bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of exposure to diesel exhaust on pulmonary prostaglandin dehydrogenase (PGDH) activity
Authors: Chaudhari A. , Farrer R. G. , Dutta S. 
Published: October 2006

AbstractThere has been evidence that an acute exposure of laboratory animals to nitrogen dioxide (NO2) for a short period of time can cause marked inhibition of pulmonary PGDH activity. Since diesel exhaust contains NO2, this investigation was undertaken to determine the effect of long‐term exposure of guinea pigs and rats to diesel exhaust. The study involves measurement of PGDH activity in the lung tissue as obtained from these animals following exposure to 250 and 1500 μg m−3 of diesel particles for various time periods in relation to the appropriate time‐matched controls. In guinea pigs, exposure for 6 weeks to 250 μg m−3 of diesel exhaust seems to stimulate the PDGH activity about two‐fold in comparison to the time‐matched controls while, paradoxically, the exposure to 1500 μg m−3 of diesel exhaust did not show any particular effect. The exposures to diesel exhaust for 12 weeks, as well as 24 weeks, seem to show concentration dependent lowering of PGDH activity as compared to the time‐matched controls. This study also documents the well‐known species difference in PGDH activity in that the rat shows much lower activity of this enzyme than the guinea pig. Because of undetectable enzyme activity in many samples, it has not been possible to draw any meaningful conclusion as to the effect of diesel exposure on the enzyme in rat.
Absorption and alveolar excretion of cyclohexane in workers in a shoe factory
Authors: Mutti A. , Falzoi M. , Lucertini S. , Cavatorta A. , Franchini I. , Pedroni C. 
Published: October 2006

AbstractThe lung uptake and excretion of cyclohexane were studied in five workers and three volunteers in a shoe factory. Air samples were collected from the breathing zones with personal samplers, and simultaneous samples of inhaled and alveolar air were collected with the aid of a Rham–Otis valve. Cyclohexane was absorbed on activated NIOSH approved charcoal tubes. The uptake was calculated from the pulmonary ventilation, the retention coefficient and environmental concentration. Alveolar excretion was monitored during a 6 h post‐exposure period. The amount of exhaled cyclohexane was calculated from the decay curve. According to experimental data, the alveolar retention of cyclohexane is about 34% of the inhaled dose. This corresponds to a lung uptake of 23%. The post‐exposure alveolar excretion does not exceed 10% of the total uptake. The difference between respiratory uptake and excretion indicates that the amount metabolized may be very large. Nevertheless, the urinary excretion of the main metabolites, cyclohexanol and cyclohexanone, was only about 1% of the absorbed dose.
Organic solvents and chronic glomerulonephritis: A cross‐sectional study with negative findings for aliphatic and alicyclic C5–C7 hydrocarbons
Authors: Mutti A. , Lucertini S. , Falzoi M. , Cavatorta A. , Franchini I. 
Published: October 2006

AbstractProteinuria, albuminuria, urinary β‐glucuronidase and serum creatinine were estimated in 182 workers exposed to organic solvents in four shoe factories, as well as 30 workers with past exposure and 80 control subjects. Ambient air concentrations at each workplace were also measured. In most of these samples, the concentration of organic solvents exceeded the ACGIH recommended threshold limit value for the mixture. Total protein excretion was significantly elevated in exposed workers, although none of the workers had abnormal albuminuria or serum creatinine. Four had increased lysozymuria. There was also a simultaneous elevation of β‐glucuronidase. These findings suggest that a mild and presumably reversible tubular lesion, but not glomerular damage, may occur in workers occupationally exposed to C5–C7 hydrocarbon mixtures.
Ames testing of direct black 38 parallels carcinogenicity testing
Authors: Gregory Arthur R. , Elliott John , Kluge Paul 
Published: October 2006

AbstractStudies have established that Direct Black 38 and two other benzidine‐based dyes are carcinogenic. The carcinogenic effect has been generally considered attributable to the metabolic release of benzidine from Direct Black 38 and similar dyes. However, Ames tests indicated that when Direct Black 38 is reduced with sodium dithionate it is more mutagenic than can be accounted for by complete release of all the benzidine present in the dye molecule. While most dyes are not mutagenic when tested with S‐9, a series of benzidine congener dyes were all found to be mutagenic with either TA 98 or TA 100 strains, if the dyes were first reduced with sodium dithionate. Unreduced dyes were not mutagenic. Neither anaerobic conditions nor addition of riboflavin induced mutagenicity of these dyes under the condition of our experiments.
Biochemical and morphological changes induced by 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin in the rat liver cell plasma membrane
Authors: Greig John B. , Osborne Glenys 
Published: October 2006

