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Biomedical subjects

E Bailey

Publications and source records attributed to E Bailey.

At least 145 records · Page 8Linked to original sources

Hepatic mitochondrial fatty acid oxidation during the perinatal period in the rat.

1. The activity of hepatic mitochondrial carnitine acyltransferase I increases rapidly after birth, is high during the suckling period and falls after weaning. In contrast, carnitine acyltransferase II and acyl-CpA dehydrogenase exhibit few developmental changes. 2. These and previous studies indicate that outer mitochondrial membrane acyl-CoA synthetase and inner membrane carnitine acyltransferase I increase in activity after birth much more rapidly than to any other enzymes of fatty acid oxidation. 3. Studies of the 18 hr after caesarian delivery indicate that whereas the major increase in the activity of acyl-CoA synthetase occurs within 3 hr of birth the change in carnitine acyltransferase I activity is less rapid. 4. Prolonged pregnancy, starvation of the mother or feeding the mother a high polyunsaturated fat content diet resulted in increased activities of acyl-CoA synthetase and carnitine acyltransferase I in the fetal liver.

Acyltransferases↗

Triiodothyronine-dietary interrelationships in the modulation of brown adipose tissue and liver lipogenesis in the rat.

The influence of diet and triiodothyronine on "in vivo" lipogenesis has been compared in liver and brown adipose tissue of the rat at weaning and in adult life. At both ages studied, hyperthyroidism increases lipogenesis only in the liver. However brown adipose tissue accumulates lipid (probably derived from white adipose tissue) thus helping to explain previous observations of low rates of lipogenesis in this tissue during the late suckling period when thermogenesis is high and plasma triiodothyronine levels rise. Suppression of lipogenesis by dietary polyunsaturated fat in both tissues at both ages studied confirms previous studies on adult animals. Malic enzyme and glucose-6-phosphate dehydrogenase activities correlate well with changes in lipogenesis in brown adipose tissue but not in liver and the hepatic enzymes exhibit a diminished response to dietary and hormonal factors with age.

Adipose Tissue, Brown↗

Linkage disequilibrium between the ELA and the A blood group systems in Standardbred horses.

The linkage group formed by the ELA and A blood group system in horses was studied in American Standardbred horses. The distance between the ELA locus and the A blood group locus was measured as 1.61 centimorgans, observing only the haplotypes contributed by the sires. Strong linkage disequilibrium was found in pacing Standardbred horses for ELA-W1 with Aa, ELA-W5 with Ab and ELA-W10 with Ab. Linkage disequilibrium was apparent at both the population and family level. Among trotting Standardbred horses, linkage disequilibrium was found for ELA-W1 with Aa and for ELA-W10 with Ab. It was not possible to investigate linkage relationships in Thoroughbred horses because of the high frequency of Aa and low frequency of other A system markers.

Animals↗

Population studies on the ELA system in American standardbred and thoroughbred mares.

336 Standardbred mares and 334 Thoroughbred mares in the vicinity of Lexington, Kentucky, were lymphocyte typed for 11 allelic antigenic specificities of the equine lymphocyte antigen (ELA) system. The Standardbred mares were divided into a population of pacers and a population of trotters. Substantial differences in ELA gene frequencies were found between the 3 groups. When the distribution of antigens within populations were compared to Hardy-Weinberg equilibrium expectations, relatively good agreement was found.

Animals↗

Studies on rat hepatic mitochondrial hydroxymethylglutaryl-CoA synthase during the perinatal period.

Rat hepatic mitochondrial hydroxymethylglutaryl-CoA (HMG-CoA) synthase activity increases throughout the perinatal period, indicating that the factors necessary for the induction of the enzyme are present in utero. Reciprocal changes occur in 3-ketoacid transferase activity during late fetal life, suggesting that ketone body formation and utilization may be subject to coordinate regulation. Cytosolic HMG-CoA synthase activity is low during fetal life and rises rapidly after birth. The activities of both cytosolic and mitochondrial enzymes in fetal liver are dependent upon maternal diet and different dietary effects are observed at different fetal ages.

Animals↗

Effects of insulin and maternal diabetes on fetal lipogenesis in the rat.

