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Träfflista för sökning "(L773:1096 0333 OR L773:0041 008X) srt2:(1995-1999)"

Sökning: (L773:1096 0333 OR L773:0041 008X) > (1995-1999)

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1.
  • DeJongh, J, et al. (författare)
  • Estimation of systemic toxicity of acrylamide by integration of in vitro toxicity data with kinetic simulations.
  • 1999
  • Ingår i: Toxicology and Applied Pharmacology. - : Elsevier BV. - 0041-008X .- 1096-0333. ; 158:3, s. 261-268
  • Tidskriftsartikel (refereegranskat)abstract
    • Neurodegenerative properties of acrylamide were studied in vitro by exposure of differentiated SH-SY5Y human neuroblastoma cells for 72 h. The number of neurites per cell and the total cellular protein content were determined every 24 h throughout the exposure and the subsequent 96-h recovery period. Using kinetic data on the metabolism of acrylamide in rat, a biokinetic model was constructed in which the in vitro toxicity data were integrated. Using this model, we estimated the acute and subchronic toxicity of acrylamide for the rat in vivo. These estimations were compared to experimentally derived lowest observed effect doses (LOEDs) for daily intraperitoneal exposure (1, 10, 30, and 90 days) to acrylamide. The estimated LOEDs differed maximally twofold from the experimental LOEDs, and the nonlinear response to acrylamide exposure over time was simulated correctly. It is concluded that the integration of the present in vitro toxicity data with kinetic data gives adequate estimates of acute and subchronic neurotoxicity resulting from acrylamide exposure.
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2.
  • Hallén, I P, et al. (författare)
  • Toxicokinetics of lead in lactating and nonlactating mice.
  • 1996
  • Ingår i: Toxicology and Applied Pharmacology. - : Elsevier BV. - 0041-008X .- 1096-0333. ; 136:2, s. 342-7
  • Tidskriftsartikel (refereegranskat)abstract
    • Toxicokinetics of lead in lactating and nonlactating mice were studied after a single intravenous injection of 0.05 mg of lead (2.5 mCi 203Pb)/kg. Lead concentrations in blood, plasma, and milk were measured for 10 days following dosing. The volume of distribution based on plasma lead was more than two times larger in lactating than in nonlactating mice, 133 and 58 liter/kg, respectively. Plasma lead clearance in lactating mice was 4.25 liter/hr/kg compared with 1.07 liter/hr/kg in nonlactating mice. However, no such pronounced difference in blood lead clearance was found between the two groups, indicating that this parameter does not reveal the kinetic characteristics during lactation. Milk was found to be an additional route of excretion for lead. About 1/3 of the administered dose of lead was excreted in milk. Accordingly, milk clearance contributed to 1/3 of the total plasma clearance in the mice. The relationships of lead in plasma to lead in whole blood as well as lead in milk to lead in whole blood were nonlinear, with a relatively higher increase in plasma and in milk lead levels at higher blood lead levels. This nonlinearity may be explained by a reduced uptake of lead in erythrocytes as the lead binding sites of these cells become saturated. In lactating mice, the maximum binding capacity of lead in red blood cells was even lower than in nonlactating mice. Similar nonlinear relationship have have also been found in human studies although at much higher levels of lead in blood. The milk:plasma concentration ratio for lead was found to be between 50 and 100 after 24 hr, demonstrating a much more efficient excretion of lead into milk than what is known from human studies. Differences in the milk composition may be one explanation for the species differences in milk excretion of lead. The present study shows that physiological changes during lactation alter the pharmacokinetics of lead in mice.
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3.
  • Hultman, Per, 1957-, et al. (författare)
  • Methyl mercury-induced autoimmunity in mice.
  • 1999
  • Ingår i: Toxicology and Applied Pharmacology. - 0041-008X .- 1096-0333. ; 154, s. 203-211
  • Tidskriftsartikel (refereegranskat)
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4.
