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L Fay

Publications and source records attributed to L Fay.

14 recordsLinked to original sources

Quantitative determination of heterocyclic amines in food products.

Heterocyclic aromatic amines (HAs) may be formed during heat-processing of proteinaceous foods. All HAs are mutagenic in the Ames test, and many are animal and non-human primate carcinogens. The information on human dietary exposure is, therefore, of primary importance to accurately assess this health risk. A sensitive multiresidue method for quantifying ng/g HA levels, i.e., MeIQx, IQx, 7,8-DiMeIQx, 4,8-DiMeIQx, IQ, MeIQ, PhIP, Glu-P-1, Glu-P-2, Trp-P-1, Trp-P-2, A alpha C and MeA alpha C, in food products by high performance liquid chromatographic analysis with ultraviolet and fluorescence detection was developed. Isolation from cooked foods was performed in a three-step solid-phase extraction procedure using cartridges of diatomaceous earth, propylsulfonic acid silica and octadecyl silica. Quantitative analysis in food products was done using the standard addition quantification model. Levels of PhIP and A alpha C exceeding 100 ng/g were found in grilled fish as well as grill scrapings, whereas of the commercial products investigated less than 50% contained detectable levels of heterocyclic amines, generally MeIQx in the range of 1 to 5 ng/g. Few samples, e.g., some Process Flavours, needed further purification and more selective detection methods to increase the sensitivity of the assay. Such products were further purified by solid-phase extraction with TSKCM650 gel, and analyzed with thermospray liquid chromatography/mass spectrometry.

Amines↗

Effects of 9, 12, 15-octadecatrien-6-ynoic acid on the metabolism of arachidonic acid in platelets and on platelet aggregation.

An acetylenic fatty acid: 9,12,15-octadecatrien-6-ynoic acid (dicranin) was extracted from Dicranum Scoparium and preincubated with platelets which were then stimulated by exogenous arachidonic acid (20:4 n-6). This molecule at 10(-4) M weakly inhibited the cyclooxygenase activity as assessed by measurement of 12-hydroxy-heptadecatrienoic acid (HHT) In contrast, the 12-hydroxy-eicosatetraenoic acid (12-HETE) synthesized by the 12-lipoxygenase was strongly increased by about 650%. The same effects were observed with 10(-5) M and with 10(-6) M of dicranin but to a lesser extent. Platelet hydroxylated dicranin metabolites were also found and the structure of the main compound determined by GC-MS was a 13-hydroxy derivative. Its origin has not yet been elucidated. Platelet aggregation induced by 1 microgram/ml of U46619, a structural PGH2 analogue was completely abolished in the presence of dicranin. Platelet aggregation induced either by thrombin or by arachidonic acid was inhibited by 10(-4) M of dicranin only after preincubation. This observation indicates that the formation of metabolites of dicranin are necessary to effect this inhibition. Dicranin is thus a new inhibitor of platelet aggregation and may prove to be useful for elucidating the effects of 12-HETE in biological systems.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

Effects of 9,12,15-octadecatrien-6-ynoic acid on the metabolism of arachidonic acid in platelets and on the platelet aggregation.

An acetylenic fatty acid: 9,12,15-octadecatrien-6-ynoic acid (dicranin), extracted from Dicranum Scoparium was preincubated with platelets stimulated by exogenous arachidonic acid (20:4 n-6). Dicranin (10(-4) M) weakly inhibited the cyclooxygenase activity as assessed by measurement of 12-hydroxy-heptadecatrienoic acid (HHT) In contrast, the 12-hydroxy-eicosatetraenoic acid (12-HETE) synthesized by the 12-lipoxygenase was strongly increased by about 650%. The same effects were observed with 10(-6) M of dicranin but to a lesser extent. The main platelet hydroxylated dicranin metabolite determined by GC-MS was a 13-hydroxy derivative Platelet aggregation induced either by thrombin or by arachidonic acid or by U46619, an structural PGH2 analogue was inhibited by 10(-4) M of dicranin.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

Physiological parameters related to distance running performance in female athletes.

The purpose of this study was to investigate the relationship between running pace for the 5 km, the 10 km, and the 16.09 km (10 mile) distances and the following variables: oxygen uptake and treadmill speed at predetermined lactate accumulation points (2.0 and 4.0 mmol.l-1), oxygen uptake (running economy) at three submaximal standardized treadmill speeds (196, 215, and 241 m.min-1), and maximal oxygen uptake. Thirteen moderately to highly conditioned (VO2max = 59.7 +/- 5.3 ml.kg-1.min-1; VO2 at 2.0 mmol.l-1 of plasma lactate = 46.6 +/- 4.1 ml.kg-1.min-1) female runners between the ages of 18 and 33 yr volunteered to participate. All subjects performed the laboratory tests and the 5 km, 10 km, and 16.09 km competitive time trials on an outdoor 5 km course. The correlation coefficients (r) between each race pace and maximal oxygen uptake (VO2max), speed (s) at 2.0 mmol.l-1 plasma lactate accumulation (PLA2s), and speed at 4.0 mmol.l-1 plasma lactate accumulation (PLA4s) ranged between 0.84 and 0.94. The oxygen costs of running at each of the three submaximal paces were correlated moderately with each race pace (r = -0.40 to -0.63). Hierarchal stepwise multiple regression analyses produced equations with two independent variables which explained 94 to 97% of the variability in race performance.

Adolescent↗

[Influence of the concentration of precursors on the biosynthesis of testosterone by the chick embryo testis].