Offspring of diabetic mothers have been investigated with regard to fetal hepatic and brown adipose tissue lipogenesis in the rat. Results, which cannot be explained by existing theory, are obtained from offspring of subdiabetic mothers and manifest diabetic mothers. In re-evaluating the effect of exogenous insulin on perinatal lipogenesis, we find important differences in hormone sensitivity between liver and brown adipose tissue.

Adipose Tissue, Brown↗

Activities of enzymes of rat hepatic mitochondrial fatty acid oxidation during increased fatty acid degradation.

The activities of the enzymes of hepatic mitochondrial fatty acid oxidation have been compared in normal and fat-fed, streptozotocin diabetic, starved and hyperthyroid adult female rats. The various experimental states resulted in hyperketonaemia and marked increases in the activities of palmitoyl-CoA synthetase and carnitine palmitoyltransferase I, but had little effect on the other enzymes involved.

Animals↗

Effect of dietary carrageenan and pectin on the reduction of nitro-compounds by the rat caecal microflora.

Rats were fed either a basal purified diet, or that diet supplemented with 50 g/kg pectin or iota carrageenan for 50 days, and caecal microbial nitroreductase activity determined using p-nitrobenzoic acid, p-nitrophenol, 2,4-dinitrotoluene, nitrofurantoin and metronidazole as substrates. Both pectin and carrageenan increased the weight of caecal contents, and pectin also increased the number of bacteria per caecum. In contrast, carrageenan decreased the caecal bacterial population. Pectin significantly increased the rate of reduction of metronidazole and the rate of conversion of p-nitrobenzoic acid to p-aminobenzoic acid, while carrageenan significantly decreased the rate of reduction of every compound studied. The results demonstrate that microbial reduction of the nitro-group may be altered by diet, although the response found with one nitro-compound may differ from that seen with another substrate.

Animals↗

Hepatic lipogenesis and ketogenesis in the mother and fetus during postmaturity in the rat.

Prolongation of pregnancy for 1.5 days by the injection of progesterone leads to a decrease in maternal liver glycogen content and an increase in blood ketones without alteration in the activity of hepatic hydroxymethylglutaryl-CoA synthase, an enzyme of ketogenesis. Fetal hepatic mitochondrial hydroxymethylglutaryl-CoA synthase activity increases with increasing postmaturity in a similar manner to that observed in normal neonates, suggesting that the factors necessary for enzyme induction are present in utero during postmaturity and that birth and the intake of the milk diet of suckling are not essential for increased enzyme activity. Hepatic in vivo lipogenesis is elevated in both mother and fetus during prolonged pregnancy and the results indicate that progesterone may have a specific effect on hepatic lipogenesis.

Animals↗

Lipogenesis at the suckling-weaning transition in liver and brown adipose tissue of the rat.

The responses of rat hepatic and brown adipose tissue in vivo lipogenesis to premature (15 days) and normal (21 days) weaning have been correlated to changes in the activities of acetyl-CoA carboxylase and two NADPH-producing enzymes, malic enzyme and glucose-6-phosphate dehydrogenase. Both tissues show an induction of lipogenesis in response to weaning. In the liver, lipogenic flux is closely linked to the activity of acetyl-CoA carboxylase, but not necessarily that of malic enzyme or glucose-6-phosphate dehydrogenase, whereas no such dissociation between enzyme activity and flux rate occurs in brown adipose tissue. Thyroid hormones, implicated in many physiological changes around weaning, do not seem to play a primary role in the adaptation of lipogenesis to the dietary change at this time, although a permissive role in both tissues is possible.

Acetyl-CoA Carboxylase↗

Determination of hydroxypropylhistidine in haemoglobin as a measure of exposure to propylene oxide using high resolution gas chromatography mass spectrometry.

