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Biomedical subjects

E Bailey

Publications and source records attributed to E Bailey.

At least 127 records · Page 7Linked to original sources
PubMed1986

Monitoring human exposure to ethylene oxide by the determination of haemoglobin adducts using gas chromatography-mass spectrometry.

Globin samples from ethylene oxide-exposed workers and non-exposed referrents were analysed by two methods: (i) gas chromatography-mass spectrometry determination of Nt-(2-hydroxyethyl)histidine as its methyl ester heptafluorobutyryl derivative, after hydrolysis of the protein and isolation of the alkylated amino acid by ion exchange chromatography. The internal standard, Nt-(2-hydroxy-d4-ethyl)histidine, was added to the protein before hydrolysis. (ii) Determination of N-(2-hydroxyethyl)valine after derivatization of the protein by a modified Edman procedure, extraction and g.c.-m.s. determination of alkylated N-terminal valine in the form of its pentafluorophenylthiohydantoin derivative. The internal standard used was in this case a globin with a known content of hydroxy-d4-ethylated amino acids. The two methods gave consistent results, especially at high levels of alkylated products. The average content of hydroxyethylhistidine was 0.6 nmol/g higher than the content of hydroxyethylvaline. Higher levels of background alkylation (of unknown origin) were recorded with the histidine method as compared with the valine method, suggesting that the latter assay should show greater sensitivity for low level ethylene oxide exposure monitoring.

Alkylation↗
PubMed1986

Joint report of the Third International Workshop on Lymphocyte Alloantigens of the Horse, Kennett Square, Pennsylvania, 25-27 April 1984.

The Third International Workshop on Lymphocyte Alloantigens of the Horse was held on 25-27 April 1984 in Kennett Square, Pennsylvania. Twelve laboratories from five countries participated. The principal purpose of this Workshop was to determine the phenotypic and gene frequencies of the 10 equine lymphocyte antigens (ELA) and a non-ELA lymphocyte antigen, ELY-2.1, in several breeds of horse. A total of 86 alloantisera characterized in previous workshops were tested against lymphocytes from 1179 horses. In addition, several experimental antisera were also tested against the same panel of lymphocytes. As a result of analysis of these data, the Workshop recognized two new equine lymphocyte alloantigens: W11 of the ELA system, and ELY-1.1, an antigen not linked to the ELA system.

Animals↗
PubMed1985

The comparative toxicology of ethyl- and methylmercury.

Neurotoxicity and renotoxicity were compared in rats given by gastric gavage five daily doses of 8.0 mg Hg/kg methyl- or ethylmercuric chloride or 9.6 mg Hg/kg ethylmercuric chloride. Three or 10 days after the last treatment day rats treated with either 8.0 or 9.6 mg Hg/kg ethylmercury had higher total or organic mercury concentrations in blood and lower concentrations in kidneys and brain than methylmercury-treated rats. In each of these tissues the inorganic mercury concentration was higher after ethyl- than after methylmercury. Weight loss relative to the expected body weight and renal damage was higher in ethylmercury-treated rats than in rats given equimolar doses of methylmercury. These effects became more severe when the dose of ethylmercury was increased by 20%. Thus in renotoxicity the renal concentration of inorganic mercury seems to be more important than the concentration of organic or total mercury. In methylmercury-treated rats damage and inorganic mercury deposits were restricted to the P2 region of the proximal tubules, while in ethylmercury-treated rats the distribution of mercury and damage was more widespread. There was little difference in the neurotoxicities of methylmercury and ethylmercury when effects on the dorsal root ganglia or coordination disorders were compared. Based on both criteria, an equimolar dose of ethylmercury was less neurotoxic than methylmercury, but a 20% increase in the dose of ethylmercury was enough to raise the sum of coordination disorder scores slightly and ganglion damage significantly above those in methylmercury-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The effect of maternal diet during late pregnancy on postnatal changes in blood and liver metabolites and hepatic hydroxymethylglutaryl-CoA synthase activity in the offspring.

Both starvation of and feeding a high linoleic acid content diet to rats during late pregnancy resulted in marked differences in the metabolism of the fed offspring immediately after birth when compared to control neonates (mother fed the normal high carbohydrate content laboratory diet during pregnancy). In particular differences in postnatal changes in blood glucose, non esterified fatty acids and ketone bodies and in hepatic triglyceride content were observed. Many of the differences appeared to be related to the variations in blood and hepatic metabolites present at birth in the various groups of animals. A similar situation also existed with respect to postnatal changes in the activity of hydroxymethylglutaryl-CoA synthase.

Animals↗
PubMed1984

Metabolic activation of acetylenes. Covalent binding of [1,2-14C]octyne to protein, DNA and haem in vitro and the protective effects of certain thiol compounds.

