni from the brain. MFA was also more effective than other structurally related compounds in enhancing urinary and faecal excretion and in lowering body burden of Pb. All the compounds significantly reduced the inhibition of the activity of blood δ‐aminolevulinic acid dehydratase (δ‐ALA‐D) and increase in the urinary excretion of δ‐aminolevulinic acid (δ‐ALA) caused by Pb. The results do not show any relationship between the nature of the substitution at the β‐position of α‐mercapto acrylic acids and their ability to reduce the concentration and the toxic effects of the two metals. However, these thiol chelating agents appear promising as antidotes to Ni and Pb poisoning.
Cyanide stimulation of tri‐N‐butyltin mediated hemolysis
Authors: Gray Brian H. , Porvaznik Martin , Lee Lanfong H. 
Published: October 2006

AbstractThe effects of tributyltin and sodium cyanide on hemolysis in human erythrocytes are described. Tributyltin has a sharp cut‐off concentration for induction of hemolysis. A 5 μM concentration of tributyltin induces hemolysis and 1 μM or less does not in erythrocyte supensions with 2.3×108 cells per ml. The kinetics for tributyltin‐induced hemolysis are sigmoidal indicating a complex molecular mechanism leading to lysis. Ten mM sodium cyanide plus 1 μM tributyltin does not stimulate hemolysis rates above levels observed with 10 mM sodium cyanide alone. Five mM sodium cyanide plus hemolytic concentrations of tributyltin stimulates hemolysis rates synergistically compared with either cyanide or tributyltin alone. Ultrastructurally, hemolytic concentrations of tributyltin can be visualized in the electron microscope by osmium staining during fixation as electron‐dense spheres penetrating the lipid bilayer of the erythrocyte plasma membrane. Ten mM sodium cyanide plus 25 μM tributyltin increases slightly the size of osmiophilic structures in erythrocyte membranes compared with those spheres seen in cells exposed to 25 μM tributyltin alone. Sodium cyanide is the only compound tested that stimulates tributyltin‐induced hemolysis. Sodium thiocynate, previously shown to be rapidly exchanged across erythrocyte membranes by tributyltin, reduces the rate of hemolysis. It is likely that sodium cyanide stimulates hemolysis in the presence of hemolytic tributyltin concentrations because the multimolecular, membrane‐intercalated, tributytin aggregates are transporting cyanide anion by the electrically silent, anion exchange mechanism demonstrated for other anions. It is suggested that this mechanism delivers cyanide anion to or near critical membrane sites where it is available for enzyme inhibition or cross‐linking of protein sulfhydryl groups.
Stimulation of lipid peroxidation and impairment of glutathione‐dependent defence system in the liver of rats repeatedly treated with carbon tetrachloride
Authors: Yalçin A. Süha , Koçak‐Toker Necla , Uysal Müjdat , Aykaç Gülçin , Sivas Ahmet , Öz Hikmet 
Published: October 2006

AbstractTo study the effect of carbon tetrachloride treatment on hepatic lipid peroxidation and glutathione‐dependent defence system, rats were injected with carbon tetrachloride (0.2 ml/kg body weight, i.p.) twice weekly for a period of 4 weeks. Carbon tetrachloride treatment caused a significant increase in hepatic lipid peroxide levels and significant decreases in hepatic glutathione levels and glutathione peroxidase and glutathione transferase activities. These results show that chronic carbon tetrachloride administration to rats leads to the stimulation of hepatic lipid peroxidation, which seems to be the consequence of impaired cellular defence by glutathione and glutathione‐related enzymes.
Effects of diflubenzuron on the mouse liver
Authors: Young Mark F. , Trombetta Louis D. , Carson Steven 
Published: October 2006