AbstractThe administration of single oral doses of 200 μg kg−1 of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin to females of the outbred, Lac: P strain of rat results in the formation of hepatic multinucleate cells by cell fusion. Liver cell plasma membranes isolated 6 or 11 days after dosing show two distinct changes. The first is a decrease of the activity of K+‐Mg2+‐ATPase, which confirms histochemical observations. The second is the formation, in those animals showing a more severe intoxication, of a population of plasma membranes which are less dense than usual and which consist of extended membrane sheets. It is suggested that these alterations are consequent on a disturbance of lipid metabolism in the hepatic cells and that they represent early manifestations of the toxic process which leads to the formation of multinucleate cells.
Laser microfabrication of hydroxyapatite‐osteoblast‐like cell composites
Authors: Doraiswamy A. , Narayan R. J. , Harris M. L. , Qadri S. B. , Modi R. , Chrisey D. B. 
Published: October 2006

AbstractWe have developed a novel approach for layer‐by‐layer growth of tissue‐engineered materials using a direct writing process known as matrix assisted pulsed laser evaporation direct write (MAPLE DW). Unlike conventional cell‐seeding methods, this technique provides the possibility for cell‐material integration prior to artificial tissue fabrication. This process also provides greater flexibility in selection and processing of scaffold materials. In addition, MAPLE DW offers rapid computer‐controlled deposition of mesoscopic voxels at high spatial resolutions. We have examined MAPLE DW processing of zirconia and hydroxyapatite scaffold materials that can provide a medical device with nearly inert and bioactive implant‐tissue interfaces, respectively. We have also demonstrated codeposition of hydroxyapatite, MG 63 osteoblast‐like cells, and extracellular matrix using MAPLE DW. We have shown that osteoblast‐like cells remain viable and retain the capacity for proliferation when codeposited with bioceramic scaffold materials. Our results on MG 63‐hydroxyapatite composites can be extended to develop other integrated cell‐scaffold structures for medical and dental applications. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Distinction between octachlorostyrene and hexachlorobenzene in their potentials to induce ethoxyphenoxazone deethylase and cause porphyria in rats and mice
Authors: Smith Andrew G. , Francis Jean E. , Bird Ian 
Published: October 2006

AbstractThe potentials of octachlorostyrene (OCS) and hexachlorobenzene (HCB) to induce liver microsomal ethoxyphenoxazone deethylation (an indicator of induction of 3‐methylcholanthrene and β‐naphthoflavone–like cytochrome P‐450 monoxygenase activity) and cause porphyria in male C57BL/6 and C57BL/10 mice and female F344 rats were compared. Ethoxyphenoxazone deethylation was induced much more by HCB than by OCS in both of these strains of mice (although neither OCS nor HCB greatly induced deethylation in the DBN/2 strain). In rats ethoxyphenoxazone deethylase was induced 26‐fold by HCB but only four‐fold by OCS, whereas dealkylation of pentoxyphenoxazone (an indicator of phenobarbital‐like induction) increased 43‐and 36‐fold, respectively. Both chemicals were poor inducers of dealkylation of pentoxyphenoxazone in mice. When fed HCB continuously but not when given OCS, C57BL/6 and C57BL/10 mice (both after pretreatment with iron) and F344 rats developed porphyria with a depression of hepatic uroporphyrinogen decarboxylase activity. The results illustrate that in these species OCS and HCB cannot be considered as equally efficient agents for inducing ethoxyphenoxazone deethylation or causing porphyria. If these effects are mediated through binding to the aromatic hydrocarbon responsiveness (Ah) receptor, HCB would appear to have a much greater affinity than OCS despite the face that neither chemical possesses a structure currently considered to be necessary for efficient binding.
Erythrocyte pyrimidine 5′‐nucleotidase inhibition by acute lead exposure in neonatal rats
Authors: Konantakieti Chalong , Beuthin Fredric C. , Louis‐Ferdinand Robert T. 
Published: October 2006