[1,2-14C]Oct-l-yne was used to investigate metabolic activation of the ethynyl substituent in vitro. Activation of octyne by liver microsomal cytochrome P-450-dependent enzymes gave intermediate(s) that bound covalently to protein, DNA and to haem. The time course and extent of covalent binding of octyne to haem and to protein were similar. However, two different activating mechanisms are probably involved. Whereas covalent binding to protein or to DNA was inhibited by nucleophiles such as N-acetylcysteine, that to haem was little affected. When N-acetylcysteine was included in the reaction mixtures, two major octyne-N-acetylcysteine adducts were isolated and purified by high-pressure liquid chromatography. G.l.c.-mass spectrometry and n.m.r. suggest that these are the cis-trans isomers of S-3-oxo-oct-1-enyl-N-acetylcysteine. Oct-1-yn-3-one reacted non-enzymically with N-acetylcysteine at pH 7.4 and 37 degrees C with a t1/2 of about 6 s also to yield S-3-oxo-oct-l-enyl-N-acetylcysteine. The same product was formed when microsomal fractions were incubated with oct-1-yn-3-ol, N-acetylcysteine and NAD(P)+. Octyn-3-one did not appear to react with haem or protoporphyrin IX. 5. A mechanism for the metabolic activation of oct-1-yne is proposed, consisting in (a) microsomal hydroxylation of the carbon atom alpha to the acetylenic bond and (b) oxidation to yield octyn-3-one as the reactive species.

Acetylcysteine↗
PubMed1984

Determination of N-7-[2H3]methyl guanine in rat urine by gas chromatography-mass spectrometry following administration of trideuteromethylating agents or precursors.

A gas chromatographic-mass spectrometric method has been developed for the determination of N-7-[2H3]methyl guanine in urine in the presence of large natural levels of N-7-methyl guanine. Urine is fractionated on heptanesulfonic acid-treated C-18 Sep-pak cartridges, followed by derivatization to give a volatile N-heptafluorobutyryl-O6-2,3,4,5, 6-pentafluorobenzyl derivative which is separated on an SE52 fused silica capillary column. Using N-7-ethyl guanine as an internal standard, the total amount of N-7-methyl guanine is determined by gas chromatography-flame ionization detection. The percentage of N-7-[2H3]methyl guanine is then measured by gas chromatography-mass spectrometry, enabling the amount of deuterated base to be determined. Preliminary experiments with [2H3]methyl methanesulfonate in rats showed measurable excretion of N-7-[2H3]methyl guanine. 4-(Di[2H3]methylamino)antipyrine alone gave no detectable amount of alkylated base, but coadministration of nitrite resulted in excretion of deuterated N-7-methyl guanine.

Alkylating Agents↗
PubMed1984

Comparison of ELY-2.1 with blood group and ELY-1 markers in the horse.

The distribution of ELY-2 was compared to the distribution of blood group factors Aa, Ab, Ac, Ae, Ca, Da, Db, Dc, Dd, De, Df, Dh, Dk, Ka, Pa, Pb, X, Qa, Qc, Ua, and W in 2465 American Standardbred horses and to ELY-1 in 193 American Standardbred horses. The distribution patterns were different in each case. The segregation of ELY-2.1 and factors at the A, C, D, K, P, Q, U and T (W) blood group loci and at the ELA locus indicated that ELY-2.1 is not a product of any of those loci. No segregation data were available for the ELY-1 locus. Family studies indicated that the gene for ELY-2.1 is not sex-linked.

Animals↗
PubMed1984

Joint report of the Second International Workshop on Lymphocyte Alloantigens of the Horse, held 3-8 October 1982.

The Second International Workshop on Lymphocyte Alloantigens of the Horse was held 3-8 October 1982. At this workshop, the 6 specificities identified at the first workshop were confirmed and an additional 5 new specificities were identified and given workshop nomenclature. Four of the new specificities, products of the ELA locus, were named ELA-W7, W8, W9, and W10. An additional specificity, designated ELY-2.1, is the product of a locus independent of the ELA locus. Cell isolation methods were compared at this workshop. Technical variation in methods clearly affected reactivity of many reagents. However, when highly selected reagents were used, antigen assignment did not differ regardless of the cell isolation method. Based on the comparison of methods, isolation procedures in which thrombin was used were more effective than those relying on carbonyl iron or slow centrifugation.

Animals↗
PubMed1984

Monitoring exposure to propylene oxide through the determination of hemoglobin alkylation.

The levels of Nt-(2-hydroxypropyl)histidine in hemoglobin were determined for eight employees of a plant where propylene oxide is used and for thirteen referents. Good agreement was obtained between the estimated exposure and the degree of alkylation of hemoglobin; values of 0.1 nmol (11 referents), 0.2 nmol (1 referent), 0.38 nmol (1 referent), 0.2 nmol (1 employee without exposure), 0.85-1.2 nmol (3 employees with low-intermediate exposure), and 4.5-13 nmol (4 employees with high exposure; 10 ppm propylene oxide during 25-75% of the work time) per gram of hemoglobin were recorded. The method gives a measure of the in vivo dose obtained during a period of about four months and is therefore superior to point measurements of concentrations for the surveillance of exposure conditions in work environments.

