Biomedical subjects
Publications and source records attributed to S L Taylor.
Few of the food allergens have been purified and characterized. Complex mixtures of allergens seem to exist in some commonly allergenic foods. Much further research will be necessary to develop any detailed understanding of the chemistry of food allergens.
Ingestion of sulfiting agents can induce wheezing in some asthmatic patients. However, neither the prevalence of sulfite sensitivity nor the clinical characteristics of the affected asthmatic population are known. In a prospective single-blind screening study, 120 non-steroid-dependent and 83 steroid-dependent asthmatic patients underwent challenge with oral capsules of potassium metabisulfite. Five non-steroid-dependent and 16 steroid-dependent asthmatic patients experienced a greater than 20 percent reduction in their one-second forced expiratory volume within 30 minutes following the oral challenge. Twelve of these sulfite reactors were rechallenged with metabisulfite capsules in a double-blind protocol. Under these conditions, only three of seven steroid-dependent patients had a positive response. Moreover, only one of five non-steroid-dependent patients had a response to double-blind challenge. On the basis of this challenge study, the best estimate of the prevalence of sulfite sensitivity in the asthmatic patients studied is 3.9 percent. This population, however, contained a larger number of steroid-dependent asthmatic patients than would be found in the general asthmatic population. It is concluded, therefore, that the prevalence of sulfite sensitivity in the asthmatic population as a whole would be less than 3.9 percent and that steroid-dependent asthmatic patients are most at risk.
Previous findings indicating that the oxidation products of cholesterol are associated with atherogenicity have led to a comparative study of the subchronic effects of feeding rabbits purified cholesterol, oxidized cholesterols free of cholesterol and cholesterol esters, or a mixture of cholesterol and oxidized cholesterols. Macroscopically, the cholesterol-fed animals exhibited 6-fold more arterial lesions than the animals fed cholesterol-free oxidized cholesterols. Microscopically, there was no statistically significant difference from the control in the number of histochemically-defined lesions in any of the groups. However, the lesions in the cholesterol-fed group were more severe, as indicated by a statistically significant increase in the magnitude of the lesions. This increased severity was also characterized by greater frequency and intensity of Azure A/Thionin, VonKossa, and Horseradish Peroxidase-Wheat Germ Agglutinin staining. Electron-microscopic studies of normal appearing arterial tissues showed an increased density of viable smooth muscle cells and an increase in vacuolar extracellular debris in the cholesterol-fed group. Oxidized cholesterols in the concentrations and relative compositions administered here are markedly less atherogenic to rabbits than highly purified cholesterol.
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Histamine poisoning can result from the ingestion of food containing unusually high levels of histamine. Fish are most commonly involved in incidents of histamine poisoning, although cheese has also been implicated on occasion. The historic involvement of tuna and mackerel in histamine poisoning led to the longtime usage of the term, scombroid fish poisoning, to describe this food-borne illness. Histamine poisoning is characterized by a short incubation period, a short duration, and symptoms resembling those associated with allergic reactions. The evidence supporting the role of histamine as the causative agent is compelling. The efficacy of antihistamine therapy, the allergic-like symptomology, and the finding of high levels of histamine in the implicated food suggest strongly that histamine is the causative agent. However, histamine ingested with spoiled fish appears to be much more toxic than histamine ingested in an aqueous solution. The presence of potentiators of histamine toxicity in the spoiled fish may account for this difference in toxicity. Several potentiators including other putrefactive amines such as putrescine and cadaverine have been identified. Pharmacologic potentiators may also exist; aminoguanidine and isoniazid are examples. The mechanism of action of these potentiators appears to be the inhibition of intestinal histamine-metabolizing enzymes. This enzyme inhibition causes a decrease in histamine detoxification in the intestinal mucosa and results in increased intestinal uptake and urinary excretion of unmetabolized histamine.
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When [14C]histamine was administered orally to rats, an average of 80% of the administered radioactivity was recovered in the urine at the end of 24 hr. About 10% of the total dose was excreted via the feces. Analysis of 4-hr urine samples found imidazoleacetic acid to be the predominant metabolite (60.6%), with N tau-methylimidazoleacetic acid (8.6%), N tau-methylhistamine (7.3%), and N-acetylhistamine (4.5%) to be the minor metabolites. Histamine metabolism was inhibited by simultaneous oral administration of aminoguanidine, isoniazid, quinacrine, cadaverine, putrescine, tyramine, and beta-phenylethylamine. The administration of inhibitors resulted in an increased amount of unmetabolized histamine and a decreased amount of metabolites reaching the urine. Pharmacologic inhibitors were found to be more potent and have a longer duration of action than foodborne ones. The inhibitors could potentiate food poisoning caused by histamine by inhibiting its metabolism.