AbstractInhibition by lead of erythrocyte pyrimidine 5′‐nucleotidase (P5N) is thought to contribute to morphological abnormalities observed in red blood cells (RBC) of lead‐exposed subjects. However, neither the mechanism of lead inhibition of P5N nor the relationship of this inhibition to blood lead levels attained in exposed subjects is known. In the present investigation, acute in vivo and in vitro lead acetate effects on erythrocyte P5N from 21‐day‐old rat pups were determined and were related to blood lead concentrations ascertained by atomic absorption spectrophotometry. Acute lead administration to rat pups resulted in a 16% to 21% reduction in erythrocyte P5N, with mean blood lead levels ranging from 77 to 108 μg/dl 24 hours later. Inhibition of erythrocyte P5N was linearly related to blood lead level (r = −0.67, P < 0.05) following acute lead administration. Lead acetate addition to RBC preparations from 21‐day‐old rats resulted in concentration‐dependent P5N inhibition which was comparable to that produced following acute in vivo exposure. The results indicate that acute P5N inhibition in lead‐treated neonatal rats is due to noncompetitive P5N inhibition by lead. The inhibition of P5N produced by acute lead treatment is linearly related to blood lead concentrations.
Potentiation of carbon tetrachloride hepatotoxicity by chlordecone: Dose‐response relationships and increased covalent binding in vivo
Authors: Britton Robert S. , Dolak James A. , Glende Eric A. , Recknagel Richard O. 
Published: October 2006

AbstractChlordecone greatly potentiates carbon tetrachloride (CC14) hepatotoxicity. In order to quantitate the degree of this potentiation, the effects of a range of doses of CC14 on two microsomal enzymatic functions and liver enzyme release were examined in chlordecone‐treated and control rats. Male Sprague‐Dawley rats were pretreated with 15 mg chlordecone per kilogram body weight (BW) intragastrically or with vehicle. After 48 hours, 0 to 250 μ1 CC14 per 100 g body weight were given intraperitoneally (IP), and the rats were killed 24 hours later. Chlordecone treatment produced approximately a 17‐fold potentiation of the CC14 dependent loss of cytochrome P‐450 and glucose‐6‐phosphatase activity, so that a dose of 6 μ1 CC14 per 100 g body weight in the chlordecone‐treated animals resulted in a similar amount of damage as observed with 100 μ1 CC14 per 100 g body weight in controls. A similar potentiation by chlordecone was seen with CC14‐ induced increases in serum glutamic‐oxaloacetic transaminase (SGOT) levels. Chlordecone treatment also increased hepatic cytochrome P‐450 levels by 67% and resulted in an increase in the covalent binding of [14‐C]‐CC14‐derived metabolites to microsomal protein and lipid in vivo.
Chlordecone does not interfere with hepatic repair after carbon tetrachloride or partial hepatectomy
Authors: Dolak James A. , Britton Robert S. , Glende Jr. Eric A. , Recknagel Richard O. 
Published: October 2006

AbstractThe effect of chlordecone (CD) on hepatic repair, measured either as recovery of microsomal enzymatic functions or as the induction of cytosolic thymidine kinase (TK) activity, was evaluated in rats given carbon tetrachloride (CC14). Carbon tetrachloride was administered to CD‐potentiated and control animals using doses of this hepatotoxin which produce similar degrees of damage at 24 hours in both groups of animals (6 and 100 μ1 CC14 per 100 g body weight, respectively). Chlordecone had no significant effect on the time course of recovery of microsomal cytochrome P‐450 content or glucose‐6‐phosphatase activity following CC14 administration. Hepatic TK activity was measured 48 hours after CC14 administration as a biochemical index of the hepatic regenerative response. Thymidine kinase activity was increased eightfold in CD‐treated rats receiving 6 μ1 CC14 per 100 g body weight, whereas in controls a similar induction of TK activity was produced by 100 μ1 CC14 per 100 g body weight. Therefore, the TK response in CD‐treated rats receiving CC14 is appropriate for the amount of damage produced, suggesting that CD does not inhibit the hepatic regenerative response to CC14‐induced injury. The effect of CD on hepatic repair was also examined in rats receiving a two‐thirds partial hepatectomy. Pretreatment of animals with CD had no significant effect on the increase in TK activity produced 24 hours after partial hepatectomy. These results offer no support for the idea that CD impairs hepatic repair after either partial hepatectomy or CC14 administration.
Changes in lung ATP concentration in the rat after low‐level phosgene exposure
Authors: Currie William D. , Hatch Gary E. , Frosolono Michael F. 
Published: October 2006

