bluuebunny/crossref_metadata_2025_split huggingface dataset:
Degeneration and regeneration of respiratory mucosa of rats after exposure to styrene
Authors: Ohashi Yoshihiro , Nakai Yoshiaki , Ikeoka Hiroshi , Koshimo Hiroyuki , Nakata Junko , Esaki Yusuke , Horiguchi Shun'Ichi , Teramoto Keiko 
Published: October 2006

AbstractThe recovery process of pathological changes in the respiratory mucosa following exposure to styrene were experimentally studied to improve the understanding of the respiratory toxicity of styrene. Thirty male SD rats were exposed to 150 ppm or 1000 ppm of styrene for 4 h a day over 3 weeks (5 days a week). They were killed for examination at 1 day or 12 weeks after completion of the exposure sequence. Bilateral mucosal samples from the nasal septum and the trachea of the animals were examined for ciliary activity and subjected to electron microscopy, Complete functional and morphological recovery of the nasal and tracheal mucosa was observed at the 12th week post‐exposure to 150 ppm of styrene. After exposure to 1000 ppm of styrene, almost normal function and morphology of the tracheal mucosa was found at the 12th week post‐exposure, but the nasal mucosa continued to show decreased ciliary activity and an affected morphology.
Platelet population profiles: Significance of species variation and drug‐induced changes
Authors: Eason C. T. , Pattison A. , Howells D. D. , Mitcheson I. , Bonner F. W. 
Published: October 2006

AbstractPlatelet counts are routinely assessed from whole blood samples and recent technical advances enable the total platelet counts to be complemented by additional information which fully profiles the platelet population. In this report the platelet count, mode and mean platelet volumes and platelet profile histograms are presented for eight mammalian species. Species and strain variation in platelet profiles and the degree of volume heterogeneity are presented, and a platelet profile is presented for the marmoset which is previously unreported. The significance of these parameters and their potential importance to the toxicologist are disussed in the light of an observation of a drug‐induced altertaino in a platelet population profile.
Dose requirements, assay procedures and tissue specificity for PCB inductation of P‐450 dependent mono‐oxygenase activity in the rat: Implications for design of studies measuring in vivo induction of human placental monooxygenases
Authors: Wong Thomas K. , Blanton Toni E. , Hunnicutt Colleen K. , Shore David L. , Everson Richard B. 
Published: October 2006

AbstractPregnant Sprague‐Dawley and Fisher 344 rats were treated on day 15 of gestation with Aroclor 1254 in a single dose ranging from 0 to 500 mg kg−1 body weight and killed on day 18 of gestation. In the small groups of animals used for this study, no effect was observed on mean maternal liver or placental weight, or the number of fetal resorptions at any of the doses tested. Measurement of aryl hydrocabon hydroxylase (AHH) and 7‐ethoxycoumarin 0‐deethylase (7ECD) activity in tissue homogenates, however, showed that administration of Aroclor 1254 (15 mg kg−1 body weight or greater) induced mono‐oxygenase activity in fetal liver. Both the AHH and 7ECD assay detected effects of PCBs with similar sensitivity, and the findings were comparable when homogenates were assayed instead of microsomes. These data were used to suggest technical approaches to the detection of mono‐oxygenase induction in placental tissue human populations exposed to PCBs.
Comparison of effects of ozone, cadmium chloride and carbon tetrachloride on [14C]antipyrine metabolism in conscious rats
Authors: Dutta Saradindu , Kamat Madhav , Gole Dilip 
Published: October 2006