The aim of this study was to determine whether substrate concentration was of crucial importance in the formation of testosterone by the chick embryo testis. Testes from 15 to 18-day old chick embryos were cultured in medium 199 with dehydroepiandrosterone 1, 2, 6, 7-3H or androstenedione-4-14C added at different concentrations. Testosterone was identified and measured by crystallization to constant specific activity or by gas chromatography-mass spectrometry. The formation of testosterone could not be demonstrated at a substrate concentration of 76 nM. Concentrations in the micromolar range yielded measurable quantities of testosterone which increased to about 10% of the added substrate when the concentration was 70 microM. However, the capacity to form testosterone was shared by other organs such as the ovary or the mesonephros. These results should settle definitively the question concerning the formation of testosterone by the chick embryo testis. When exposed to high substrate concentrations, the testis can form testosterone, but under physiological conditions there is no such testosterone formation. This conclusion is in agreement with the absence of any physiological role of testosterone in the chick embryo.

Androstenedione↗

Oxidoreductive and hydroxylating metabolism of progesterone in rat liver epithelial cell lines.

Mechanisms and sequences of reduction and hydroxylation of progesterone into 6-hydroxypregnanolones were studied in proliferating rat liver epithelial cell cultures. These cell lines had an intense metabolic activity and all the metabolites were unconjugated. The formation of 3 alpha,6 alpha- and 3 beta,6 alpha-dihydroxy-5 alpha-pregnan-20-one was observed when the cells were incubated with progesterone, 5 alpha-pregnane-3,20-dione, 3 alpha- or 3 beta-hydroxy-5 alpha-pregnan-20-one and 6 alpha-hydroxy-5 alpha-pregnane-3,20-dione but not with 6 alpha- or 6 beta-hydroxyprogesterone, 5 beta-pregnane-3,20-dione, 3 alpha- or 3 beta-hydroxy-5 beta-pregnan-20-one. These findings indicate that the potential precursors of the 6 alpha-hydroxypregnanolones have a 5 alpha-configuration. The reduction of 5 alpha-pregnane-3,20-dione at C-3 followed by a 6 alpha-hydroxylation can be postulated as the major, if not the only, metabolic pathway. However, the possibility that 6 alpha-hydroxylation may occur prior to reduction of the C-3 oxo group cannot be entirely ruled out. The stereospecificity of reduction at C-5 and hydroxylation at C-6 are discussed and compared with 6-hydroxylated progesterone metabolites found in man and some other mammals during pregnancy and the neonatal period.

Aging↗

Botulinum A toxin for the treatment of spasmodic torticollis: dysphagia and regional toxin spread.

Chemodenervation of cervical muscles with botulinum A toxin, although useful in treating spasmodic torticollis, has been associated with dysphagia. Retrospective analysis of dose and injection site (sternomastoid vs. posterior cervical muscle groups) in 26 patients (49 injections) suggested that dysphagia was related to the quantity of toxin injected into the sternomastoid muscle: dysphagia, median 150 IU (7 injections); and no dysphagia, median 100 IU (42 injections; p = 0.026 Wilcoxon test). In a prospective study (31 injections to 24 patients), limiting the dose administered to the sternomastoid to 100 IU, substantially reduced the incidence of dysphagia (0 of 31, p = 0.27, Fisher's exact test). Denervation of human orbicularis muscle fibers, 5 weeks to 4 months after injection of botulinum A toxin for the treatment of blepharospasm, was successfully demonstrated by intense, diffuse acetylcholinesterase staining. A weight-adjusted dose similar to that given for torticollis was injected into longissimus dorsi muscle in 6 albino rabbits. Using the acetylcholinesterase stain as a marker, a diffusion gradient was noted over a distance of 30 to 45 mm from the point of injection and in contralateral muscle 15 to 25 mm from this point. Thus, denervation was demonstrated to occur within a definable area which crossed anatomic barriers, such as fascia and bone. These clinical and laboratory data suggest that dysphagia following botulinum toxin therapy results from toxin spread to pharyngeal musculature from the sternocleidomastoid injection site. Limiting of the injection dose to 100 IU or less to the sternomastoid substantially decreases the incidence of this complication.

Acetylcholinesterase↗

A multicentre open comparison of isosorbide-5-mononitrate and nifedipine given prophylactically to general practice patients with chronic stable angina pectoris.

A total of 126 patients from general practice with chronic stable angina pectoris entered the treatment phase of this open, randomized, crossover comparison of 20 mg isosorbide-5-mononitrate, and 20 mg nifedipine. Both treatments were given orally, three times daily, for 4 weeks and sublingual administration of glyceryl trinitrate was allowed throughout. Over the whole treatment period, there was no statistically significant difference between treatments for anginal attacks. However, significantly fewer glyceryl trinitrate tablets were required by patients receiving prophylaxis with nifedipine, although this difference was too small to be of clinical significance. No statistical difference existed between treatments in respect of scores for 'overall intensity of pain', 'physical exercise ability' and 'general well-being'. Of those patients who expressed a preference, the majority preferred the second treatment with no statistically significant difference between isosorbide-5-mononitrate and nifedipine. Both treatments showed similar levels of adverse events, the major difference (not significant) being for flushing of the skin which occurred in five patients given nifedipine compared with one patient given isosorbide-5-mononitrate. It is concluded that, in clinical terms, the two treatments were similar. Headache and dizziness/giddiness were the most frequently recorded adverse events.

Angina Pectoris↗

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Anti-Bacterial Agents↗