AbstractInhibition of mitochondrial respiratory activity and decreased lung adenosine triphosphate (ATP) concentration occur following exposure to 240 ppm·min phosgene. To determine the relationship between energy stores and the onset of phosgene‐induced pulmonary edema, we measured the ATP concentration in rapidly frozen rat lung tissue before and during pulmonary edema. Male Sprague‐Dawley rats were exposed to phosgene for four hours at concentrations of 0.05 to 1.0 ppm (12, 30, 60,120, and 240 ppm·min). Lung wet and dry weight and ATP concentration were measured immediately after exposure and for three days postexposure. The accumulation of lavage fluid protein (LFP) was also measured as an index of damage or edema due to phosgene. Lung dry weight was significantly elevated one day postexposure to 0.5 ppm phosgene, while the LFP was elevated by 0.2 ppm phosgene. Time course studies at these doses of phosgene showed that decreased ATP levels preceded the onset of edema or increase in lung weight. The ATP values expressed on a per‐lung basis showed that ATP levels were significantly lowered immediately following phosgene exposure, suggesting that the ATP changes were not the result of edema. This study is the first demonstration of a biochemical change that occurs following exposure to phosgene at a level significantly below the threshold limit value for this gas.
Effects of tricyclohexylhydroxytin on the kinetics of adenosine triphosphatase system and protection by thiol reagents
Authors: Prasada Rao Kodavanti S. , Chetty Sreeramulu C. , Desaiah Durisala 
Published: October 2006

AbstractTricyclohexylhydroxytin, commonly known as Plictran® inhibited Na+, K+ ‐ATPase activity of rat brain synaptosomes in a concentration‐dependent manner with median inhibitory concentration (IC‐50) of 2 μM. Both K+ ‐stimulated para‐nitrophenylphosphatase and [3‐H]‐ouabain binding to synaptosomes were also inhibited by Plictran with IC‐50 values of 11 and 30 μM, respectively. Altered pH and Na+, K+ ‐ATPase activity curves demonstrated comparable inhibition in buffered neutral and alkaline pH ranges, and no inhibition was observed in acidic pH. The inhibition of Na+, K+ ‐ATPase was independent of temperature. Kinetic studies of substrate (ATP) activation of Na+, K+ ‐ATPase indicated uncompetitive inhibition. Results also showed noncompetitive inhibition for p‐nitrophenylphosphate and uncompetitive inhibition for K+ activations of p‐nitrophenylphosphatase. Preincubation of synaptosomes with dithiothreitol, a sulfhydryl (SH) agent, resulted in the complete protection of Plictran inhibition of Na+, K+ ‐ATPase, K+ ‐para‐nitrophenylphosphatase, and [3‐H]‐ouabain binding. The protection was specific and concentration dependent since cysteine and glutathione did not afford protection. These results indicate that Plictran inhibited Na+, K+ ‐ATPase by interacting with dephosphorylation of the enzyme‐phosphoryl complex and exerted a similar effect to that of SH‐blocking agents.
Induction of single‐strand breaks and interstrand cross‐links in liver DNA after the administration of 2‐acetylaminofluorene and trans‐4‐acetylaminostilbene to rats
Authors: Ruthsatz M. , Neumann H.‐G. 
Published: October 2006

Abstract2‐Acetylaminofluorene (AAF) or trans‐4‐acetylaminostilbene (AAS) was orally or intraperitoneally administered to female Wistar rats. DNA from liver cells was analyzed for single‐strand breaks by the alkaline elution assay. Only borderline effects were observed with doses (100 μMol/kg) used in animal carcinogenesis experiments. Even high doses of AAF (1,000 μMol/kg) were not effective. Methyl methanesulfonate (MMS) in vivo and gamma irradiation in vitro were shown to produce dose‐dependent DNA single‐strand breaks (positive control). Only a marginal effect was obtained with 100 μMollkg MMS. The elution rate of DNA was increased by a factor of 34 in liver cells in vitro with 400 rad of gamma irradiation. Only a fraction of this rate could be demonstrated immediately after irradiation in vivo, and no lesions were found two hours later. This strongly indicates the rapid repair of single‐strand breaks. Additional experiments showed that AAS, a nonhepatocarcinogen, produced more interstrand cross‐links in the rat liver DNA than did AAF.
Effects of cadmium‐metallothionein on renal organic ion transport and lipid peroxidation in rats
Authors: Suzuki Catherine A. M. , Cherian M. George 
Published: October 2006