AbstractPreviously, Graham et al. found evidence that pentobarbital‐induced sleeping time was enhanced in various animals following exposure to 1 ppm of ozone in air. The present study was undertaken to investigate whether similar ozone exposure would cause inhibition of metabolism of another model drug, [14C]antipyrine, in conscious rats. Furthermore, this study also investigated whether, like that of ozone, other lipid‐peroxidizing agents such as cadmium and carbon tetrachloride would affect metabolism of [14C]antipyrine in conscious rats.The results showed no significant effect of ozone exposure on subsequent metabolism of [14C]antipyrine in conscious rats as revealed by very similar 14CO2 exhalation rate (CER)‐time profiles before and after ozone treatment under various exposure protocols. Even though the exposure to ozone caused no inhibition of antipyrine metabolism in conscious rats, cadmium and carbon tetrachloride, on the other hand, markedly inhibited metabolism of this model drug. In agreement with the reported sex‐difference in toxic effects of cadmium, during the present study the cadmium‐induced inhibitory effect on the CER‐time profiles was observed in male but not in female rats. In contrast, no clear sex‐dependency was noted in the inhibitory effect of carbon tetrachloride on [14C]antipyrine metabolism.
Biotransformation of dimethylarsinic acid in mouse, hamster and man
Authors: Marafante Erminio , Vahter Marie , Norin Harald , Envall Jeanette , Sandström Margareta , Christakopoulos Alexandros , Ryhage Ragnar 
Published: October 2006

AbstractThe metabolism of dimethylarsinic acid (DMA) a common pesticide and the main metabolite of inorganic arsenic in mammals, has been studied in mice, hamsters and man. Mice and hamsters were administered a single dose of 74As‐DMA (40 mg As/kg body weight) orally, while a human subject ingested DMA corresponding to 0.1 mg As/kg body weight. Ion exchange chromatography, paper electrophoresis, thin layer chromatography as well as arsine generation—gas chromatography combined with atomic absorption spectrophotometry or mass spectrometry were used to characterize the arsenic metabolites in urine and feces collected over 48 hours after treatment.In mice and hamsters 3.5% and 6.4% of the dose, respectively, were excreted in urine in the form of trimethylarsine oxide (TMAO). No TMAO was found in feces. A DMA‐complex was detected in urine and feces. It amounted to about 13% of the dose in mice and 15% in hamsters. About 80–85% of the dose was eliminated in urine and feces in the form of unmetabolized DMA. No demethylation of DMA to inorganic arsenic was observed. In man, about 4% of the dose was excreted in urine as TMAO and about 80% as DMA.
Measurement of polycyclic aromatic hydrocarbons and other pollutants
Authors: Garcia M. Espigares , López J. A. Pérez , Larrubia A. Mariscal , Fernandez‐Crehuet M. , Vargas R. Gálvez 
Published: October 2006

AbstractA single point study of atmospheric pollution has been carried out in Granada (Spain); suspended particulate matter, sulphur oxides, ammoniac, nitrogen dioxide and polycyclic aromatic hydrocarbons were determined. There were variations in relation to the month and the day of the week. The PAHs have been determined through HPLC, with a mobile phase of acetonitrile–water (75–25). The results of measurements of benzo(a)pyrene were between 1.006 and 0.485 μ m−3 in two different periods of sampling.
The development of contact hypersensitivity in mouse skin is suppressed by tumor promoters
Authors: Czerniecki Brian , Witz Gisela , Reilly Christopher , Gad Shayne C. 
Published: October 2006