AbstractDiflubenzuron (DFB), a potent inhibitor of insect chitin synthesis, was administered to Swiss Webster mice in a 30‐day oral intubation study. Animal groups received either no treatment, vehicle control (Polyehylene glycol 400), or DFB suspensions at doses of 125, 500, and 2000 mg/kg body weight. Hepatic gluta thione S‐transferase activity as well as morphological characteristics were studied. DFB was shownn to elicit hepatocellular changes at all dose levels. The activities of three glutathione S‐transferases (S‐aryl, S‐aralkyl, and S‐epoxide) were all altered after DFB administration. Light microscopy revealed radial arrays of hepatocellular vacuolization between the portal and central vein areas. Electron‐microscopic examination, verified by morphometric analysis, revealed degenerativ changes as well as an increased volume density of the endoplasmic reticulum.
Teratologic studies on alcide Allay® gel in rabbits
Authors: Abdel‐Rahman Mohamed S. , Skowronski Gloria A. , Gerges Samy E. , von Hagen Stanley , Turkall Rita M. 
Published: October 2006

AbstractAlcide Allay® gel, a highly effective germicidal compound, was evaluated for teratogenic potential in rabbits. Pregnant rabbits were administered 2 g/kg Allay® get (containing either of two concentrations of sodium chlorite as active ingredient) or placebo topically on days 6–18 of gestation. Moderate to severe erythema was recorded in the high‐dose gel group on day 11 (Draize score = 3.5). By day 18, the skin of all rabbits in the high dose treatment group appeared normal. Decreased maternal body weight gain was observed in the low dose and placebo gel groups. Fetal weights and lengths were significantly reduced in all gel groups. There was some incidence of skeletal anomalies in all gel treated groups, however, these incidences were not statistically different from the control group. The commonly occurring skeletal defects were incomplete ossification of skull bones, small or missing sternebrae, and extra ribs. The incidence of visceral abnormalities in all gel groups was not statistically different from control animals. Visceral anomalies included heart displacement, fusion or serration of the liver, and kidney displacement. Alcide Allay® gel at 2 g/kg was non‐teratogenic to rabbit fetuses.
Pithomyces chartarum spore counts in rumen contents and faeces of sheep exposed to autumn pasture at three different grazing pressures
Authors: Smith B. L. , Embling P. P. , Gravett I. M. 
Published: October 2006

AbstractThree groups, each of 18 lambs were grazed during autumn in paddocks which had been divided longitudinally by temporary fencing to give twofold differences in grazing intensity between the groups. During the period when spore numbers were elevated the high grazing pressure (HGP) group lost some body weight (−34 g/day). The low grazing pressure (LGP) group gained +90 g/day and the intermediate grazing pressure (IGP) group gained weight slightly (+14 g/day). There were two spore rises during the experimental grazing period, a minor and a major rise. Peak pasture spore counts were 88 000, 130 000 and 282 000 spores/g grass for the LGP, IGP and HGP groups respectively. These were reflected in the peak rumen content counts which were 6640, 17 050 and 24 470 spores/g and the faecal peak counts which were 141 400, 330 800 and 568 200 spores/g for the LGP, IGP and HGP groups respectively. Liver injury scores were 0.9, 2.6 and 1.7 and peak mean serum GGT levels were 139, 312 and 220 U/I for the LGP, IGP and HGP groups respectively. The greater liver injury in the IGP groups was considered due to the greater total consumption of spores caused by the combination of pasture spore concentration and dry matter intake.
Aluminium induced damage of the lysosomes in the liver, spleen and kidneys of rats
Authors: Stein Günter , Laske Volker , Müller Andreas , Bräunlich Helmut , Linß Werner , Fleck Christian 
Published: October 2006