AbstractThe effects of cadmium‐metallothionein (Cd‐MT) on organic ion uptake in renal cortical slices and lipid peroxidation in the kidney were studied in rats. For in vitro studies, slices were prepared from kidneys of control animals and incubated in buffer containing either cadmium chloride (CdCl2) or Cd‐MT in equimolar Cd concentrations ranging from 5 × 10−6 to 2 × 10−4 M. Uptake into the slices of the organic anion p‐aminohippuric acid (PAH) was found to be inhibited by both forms of Cd in a dose‐dependent manner. Although this inhibition was slightly greater in the presence of Cd‐MT, accumulation of Cd into the slices was approximately 12 times greater with CdCl2 than Cd‐MT. Tetraethylammonium (TEA) uptake was less sensitive to the inhibitory effects of both CdCl2 and Cd‐MT, although a dose‐dependent inhibition did occur with higher Cd concentrations.To study the in vivo effects of Cd‐MT on transport function and lipid peroxidation in the kidney, rats were injected with Cd‐MT (0.3 mg Cd per kilogram body weight [bw]) and sacrificed at specific time intervals. Similar to the in vitro studies, PAH uptake into the renal cortical slices was markedly inhibited within 12 hours after Cd‐MT injection whereas inhibition of TEA uptake was less and not observed until 48 hours after injection. Only a small increase (1.4‐fold) in lipid peroxidation, as measured by generation of malondialdehyde (MDA), in the kidney was detected at four hours postinjection, and no further increase was observed at later time periods.The results suggest that Cd‐MT affects the transport of organic anions and cations during its renal uptake but that lipid peroxidation may play only a minor role in Cd‐MT‐induced renal toxicity.
Morphological and biochemical effects of gentamicin and cyclosporin‐a on urinary cell phospholipids and phospholipases in man
Authors: Chatterjee Subroto , Bose Sharmistha 
Published: October 2006

AbstractThe morphology, lipid composition, and activity of sphingomyelinase (E.C. 3.1.4.12) and phospholipases A (E.C. 3.1.1.32) and C (E.C. 3.1.4.3) were studied in the urinary cells from four normal subjects, four patients receiving gentamicin (G), and four patients receiving cyclosporin‐A (CsA). We report that abnormal urinary excretion of proximal tubular cells occurred in patients receiving G and CsA. Membrane‐enclosed sudanophilic material and numerous vacuoles were found in the cytoplasm of the proximal tubular cells from both patients receiving G and those receiving CsA. Patients receiving G shed higher levels of phosphatidylcholine (PC), phosphatidylethanolamine (PE), and sphingomyelin (SM) in the order of 78%, 38%, and 30% relative to normal. In contrast, the excretions of phosphatidylinositol (PI) and PC were 50% and 30% lower, respectively, in patients receiving CsA as compared to control. Sphingomyelin levels, however, were moderately elevated in these patients' urinary renal tubular cells.The activity of acid sphingomyelinase was one half the normal level in the cells of patients receiving G and CsA. The most striking result was a tenfold decrease in the activity of neutral sphingomyelinase in patients receiving G. In contrast, the activity of neutral sphingomyelinase in patients receiving CsA was similar to control. Phospholipase A activity was decreased and increased 35% and 15%, respectively, in urinary proximal tubular cells from patients receiving G and CsA.We conclude that deficient neutral sphingomyelinase activity precedes phospholipid (PL) overloading and gross pathological changes in patients receiving gentamicin but not in patients receiving cyclosporin‐A.
Modulations in the biotransformation of tobacco extract and N′‐nitrosonornicotine under differential dietary protein status
Authors: Ammigan N. , Nair U. J. , Amonkar A. J. , Bhide S. V. 
Published: October 2006

AbstractThe modulation of the phase I and phase II biotransformation enzymes upon treatment with tobacco extract (TE) and N'‐nitrosonornicotine (NNN) was investigated using male Sprague‐Dawley rats fed differential protein diets. It was observed that the animals fed a low protein diet showed an overall decrease in the basal levels of hepatic and pulmonary phase I and II enzymes. TE and NNN significantly decreased the detoxifying system in the low‐proteinfed animals. Animals fed 20% protein, however, showed significant increases in glutathione and glutathione S‐transferase upon treatment. Furthermore, TE and NNN treatment brought about a significant depletion in the hepatic pool of vitamin A with a concomitant increase in the vitamin C levels.