AbstractThe ability of tumor promoters to suppress the development of contact hypersensitivity (CHS) was assessed by the mouse ear swelling assay. Application of the complete or second stage tumor promoters phorbol‐12‐myristate‐13‐acetate (PMA, 2 μg), croton oil (1%), benzoyl peroxide (20 mg), mezerein (2 μg), or phorbol‐12‐retinoate‐13‐acetate (PRA, 2 μg) to the abdominal surface of CF‐1 female mice for 1 week (three treatments) prior to the sensitization of the same location with 0.5% 1‐chloro‐2,4‐dinitrobenzene (DNCB) resulted in a 50% suppression (p <0.05) of the CHS response to DNCB. The first stage tumor promoters 4‐O‐Me‐PMA (80 μg), calcium ionophore A23187 (80 μg), hydrogen peroxide (15%) and the non‐promoting analogs phorbol‐12,13‐diacetate (PDA, 20 μg), phorbol (80 μg) or acetone did not suppress the response. The suppression of the development of CHS caused by PMA was dependent on the promoter being applied at the site of induction and was inhibited by application of the phospholipase A2 inhibitor dibromoacetophenone (100 μg), the lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA, 100 μg), or the antiinflammatory steroid fluocinolone acetonide (2 μg). Application of PMA or mezerein 24 h prior to challenge with DNCB, to the ears of mice previously sensitized with DNCB resulted in a significant enhancement of the ear swelling response by 60% and 110%, respectively, compared with controls. The results demonstrate that tumor promoters suppress the development of CHS, and suggest the possibility that second stage promotion may involve suppression of the development of a tumor specific immune response.
The effects of caffeine on the ultrastructure and mitochondrial function of the embryonic chick heart
Authors: Bruyere Harold J. , Noonan John J. , Dong Sophie , Oberley Terry D. , Schmidt Mary J. , Gilbert Enid F. , Shug Austin L. 
Published: October 2006

AbstractResults from this study indicate that caffeine at an embryotoxic dose equal to the LD40 administered to 3‐day chick embryos produced both ultrastructural and functional abnormalities in embryonic cardiac mitochondria. The principal effects of caffeine on the ultrastructure of embryonic myocardial cells were clearly suggestive of cellular injury and included: (1) a marked disruption of mitochondrial cristae with formation of intramitochondrial myelin‐like figures and (2) intracellular edema. A biochemical analysis of mitochondrial function revealed that caffeine inhibited the capacity of mitochondria to oxidize succinate. However, when pyruvate and malate were employed as substrates for isolated mitochondria, caffeine did not significantly alter mitochondrial function. Interference with embryonic cardiac mitochondrial succinate oxidation and/or fragmentation of mitochondrial membranes are suggested as possible events in the pathogenesis of caffeine‐induced cardiac cell injury which, in turn, may lead to the embryonic death of the chick.
Changes in some histochemically demonstrable enzymes in macrophages exposed to quartz dust in vitro
Authors: Dogra Shashi , Kaw Jawahir Lal 
Published: October 2006

AbstractCytochemical studies were carried out on rat alveolar and peritoneal macrophage cultures following exposure to quartz and corundum dusts. Quartz increased the number of ATPase positive cells and brought about an enhancement in the peroxidase and diffusion of the acid phosphatase activity of the exposed cells. In unexposed cell cultures, acid phosphatase activity was higher in alveolar than in peritoneal macrophages and was dependent upon the duration of incubation. Corundum produced no significant effect on the enzyme activity. Quartz treatment did not alter esterase activity whereas corundum exposed cultures showed a decline. A significant increase in mitochondrial succinic dehydrogenase activity was observed in peritoneal macrophages after quartz treatment. The results demonstrate alteration in the marker enzymes of plasma membranes, mitochondria and lysosomes during phagocytosis of quartz dust as the key event of dust cell interaction in vitro.
The effects of amrinone, cyclophosphamide and anti‐platelet serum on platelet production in the gunn rat
Authors: Eason C. T. , Pattison A. , Howells D. D. , Bonner F. W. , Martin J. F. 
Published: October 2006