The alkylating agent propylene oxide is a potential carcinogen. Exposure to this compound leads to the formation of N-3'-(2-hydroxypropyl)histidine in protein. A sensitive and specific method has been developed for the determination of this alkylated amino acid in rat and human haemoglobin using high resolution gas chromatography with selected ion monitoring. Globin isolated from blood was hydrolysed with 6 M HCl and the protein hydrolysate chromatographed on a Dowex 50W H+ column. The amino acids in the partially purified extract were analysed as N-heptafluorobutyryl methyl esters using an SE-52 fused silica capillary column. Quantification was made by monitoring the ion m/z 560 [M-COOCH3)+ derived from the derivatized hydroxypropylhistidine in the sample and the corresponding ion at m/z 565 from the pentadeutero analogue of the alkylated amino acid added initially to the globin as an internal standard. The method has been used to quantify hydroxypropylhistidine down to levels of 2 microgram gm-1 haemoglobin and has been applied to studies in rats exposed to propylene oxide.

Animals↗

Dimethylphosphorothioates. Reaction with malathion and effect on malathion toxicity.

Five dimethylphosphorothioates were tested for their toxicity to rats, potentiation of malathion toxicity in rats, inhibition of carboxylesterase in vitro, and reaction with malathion in vitro. The compounds were: potassium salts of (CH3S)2P(O)O-(I), (CH3O)(CH3S)P(O)S-(II), (CH3O)2P(O)S-(III), (CH3O)2P(S)S-(IV), and (CH3O)(CH3S)P(O)O-(V). The dimethylphosphorothioates are not toxic to rats (up to 1 g/kg, orally), they do not potentiate malathion toxicity in rats, and do not inhibit carboxylesterase activity in vitro (up to 1 mM concentrations). However, when the S-acid diesters (II, III, IV) are incubated with malathion for serveral days at room temperature or for several hours at 50 degrees C they become methylated forming the trimethylphosphorothioates OSS-trimethyl phosphorodithioate, OOS-trimethyl phosphorothioate and OOS-trimethyl phosphorodithioate respectively, which potentiate malathion toxicity. Furthermore, these same acid diesters increase the rate of isomerization of malathion into OS-dimethyl-S-(1,2-dicarbethoxyethyl) phosphorodithioate (isomalathion) particularly, diester IV. The formation of the trimethylphosphorothioates and isomalathion from the interaction of the S-acid diesters with malathion was determined by thin layer chromatography (TLC), gas chromatography and mass spectrometry and could be detected by in vitro inhibition of carboxylesterase. TLC methods can detect 1 mg of the trimethylphosphorothioates and isomalathion per gram malathion.

Animals↗

Perinatal lipogenesis in the liver and brown adipose tissue of the rat.

1. Hepatic lipogenesis falls during late foetal life, reaching low levels soon after birth. 2. Of the lipogenic enzymes studied only changes in foetal liver acetyl-CoA carboxylase activities correlate well with the changes in lipogenic flux. 3. In contrast to liver, brown adipose tissue lipogenesis increases during late foetal life. 4. A similar developmental pattern in foetal brown adipose tissue was observed for the activities of a number of enzymes normally associated with lipogenesis. 5. The studies suggest the existence of different controls over the development of lipogenesis in the two tissues investigated during the perinatal period.

Adipose Tissue, Brown↗

Pharmacokinetics of cisplatin regional hepatic infusions.

Cisplatin (DDP), a potent antineoplastic agent, is usually administered via a peripheral vein. Recently, there has been considerable interest in intraarterial regional infusions of DDP. The pharmacokinetics of DDP when administered by this technique have not been explored in detail. We studied DDP pharmacokinetics in dogs given DDP by infusion and bolus injection in the hepatic artery (H.A.), portal vein (portal V), and peripheral vein (P.V.). Blood and biliary platinum concentrations ([Pt]) were assayed by flameless atomic absorption spectrophotometry. During an infusion into the H.S., peak [Pt] in the vessel were markedly higher (mean value 19 micrograms/ml) than those found, simultaneously, in the portal V or superior vena cava. Following a bolus injection of DDP into the H.A., higher H.A. [Pt] were also seen, but [Pt] rapidly (within 5-10 minutes) equilibrated in all sites sampled. During the H.A. infusion, most [Pt] was in its free (active) form. Bile and hepatic tissue were also sampled. Hepatic artery infusions of DDP give high drug concentrations in the perfusing blood, while systemic [Pt] are much lower. During the infusion, the majority of DDP is in its active (unbound) state.

Animals↗