  • Lind, Monica, et al. (författare)
  • Effects of the antiestrogenic environmental pollutant 3,3',4,4', 5-pentachlorobiphenyl (PCB #126) in rat bone and uterus : diverging effects in ovariectomized and intact animals
  • 1999
  • Ingår i: Toxicology and Applied Pharmacology. - : Elsevier BV. - 0041-008X .- 1096-0333. ; 154:3, s. 236-244
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • The purpose of this study was to compare effects on rat bone and uterus of estrogen depletion and exposure to the coplanar PCB-congener 3,3',4,4',5-pentachlorobiphenyl (PCB #126) which exhibits anti-estrogenic properties. Half of the rats were ovariectomized (n = 20) and the other half were sham-operated. Ten of the ovariectomized rats and ten of the sham operated were exposed to PCB #126 (ip injections) for 3 months (total dose: 384 microgram/kg body wt). The remaining control rats were injected with corn oil (vehicle). The rats were killed and the tibiae and uteri were dissected. The left tibia was used for measurements of weight, length, and bone mineral density and the right for histomorphometrical analysis. The uteri were analyzed with respect to estrogen receptor content. PCB #126 exposure did not affect bone mineral density or trabecular bone volume of tibia in sham-operated rats. In ovariectomized rats PCB #126 exposure resulted in a decreased length and an increased bone mineral density of tibia. An obvious PCB #126 induced increase in osteoid surface was observed in sham-operated rats. The cortical thickness and the organic content of the tibia were also increased in these rats. In estrogen deprived tissue like the uteri of ovariectomized rats, PCB #126 showed weak estrogen agonistic activity. The observed effects of PCB #126 on bone and uterine tissues differed between ovariectomized and sham-operated rats.
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5.
  • Lindh, Christian, et al. (författare)
  • Human hemoglobin adducts following exposure to hexahydrophthalic anhydride and methylhexahydrophthalic anhydride
  • 1998
  • Ingår i: Toxicology and Applied Pharmacology. - : Elsevier BV. - 1096-0333 .- 0041-008X. ; 153:2, s. 152-160
  • Tidskriftsartikel (refereegranskat)abstract
    • Hexahydrophthalic anhydride (HHPA) and methylhexahydrophthalic anhydride (MHHPA) are highly allergenic compounds used in the chemical industry. The aim of this study was to characterize the protein adducts in erythrocytes following exposure to HHPA and MHHPA. Blood and urine samples were obtained from 51 HHPA- and MHHPA-exposed workers. Erythrocytic proteins from HHPA- and MHHPA-exposed workers were fractionated by gel filtration and ion exchange chromatography. In vitro synthesized conjugates between tritium-labeled and unlabeled HHPA and hemoglobin (Hb) were hydrolyzed by acid or digested by Pronase E. Levels of in vivo formed anhydride-Hb adducts and urinary/plasma levels of the corresponding acids were analyzed by gas chromatography-mass spectrometry (GC-MS) and correlated. The decay of adducts was studied in workers leaving employment or during vacation. More than 85% of the adduct forming protein in vivo coeluted with Hb in gel filtration and ion exchange chromatography. At least 70% of the HHPA in the in vitro formed adducts was found on lysine by GC-MS. Similar findings were obtained using Pronase E-digested tritium-labeled Hb-HHPA. The adduct levels in workers ranged 0-26 pmol/g Hb (mean 2. 7 pmol/g Hb) for HHPA, and the range for MHHPA was 0-55 pmol/g Hb (mean 4.1 pmol/g Hb). The Spearman's rank correlation coefficient between urine data and adducts was for HHPA rs = 0.80 and for MHHPA, rs = 0.78. For the plasma, the correlation using HHPA data was rs = 0.80 and for MHHPA, rs = 0.69. The adducts seemed to be stable in vivo. The adduct levels may be used as biomarkers of exposure to HHPA and MHHPA.
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6.