We have previously demonstrated that peanut oil is not allergenic to peanut-sensitive individuals. Seven soybean-sensitive patients were enrolled in a double-blind crossover study to determine whether ingestion of soybean oil can induce adverse reactions in such patients. All subjects had histories of systemic allergic reactions (urticaria, angioedema, wheezing, dyspnea, and/or vomiting) after soybean ingestion and had positive puncture skin tests with a 1:20 w/v glycerinated-saline whole soybean extract. Sera from six of the seven subjects were tested by RAST assay for the presence of specific IgE antibodies to soybean allergens. All patients had elevated levels of serum IgE antibodies to the crude soybean extract; binding values ranged from 2.3 to 28.1 times that of a negative control serum. Before the oral challenges, all patients demonstrated negative puncture skin tests to three commercially available soybean oils and to olive oil (control). On four separate days, patients were challenged with the individual soybean oils and olive oil in random sequence. At 30-minute intervals, under constant observation, patients ingested 2, 5, and 8 ml of one of the soybean oils or olive oil contained in 1 ml capsules. No untoward reactions were observed with either the commercially available soybean oils or olive oil. Soybean oil ingestion does not appear to pose a risk to soybean-sensitive individuals.
A histamine-producing strain of Lactobacillus buchneri was isolated from Swiss cheese that had been implicated in an outbreak of histamine poisoning. It produced up to 4,070 nmol of histamine per ml in MRS broth supplemented with 0.1% histidine. The identification of this isolate was based on its biochemical, bacteriological, and DNA characterizations.
A method was developed for the production and purification of gregatin A from Phialophora gregata NRRL 13198 cultured on rice at 20 degrees C for 28 days. Liquid extraction followed by high-pressure liquid chromatography afforded 247.0 mg of crystalline gregatin A per kg of rice.
A reversed-phase ion-pair high-performance liquid chromatographic procedure for quantitative determination of histamine and its metabolites in rat urine is described. This method allows simultaneous analysis of five major histamine metabolites. Good separations were obtained by using 1-pentanesulfonic acid as the ion-pair reagent. A gradient elution program was used; the total elution time was less than 22 min. Linear standard curves with high correlation coefficients were obtained. This procedure has the advantage of requiring little sample preparation time and handling, and therefore maximizes the recovery of metabolites.
Monolayers of L-cell cultures were incubated with oxygenated cholesterols and cellular protein was subsequently measured to assess the cytotoxicity of the cholesterol oxides. The site of oxidation of the cholesterol molecule was not reflected in the degree of cytotoxicity. Of the 12 cholesterol oxides tested, cholestan-3 beta, 5 alpha, 6 beta-triol and cholestan-3,5-diene-7-one exhibited the greatest cytotoxicity, approximately 45% inhibition (reduction) in protein compared to the control at concentrations of 10 micrograms/ml, after 1 day of incubation with the compounds. 5-Cholesten-3 beta, 25-diol and 5-cholesten-3 beta-ol-7-one were the most cytotoxic after 5 days' exposure with concentrations of 10 micrograms/ml reducing the protein content to approximately 10% of the control. Lipid accumulation in the L cells (steatosis), as measured by Oil Red O-stainable droplets formed in response to cholesterol oxides was also investigated. Grade 3 steatosis (an increase in lipid droplets so that more than 75% of the L-cell cytoplasm was occupied by lipid droplets) after 1 day of exposure to cholesterol oxides generally reflected the cytotoxic effect of the same cholesterol oxides after 5 days' exposure. However some of the steatotic cholesterol oxides, such as the alpha and beta epimers of cholestan-5,6-epoxy-3 beta-ol were highly active with respect to steatosis, increasing the grade 3 value to 209 and 390% of control, respectively, but were not cytotoxic. This has led to the suggestion that the cholesterol oxides have more than one mode of action in L cells.
Staphylococcal enterotoxin A (SEA) was administered orally (15 micrograms) to two groups of rats. A marked immune reaction was evoked in the stomach and proximal small intestine of the first group. The second group of rats was used to study the absorptive fate and sites of action of orally administered SEA, utilizing immunoperoxidase staining. After oral dosing of the second group of rats. SEA-related immunoperoxidase staining was confined to: (i) neutrophils and macrophages, principally in the duodenum, and (ii) glomerular neutrophils and cells of the proximal convoluted tubules. Peroxidase staining of the kidney was noted within 15 min of exposure, indicating that SEA or some major postabsorption antigenic product can promptly pass through an intact gastrointestinal mucous membrane and become renally localized. Intestinal and renal detoxification and removal was indicated by an absence of detectable antigen in rats 180 min postexposure. Neuronal binding of SEA in the gastrointestinal tract was not demonstrable.