AbstractThe effect of amrinone on platelet production was differentiated from that of a known bone‐marrow cytotoxic agent (cyclophosphamide) and anti‐platelet serum (APS). The rate of platelet production has been observed over a 4‐day period in the Gunn rat using [75Se]selenomethionine cohort labelling of platelets following administration of either amrinone, 160 mg kg−1 day−1, cyclophosphamide, 30 mg kg−1 day−1 or APS, 0.75 ml. Platelet numbers were reduced by amrinone, cyclophosphamide and APS. The rate of platelet production was increased following APS and suppressed by cyclophosphamide, but the rate of platelet production when expressed as the selenomethionine incorporation in counts per minute (cpm) per 108 platelets appeared to be increased in amrinone‐treated animals. When these values are expressed as radioactivity per unit platelet volume the difference between the control and the amrinone‐treated group was reduced but the difference between the control, APS‐ and cyclophosphamide‐treated groups remained unchanged. It is concluded that in the Gunn rat amrinone affects platelet production by producing fewer, larger platelets.
Acute and neurotoxicity of two structurally related acetylenic compounds: 5,7,11‐dodecatriyn‐1‐ol and 5,7,11,13‐octadecatetrayne‐1,18‐diol
Authors: Gad Shayne C. , Dunn Brendan J. , Gavigan Frances A. , Reilly Christopher , Peckham John C. 
Published: October 2006

AbstractTwo structurally related acetylenic compounds, 5,7,11‐Dodecatriyn‐1‐ol, (Compound A), and 5,7,11,13‐Octadecatetrayne‐1,18‐Diol (Compound B), were evaluated in a tier I toxicology testing program as part of an ongoing research and development program. This battery of acute tests included acute oral, guinea pig maximization, photosensitization, dermal irritation, Ames and multiple genetic endpoint and a 2 week oral fetotoxicity study. Compound A was found to have an oral LD50 of 0.25 ml/kg, be an extreme dermal sensitizer, a mild dermal irritant (PDII of 1.7), and not mutagenic or fetotoxic in the tests employed. Compound B had an oral LD50 greater than 4 g/kg, was a moderate dermal sensitizer and mild dermal irritant (PDII of 1.4), was not mutagenic in the Ames test but weakly increased the incidence of SCEs and gene mutations in Chinese Hamster Ovary cells, and was not fetotoxic. Neither compound was found to be a photosensitizer, but during the course of the photosensitization study Compound A was found to cause neuromuscular signs (including hind limb paralysis) and a bilaterial necrosis of the medulla oblongata in female guinea pigs. A similar lesion was found in female rats receiving a single oral dose of 0.25 ml/kg and in nonpregnant females dosed daily for two weeks at 0.03 ml/kg. Compound B was not found to produce any of these neurologic effects.
Effect of hexacarbons on selected lipids in developing rat brain and peripheral nerves
Authors: Bhatt A. , Khan S. , Pandya K. P. , Sabri M. I. 
Published: October 2006

AbstractThe effects of neurotoxic solvents, i.e. 2,5‐hexanedione (2,5‐HD), 2,5‐hexanediol (2,5‐HDiol) and the non‐neurotoxic solvent, 2,4‐hexanedione (2,4‐HD) (500 mg/kg body wt./day, i.p.), have been studied on the lipid composition of brain and sciatic nerves in weanling rats. Five‐day‐old rats were administered a solvent daily for 21 days. Clinical signs of peripheral neuropathy appeared in 2,5‐HD and 2,5‐HDiol treated groups. Absolute weights of brain, spleen, thymus significantly decreased with 2,5‐HD. Cholesterol content in whole brain homogenates and myelin was significantly reduced with 2,5‐HD and 2,5‐HDiol treatment. There was also a significant reduction in ubiquinone content of brain with 2,5‐HD and 2,5‐HDiol treatment. On exposure to neurotoxic chemicals to weanling rats, significant alteration in lipid profile was observed in the brain, which may be one of the key factors in the development of neuropathy.
An experimental study on the respiratory toxicity of isopropyl alcohol
Authors: Ohashi Yoshihiro , Nakai Yoshiaki , Ikeoka Hiroshi , Koshimo Hiroyuki , Esaki Yusuke , Horiguchi Shuńichi , Teramoto Keiko , Nakaseko Hiroyuki 
Published: October 2006