Alkylation↗
PubMed1984

Usefulness of lymphocyte typing to exclude incorrectly assigned paternity in horses.

Lymphocyte typing can be used to detect incorrectly identified parentage of horses. Efficacies of lymphocyte typing to solve paternity questions were calculated using gene frequency estimates of equine lymphocyte antigen (ELA) markers for Thoroughbreds and Standardbreds. Probabilities that ELA typing will detect an incorrectly assigned sire were 68.7% in Thoroughbreds, 67.9% in pacing Standardbreds, and 62.0% in trotting Standardbreds. These calculations demonstrate that ELA typing is among the most efficacious genetic systems for solving paternity questions in horses. Likewise, it could also be effective for blood type identification and solving other questions of parentage in horses.

Animals↗
PubMed1984

Use of alkylated proteins in the monitoring of exposure to alkylating agents.

Measurement of reaction products of alkylating agents with proteins has been used as a monitor of in-vivo exposure to over 30 such compounds. Doses in animals exposed to directly-acting alkylating agents (e.g., methyl methanesulfonate, ethylene oxide) are directly related to the production of alkylated amino acids in haemoglobin. The erythrocyte dose of alkylating agent, calculated from the extent of haemoglobin alkylation, is in some cases related to liver and extra-hepatic DNA doses; thus, detection of alkylation of haemoglobin may be taken as an indication of a reaction at the carcinogenic target site.

Albumins↗
PubMed1984

The effect of maternal diet on maternal and fetal hepatic and brown adipose tissue lipogenesis and blood and tissue metabolites.

Both starvation of and feeding a high linoleic acid content diet to rats during late pregnancy resulted in (relative to stock diet fed controls) a decrease in maternal hepatic glycogen content and lipogenesis, reduced blood glucose levels and an increase in blood ketone levels whereas only fat feeding caused an increase in blood triglyceride levels and only starvation resulted in a decrease in the amount of brown adipose tissue. Maternal starvation resulted in decreased fetal body, liver and brown adipose tissue weights, diminished liver and brown adipose glycogen content and lipogenesis and lowered blood glucose levels. Both maternal fat feeding and starvation caused triglyceride accumulation in fetal liver, elevated blood ketone levels and an increased proportion of fetal liver and carcass fatty acids accounted for by linoleic acid.

Adipose Tissue↗
PubMed1983

Dosimetry of ethylene oxide in the rat by quantitation of alkylated histidine in hemoglobin.

Blood samples were obtained from male Fischer 344 rats exposed to controlled air concentrations of ethylene oxide; 0, 10, 33, and 100 ppm, 6 h/day, 5 days/week, for 2 years. N tau-(2-hydroxyethyl)histidine was isolated from hemoglobin hydrolysates and analyzed quantitatively by means of gas chromatography--mass fragmentography and by amino acid analysis. The degrees of alkylation found were 1.3 and 2.8 nmol hydroxyethylhistidine per gram hemoglobin in two groups of unexposed rats, and 14, 34, and 82 nmol per gram hemoglobin, respectively, at the three air levels of ethylene oxide. Rats of the same breed were given two concentrations of radiolabeled ethylene oxide by IP injection. The degrees of alkylation of amino acids in hemoglobin and of guanine-N-7 in DNA from livers and testes were determined. The degrees of alkylation of liver and testicular DNA were about 150% and 50%, respectively, of the values expected from the degree of alkylation of hemoglobin, basing the expectancy on a direct proportionality between the reactivity of the specific nucleophilic sites and the degree of alkylation obtained at these sites, assuming that the dose of ethylene oxide was the same in the different tissues studied. The in vivo dose of ethylene oxide determined from data on hemoglobin alkylation thus gives a reasonable approximation of the DNA dose. The data were in agreement with a fast elimination of ethylene oxide from the tissues, the biological half-life being estimated as about 10 min.

Alkylation↗
PubMed1983

Hydrolysis of oleylanilide in the rat.

The fate of oleylanilide, administered as a single intragastric dose in rape oil, has been studied in Porton Wistar rats. Following a dose of oleyl[U-14C]anilide approximately 60% of the label was recovered in the faeces over a 3 day period, and identified principally as unchanged anilide. Most of the remainder of the dose was recovered in urine as hydrophilic metabolites. p-hydroxyacetanilide, which is a major metabolite of aniline in the rat was identified in the hydrolysed samples of urine from anilide treated rats. Following administration of [9,10(n)-3H]oleyl[U-14C]-anilide to rats which had been fitted with a cannula in the thoracic lymph duct the [3H] label which was absorbed was recovered principally in triglycerides showing that extensive hydrolysis of the anilide occurs prior to or during uptake from the gut. Oleylanilide was identified in lymph by gas chromatography but amounted to less than 6% of the dose.

Acetanilides↗