  • Nihlén, Annsofi, et al. (författare)
  • Experimental exposure to methyl teriary-butyl ether : II. Acute effects in humans
  • 1998
  • Ingår i: Toxicology and Applied Pharmacology. - : Elsevier BV. - 0041-008X .- 1096-0333. ; 148:2, s. 281-287
  • Tidskriftsartikel (refereegranskat)abstract
    • Methyl tertiary-butyl ether (MTBE) is widely used in gasoline as an oxygenate and octane enhancer. Acute effects, such as headache, nausea, and nasal and ocular irritation, have been associated with the exposure to gasoline containing MTBE. The aim of this study was to assess acute health effects up to the Swedish occupational exposure limit value, both with objective methods and a questionnaire. Ten healthy male volunteers were exposed to MTBE vapor for 2 h at three levels (5, 25, and 50 ppm), during light physical work (50 W). All subjects rated the degree of irritative symptoms, discomfort, and CNS effects before, during, and after all three exposure occasions using a questionnaire. Answers were given on a 100-mm visual analog scale, graded from "not at all" to "almost unbearable." Ocular (redness, tear film break-up time, self-reported tear film break-up time, conjunctival epithelial damage, and blinking frequency) and nasal (mouth and nasal peak expiratory flow, acoustic rhinometry, biochemical inflammatory markers, and cells in nasal lavage) measurements were performed mainly at the highest exposure level. The ratings of solvent smell increased dramatically (ratings up to 50% of the scale) as the volunteers entered the chamber and declined slowly with time (p < 0.05, repeated-measures ANOVA). All other questions were rated from "not at all" to "hardly at all" (0-10% of the scale) with no significant relation to exposure. The eye measurements showed no effects of MTBE exposure. Blockage index, a measure of nasal airway resistance calculated from the peak expiratory flows, increased significantly after exposure; however, the effect was not related to exposure level. In addition, a nonsignificant tendency of decreased nasal volume was seen in the acoustic rhinometry measurements, but with no clear dose-effect relationship. In conclusion, our study suggests no or minimal acute effects of MTBE vapor upon short-term exposure at relatively high levels.
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7.
  • Palminger Hallén, I, et al. (författare)
  • Kinetic observations in neonatal mice exposed to lead via milk.
  • 1996
  • Ingår i: Toxicology and Applied Pharmacology. - 0041-008X .- 1096-0333. ; 140:1, s. 13-8
  • Tidskriftsartikel (refereegranskat)abstract
    • The absorption and disposition of lead in blood was examined in 10-day-old suckling mice exposed via milk. Lactating dams were administered a single intravenous injection of 0.05 mg Pb (2.5 mCi 203Pb)/kg body wt. Lead concentrations in blood of the suckling offspring were measured for 10 days after administration to the dams. Maximum blood lead concentrations in the pups were recorded between 50 and 74 hr after dams' administration despite the fact that the majority of the lead dose to the sucklings was delivered within 24 hr after dams' administration. Kinetic analysis of pups' blood lead data revealed a rate-limited absorption in the suckling pups with an absorption half-life of approximately 17 hr in the pups. This delayed absorption is most likely due to a retention of casein-bound lead in the ileal mucosa which has a high pinocytotic activity of dietary proteins in infant rodents. The present results also indicated that the distribution of lead to the peripheral tissues in the suckling mice was different than that of adults. The conflicting evidence on whether milk enhances or inhibits the absorption of lead in infant rodents may thus be explained by measurements of lead absorption at different time periods after administration to the animals. It is also suggested that the milk diet is one reason for the increased absorption of lead seen in immature rodents.
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8.
  • Sundberg, J, et al. (författare)
  • Kinetics of methylmercury and inorganic mercury in lactating and nonlactating mice.