AbstractThe influence of repeated aluminium (Al) administration (0.05 or 0.5 mg 100 g−1 b.w.t. i.p. 5 times weekly for 12 weeks) on the lysosomal enzymes N‐acetyl‐beta‐D‐glucosaminidase (β‐NAG) and beta‐glucuronidase (β‐Gluc) in serum, liver, spleen and kidneys of adult female rats with intact kidneys, (NR), or following partial nephrectomy (5/6 NX) was investigated. After Al loading, at the high dose only, the β‐NAG in serum and the free β‐NAG in liver, spleen and kidneys increased. Latent β‐NAG levels decreased in all three organs the effect being dose related. Following Al loading no elevation in total enzyme activity was observed, with one exception. Depending on Al doses the spleen of the non‐operated animals, the liver of both groups of animals and the serum showed a decrease in β‐Gluc activity. No effect on β‐Gluc activity was observed in the spleen of 5/6 NX animals or in the kidneys of either group of animals. The results confirm that high doses of Al induce toxic effects and damage the lysosomes in the liver, the spleen and the kidneys. The results indicate that the extent of lysosomal damage correlates with dose and duration of Al loading. Repeated administration of Al also interferes selectively with enzyme synthesis.
A programmed feedback control of solvent vapour concentrations in experimental inhalation chambers
Authors: Bonnet P. , Raoult G. , Delcourt J. , Jeandel B. , de Ceaurriz J. 
Published: October 2006

AbstractThis paper describes a computer‐controlled system to regulate solvent vapour concentrations in experimental inhalation devices. This system consists of an exposure chamber, a bubbler with a mass flow‐meter, a monitor gas chromatograph and a computer. The frequency of automatic sampling was dependent upon the retention time of test materials. Flow‐rate was corrected through a computer regulated bubbler as soon as the mean chamber concentration varied by more tham 2.5% of a command level. Regulation coefficients were calculated by relating the concentration of vapours sampled with adsorbent tubes to the mean peak areas given by the mantor gas chromatograph. They were then fed into the computer allowing the actual concentration to be adjusted to the command level. Deliberately induced fluctuations in the level of acetone, ethanol and trichloroethylene, either sudden or progressive, were satisfactorily corrected as were fluctuations occurring normally during repeated exposures to ethanol. Variations were generally inferior to 5% of the command level.
Renal and hepatic lesions induced by 2,2,4‐trimethylpentane
Authors: Fowlie A. J. , Grasso P. , Bridges J. W. 
Published: October 2006

AbstractThe renal changes produced by 2,2,4‐trimethylpentane, a constituent of unleaded gasoline, are studied in Wistar rats. The compound was given at a dose of 2 ml/kg daily by gavage dissolved in corn oil (2:1) to nine Wistar Albino rats. Nine control male rats received an equivalent dose of corn oil. Six animals were housed in metabowls to allow the collection of urine for enzyme and urinanalysis. The remaining three animals of each group were housed in a normal animal cage. After 2 days of treatment, all the test rats were noted to have lost weight and were killed on this or on the subsequent day. Macroscopic examination of the livers and kidneys revealed no visible lesions on the kidney, but two of the rats had white, slightly raised patches on the liver. Microscopic examination demonstrated centrilobular and confluent necrosis, hydropic degeneration and vaculolation of hepatocytes. Microscopic examination of the kidneys indicated eosinophilic hyaline droplet accumulation in the cells of the tubules, and tubular dilation. Analysis of plasma alkaline phosphatase and aspartate transominase activity revealed increases consistent with liver damage. Analysis of urinary N‐acetyl‐β‐glucosaminidase and alkaline phosphatase activity showed increases consistent with renal toxicity. An apparent increase in the amount of cellular debris in the urine was also found, when the sediment was examined microscopically.From this study, it would appear that 2,2,4‐trimethylpentane possess hepatotoxic as well as nephrotoxic properties.
Aspirin disposition in rats acutely intoxicated with CCl4
Authors: Favari Liliana , Mourelle Marisabel , Amezcua Joseg Luis 
Published: October 2006