Examination of the serosal fluid following in vitro luminal perfusion of rat intestinal segments with 1 mg/ml [3H]histamine for 2 hr showed that histamine constituted only 22.1% of the total serosal radioactivity. The remainder of the radioactivity was comprised of histamine metabolites. When equimolar amounts of either aminoguanidine and cadaverine were added to the luminal perfusate, the percentage of the serosal radioactivity as histamine increased to 67.0 and 60.4%, respectively. However, when equal amounts of histamine and anserine were added to the luminal perfusate, only 30.6% of the 3H translocated within 2 hr was [3H]histamine. In all cases, the gross translocation rate based on the percentage of total serosal radioactivity for total radioisotope [( 3H]histamine plus [3H]histamine metabolites) was unchanged by the addition of these substances to the luminal perfusate. The results indicate that the potentiation of histamine toxicity by putrefactive amines, such as cadaverine, results from the inhibition of histamine metabolism which leads to increased uptake of unmetabolized histamine. The results do not support the hypothesis that potentiation occurs via an overall increase in the absorption of histamine and its metabolites due to some disruption in the barrier function of the intestine.
A high pressure liquid chromatographic (HPLC) procedure is described for determining the following putrefactive amines: histamine, tyramine, putrescine, cadaverine, tryptamine, and beta-phenylethylamine. The amines were extracted from tuna or cheese with methanol. Further cleanup was performed by sequential extractions with butanol and HCl. The acid extract was dried, and residues were derivatized with dansyl chloride. HPLC separations were performed on an Ultrasphere-ODS column at 33 degrees C. A gradient elution program was used; the total elution time was less than 17 min. Linear standard curves with high correlation coefficients were obtained. The procedure allowed good recoveries of histamine, tyramine, putrescine, and cadaverine; recoveries of tryptamine and beta-phenylethylamine were lower but constant. With this method, some swiss cheese samples were found to contain considerable amounts of histamine, tyramine, putrescine, cadaverine, and beta-phenylethylamine. Canned tuna samples had very low levels of these amines. Since the presence of amines at high levels has been associated with tuna decomposition, this method may be useful in identifying decomposed fish.
The basic methylene chloride extract from 20 of 30 samples of foods fried in deep fat failed to elicit any mutagenic response that could be detected in the Salmonella typhimurium/mammalian microsome assay. The basic extracts of the remaining ten samples (all three chicken samples studied, two of the four potato-chip samples, one of four corn-chip samples, the sample of onion rings, two of six doughnuts, and one of three samples of french-fried potato) showed evidence of weak mutagenic activity. In these samples, amounts of the basic extract equivalent to 28.5-57 g of the original food sample were required to produce revertants at levels of 2.6-4.8 times the background level. Only two of the acidic methylene chloride extracts from the 30 samples exhibited mutagenic activity greater than 2.5 times the background reversion level, and in both cases (one corn-chip and one shrimp sample) the mutagenic response was quite weak. The basic extract of hamburgers fried in deep fat in a home-style fryer possessed higher levels of mutagenic activity (13 times the background reversion level). However, the mutagenic activity of deep-fried hamburgers is some four times lower than that of pan-fried hamburgers.
Peroral and intraduodenal administration of staphylococcal enterotoxin A (SEA) to weanling pigs elicited an emetic response. Peroral administration of an emetic dose of SEA resulted in a single emetic episode occurring 90 to 180 min after dosing. Intraduodenal administration via a surgically implanted catheter of 100 or 150 micrograms of SEA resulted in multiple emetic episodes occurring 150 to 210 min after dosing, suggesting an intestinal site of action for SEA. The 50% emetic dose for perorally administered SEA was between 40 and 50 micrograms for 4.1- to 9.1-kg weanling pigs and 20 micrograms in 0.9- to 2.3-kg weanling pigs. Neurobehavioral responses, including alternating periods of drowsiness and restlessness, staggering, temporary loss of the righting reflex, and refusal to feed were also observed in pigs given an oral dose of SEA. Based on the demonstrated responsiveness of pigs to SEA, pigs should be considered suitable animal models for studies on the sites and mode of action of the toxin.