  • 1998
  • Ingår i: Toxicology and Applied Pharmacology. - : Elsevier BV. - 0041-008X .- 1096-0333. ; 151:2, s. 319-29
  • Tidskriftsartikel (refereegranskat)abstract
    • The elimination of mercury was followed for 9 days (Days 10-19 of lactation) in milk and/or 21 days in blood and plasma of lactating and nonlactating mice administered a single iv injection of either 203Hg-labeled methylmercuric chloride or 203Hg-labeled mercuric chloride (0.5 mg Hg/kg body wt). Demethylation of methylmercury to inorganic mercury was taken into consideration by analyzing the data with a combined pharmacokinetic model based on the assumption of constant blood plasma ratios for methylmercury and inorganic mercury. A three-compartment model fitted the blood and plasma concentrations vs time profiles for both compounds. Plasma clearance and volume of distribution at steady state for methylmercury were 95. 3 ml/h/kg and 18,500 ml/kg, respectively, in lactating mice, and significantly higher than in nonlactating mice with values of 47.1 ml/h/kg and 9400 ml/kg, respectively. The terminal half-lives of methylmercury in plasma were similar, 170 h in lactating and 158 h in nonlactating mice. No differences were observed between the pharmacokinetic parameters in lactating and nonlactating mice administered inorganic mercury. The lactational transfer of mercury was more efficient following administration of inorganic mercury than after administration of methylmercury, with a five times higher peak concentration in milk, higher milk:plasma concentration ratios, and 8% of the administered dose excreted in milk compared with 4% for methylmercury. Mercury concentrations in milk following an iv dose of inorganic mercury decreased with a terminal half-life of 107 h, whereas after administration of methylmercury, the concentration of total mercury in milk remained at an almost constant level during the whole period of investigation. There was a nonlinear relationship between mercury in milk and plasma following inorganic mercury administration. It is suggested that inorganic mercury enters the mammary gland by a carrier-mediated transport system, which is saturated at high plasma levels of inorganic mercury. The present study shows that physiological changes during lactation alter the pharmacokinetics for methylmercury in mice but not for inorganic mercury.
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9.
  • Sundberg, J, et al. (författare)
  • Lactational exposure and neonatal kinetics of methylmercury and inorganic mercury in mice.
  • 1999
  • Ingår i: Toxicology and Applied Pharmacology. - : Elsevier BV. - 0041-008X .- 1096-0333. ; 154:2, s. 160-9
  • Tidskriftsartikel (refereegranskat)abstract
    • The concentration of mercury in milk and the distribution pattern in the sucking pup was followed over time after administration of a single iv injection of 0.5 mg/kg body wt of 203Hg-labeled methylmercuric chloride or mercuric chloride to lactating mice on Day 10 of lactation. Mercury concentrations in milk of the dams and in whole body, blood, plasma, GI-tract, liver, kidneys, and brain of the offspring were followed up to 11 days after dosing (until lactational Day 21). Following the inorganic mercury dose to the dams, most of the mercury in milk was delivered to the pups during the first 24 h, but the maximum mercury concentration in plasma and tissues of pups was not reached until 7 days after dosing, indicating a prolonged absorption of inorganic mercury in the sucking pup. Pups of dams given methylmercury were exposed to a much lower and constant mercury concentration in milk. The estimated accumulated mercury dose via milk per pup of dams given methylmercury was less than half of that estimated after the inorganic mercury dose. When the accumulated dose via milk from methylmercury-exposed dams was compared to the amount of mercury in pup's carcass (whole body minus GI-tract including content), it was revealed that almost all mercury delivered via milk was absorbed, and that the suckling pups had a very low elimination of mercury until lactational Day 17. Lactational exposure following a maternal methylmercury or inorganic mercury dose resulted in almost similar mercury concentrations in liver, kidneys, and plasma of the suckling, but higher concentrations in brain (as most 14 times) and also twice as high mercury body burden in the methylmercury group. Thus, differences in kinetics indicate that lactational exposure of methylmercury is a greater hazard for the breast-fed infant than inorganic mercury.
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10.
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