AbstractThe profile of urinary salicylate metabolites was determined after an oral administration of acetylsalicylic acid (ASA) to: 1, control rats; 2, rats treated with CCl4 and 3, rats intoxicated with CCl4 and also pretreated with colchicine for 7 days. The following enzymatic activities were determined: liver and plasma ASA‐esterase, liver UDP‐glucuronyltransferase and liver aniline hydroxylase. The time course of plasma concentration of salicylates in similar groups were followed after the intraperitoneal administration of acetylsalicylic acid (ASA), salicylic acid (SA) or gentisic acid (GA). The animals acutely intoxicated with CCl4 showed a reduction in urinary excretion of glucuronates and an increased urinary excretion of gentisic and salicylic acids. The activities of plasma and liver ASA‐esterases were significantly increased in CCl4‐treated rats while the aniline hydroxylase was reduced and the UDP‐glucuronyltransferase remained unchanged. The plasma half lives of salicylates were reduced in CCl4‐treated rats regardless of the administered parent compound. Colchicine pre‐treatment completely prevented the alterations produced by acute intoxication with CCl4. The heterogeneity of liver metabolic disfunctions present in acute liver damage was evidenced. It is emphasized that the pharmacokinetic alterations produced by acute liver injury can be the result of complex factors that may involve changes in circulation, hepatic binding protein and other routes of elimination.
Haemotoxicity to chicken (Gallus gallus domesticus) by technical and formulation grades of some phosphoric and synthetic pyrethroid esters
Authors: Qadri Syed S. H. , Jabeen K. , Mahboob M. , Mustafa M. 
Published: October 2006

AbstractAcute toxicity was studied by administering an encapsulated single dose to chickens (G.g. domesticus) and observing them for 21 days. Azodrin‐71 (Tech.) was found to be extremely toxic, whereas Cypermethrin‐92 (Tech.), Cypermethrin‐25 EC and Permasect‐25 EC (Form.) were practically non‐toxic based on LD50 value determinations.Sub‐acute oral haemotoxicity of technical and formulation grades of these insecticides was also studied by administering encapsulated low, medium and high daily doses for 21 days to chickens and recording clinical symptoms, mortality and haematological parameters pre and post‐dosing.Clinically high doses of Azodrin‐71 (Tech.) caused tremors and ataxia among chicks on the 10th day after dosing. Synthetic pyrethroids caused slight tremours in the whole body accompanied by salivation. In general, hyperactivity to external stimuli and loss of appetite and body weight were also observed.With sab‐acute oral doses, Permasect‐25 EC (Form.) more potently affected haemoglobin (Hb), red cell (RBC) counts and chloride level. Cypermethrin‐92 (Tech.) was most potent towards thrombocytes and clotting time. Azodrin‐71 (Tech.) was more potent to white cell (WBC) counts and serum protein level.The present Haematological studies have disclosed the possible reaction of blood and blood ferming organs to these insecticides.
Inhibition of hepatic microsomal lipid peroxidation by endogenous glycogen in the rat
Authors: Iba Michael M. 
Published: October 2006

AbstractThe effect of endogenous glycogen on lipid peroxidation was examined in hepatic microsomes from rats. Microsomes were prepared to retain endogenous hepatic glycogen (P) or to minimize it (P). The indices of lipid peroxidation examined included the rate of NADPH‐dependent formation of malondialdehyde (MDA) and the concomitant destruction of cytochrome P‐450 and decline in the linearity of benzphetamine N‐demethylase activity in microsomes. Cytochrome P‐450 was destroyed during benzphetamine N‐demethylation in microsomes with the loss being more extensive in P than in P. The destruction of cytochrome P‐450 and the concomitant loss in linearity of benzphetamine N‐demethylation in P were prevented by added EDTA. Added linoleic acid hydroperoxide (LAHP) also caused a time‐dependent loss of cytochrome P‐450 in microsomes with the rate being greater in P than in P. The results show that glycogen inhibits hepatic microsomal lipid peroxidation and suggest that variations in glycogen content may contribute to disparities in in vitro oxidative activities between different microsomal samples. Such disparities may be minimized by the removal of glycogen during the preparation of microsomes and then supplementing the incubation mixtures with EDTA. The in vivo relevance of the observed antioxidant effect of glycogen is discussed in terms of the possible modulation by the polysaccharide of hepatotoxicity by agents whose effects may be mediated by lipid peroxidation.