AbstractGuinea‐pigs were exposed to 400 ppm or 5500 ppm of isoprophyl alcohol (IPA) for 24 successive hours, and they were killed immediately after the exposure period. The ciliary activities of the nose and trachea were examined. In addition, the epithelium of the nose and trachea was observed by scanning and transmission electron microscopy.The present study showed that exposure to 400 or 5500 ppm of IPA vapor caused deterioration of the ciliary activity and also some pathological changes. Although our study revealed that exposure to 400 ppm of IPA vapor can affect the mucosa of the nose and trachea, the ciliary activity of the 400‐ppm exposure group was not too poor and morphological changes were rather mild. Recovery from such degeneration might be rapid. Therefore, our study supports the justification of the allowable IPA level recommended by ACGIH.
Removal of urea from alcoholic beverages with an acid urease
Authors: Kobashi Kyoichi , Takebe Sachiko , Sakai Tatsuo 
Published: October 2006

AbstractUrethan, a cancer causing chemical, was reported to contaminate some alcoholic beverages. Since urethan is formed by heating urea with ethylalcohol, removal of urea is necessary to prevent urethan formation in alcoholic beverages. Acid urease, whose optimal pH lies around 4, lowered urea concentrations in Japanese sake. This finding indicates a protective effect of acid urease on urethan's potential hazards in alcohol.
Heart and lung hypertrophy, changes in blood volume, hematocrit and plasma renin activity in rats chronically exposed to increasing carbon monoxide concentrations
Authors: Penney David G. , Davidson Scott B. , Gargulinski Richard B. , Caldwell‐Ayre Therese M. 
Published: October 2006

AbstractChanges in blood volume, heart and lung mass and composition and plasma renin activity were examined in two strains of male albino rats inhaling incrementally‐increasing concentrations of CO: 250 ppm for 17 days, 500 ppm for 13–14 days, 750 ppm for 10 days, and 1300 ppm for 10 days. Blood volume increased 86% and erythrocyte mass increased 212% at 1300 ppm, while plasma volume was unchanged or decreased slightly. “Real” hematocrit (hematocrit corrected for plasma trapping) increased from 50% in controls to a peak of 75% at 1300 ppm CO. Wet weight of right ventricle (RV) and combined right and left atria (2A) increased linearly with CO concentration, paralleling changes in blood volume; while real hematocrit increased nonlinearly. Left ventricle + interventricular septum (LV+S) wet weight increased less than RV, but more in Sprague‐Dawley than in Wistar rats. Plots of RV, LV+S and 2A weight vs real hematocrit showed sharp upward inflections at real hematocrit 65%, suggesting a possible role of increased viscosity in CO cardiomegaly at the higher hematocrit. Assymetric septal hypertrophy was not present. Lung weight increased with CO concentration, but was not due to increased lung blood volume or edema. Hydroxyproline measurements on heart and lung failed to show increased collagen content. Plasma renin activity measured by radioimmunoassay was depressed at 500 ppm, but was normal at 750 and 1300 ppm CO. Neither heart, lung,liver nor plasma renin measurements suggest congestive heart failure, supporting previous studies in the rat with chronic carboxyhemoglobinemia, in spite of enormously increased blood volume, hematocrit and heart weight.
Mutagenic activity of acetonitrile and fumaronitrile in three short term assays with special reference to autoinduction
Authors: Schlegelmilch R. , Krug A. , Wolf H. U. 
Published: October 2006

AbstractTwo aliphatic nitriles, acetonitrile and fumaronitrile were tested for their genotoxic potential in three mutagenicity test systems: the Salmonella/microsome‐assay, an assay using Saccharomyces cerevisiae (strain D7), and the bone marrow micronucleus test.Both compounds were tested with and without metabolic activation in the yeast and the bacterial test systems using S9 preparations from phenobarbitone‐pretreated and autoinduced rats. Autoinduction was performed by chronic (7 days) application of a dose equivalent to a 5% oral LD50‐value of the respective compound.With yeast strain D7 both nitriles induced low levels of gene conversion in the presence of phenobarbitone‐induced liver homogenate. An increase in the number of ile+‐revertants was not detectable under any condition.Neither of the compounds showed mutagenic activity in the Ames test with or without metabolic activation.A weak positive effect of acetonitrile could be detected in the micronucleus test 24 h after i.p.‐injection of the compound using a dose of 60% LD50. Fumaronitrile showed positive results with a 50% LD50 dose 48 h after administration to mice not preinduced. After 1 week of autoinduction these effects did not appear anymore, with the exception of acetonitrile 72 h after application of a dose amounting to 60% of the oral LD50‐value.
Effect of four‐week repeated inhalation exposure to unconjugated azodicarbonamide on specific and non‐specific airway sensitivity of the guinea pig
Authors: Gerlach Robert F. , Medinsky Michele A. , Hobbs Charles H. , Bice David E. , Bechtold William E. , Cheng Yung‐Sung , Gillett Nancy A. , Birnbaum Linda S. , Mauderly Joe L. 
Published: October 2006

AbstractReports of respiratory problems among industrial workers exposed repeatedly by inhalation to azodicarbonamide (ADA) raised concern that ADA might be a pulmonary sensitizer. We used a non‐invasive method for measuring specific airway conductance to evaluate the potential for repeated inhalation of unconjugated ADA to cause specific or non‐specific pulmonary sensitization in the guinea pig. Two groups of male Hartley guinea pigs were exposed 6 h/day, 5 days/week for 4 weeks to aerosolized ADA at 51 or 200 mg/m3, or to filtered air as controls. One group was tested for specific sensitization to ADA by measuring specific airway conductance during inhalation challenge with ADA before and on the third day after the 4‐week ADA exposure. The ADA concentrations for the challenges were identical to the repeated exposure concentrations (51 or 200 mg/m3, 200 mg/m3 for controls). The other group was tested for non‐specific airway sensitization by inhalation challenge with aerosolized histamine before and after the 4‐week ADA exposure. Histamine was administered in stepwise increasing concentrations to elicit an airway response in each guinea pig. Skin tests for immunological responses to ADA, body weight and histopathology of the respiratory tract and skin test sites were also evaluated. The 4‐week exposure to ADA did not result in either specific or non‐specific airway sensitization. The ADA exposure did not induce positive skin reactions, influence body weight or cause histopathological responses. These results indicate that ADA, acting alone (i.e. not conjugated to a protein), is not a pulmonary sensitizer in the guinea pig exposed repeatedly for 4 weeks and challenged to simulate a ‘Monday morning’ exposure.
Influence of particulate trap oxidizers on emission of mutagenic compounds by diesel automobiles
Authors: Rasmussen Ronald E. , Devillez Gary , Smith Lawrence R. 
Published: October 2006

AbstractDiesel exhaust particles are known to contain mutagenic and carcinogenic chemicals. The aim of this study was to determine whether, and to what extent, catalytic particulate trap oxidizers on light‐duty diesel engines may reduce the emission of particle‐associated mutagenic chemicals into the environment. Exhaust particles were collected from Mercedes Benz and Volkswagen diesel automobiles, equipped with or without the manufacturer's exhaust traps, while running on a chassis dynamometer under specified load conditions. Exhaust particles were collected from a dilution tunnel onto 20″ × 20″ Teflon®‐coated fiberglass filters. Mutagenesis tests of dichloromethane (DCM) extracts of the particles were conducted using the Ames Salmonella bacterial test system. The mutation rate was calculated in terms of histidine revertants per mile of travel during a set of standard test cycles. With both vehicles the traps produced an 87–92% reduction in the total amount of particulate material collected by the filters. There was no significant change in the specific mutagenic activity (revertants per microgram of DCM particle extract) with or without the traps. These studies support the notion that installation of exhaust traps which reduce particulate emission on diesel‐powered vehicles will also reduce the emission of particle‐associated mutagenic and carcinogenic materials into the environment.