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Biomedical subjects

D L Park

Publications and source records attributed to D L Park.

At least 37 records · Page 2Linked to original sources
PubMed1992

Mutagenic potentials of fumonisin contaminated corn following ammonia decontamination procedure.

Naturally contaminated corn implicated in an outbreak of equine leukoencephalomalacia (ELEM) in southeastern Arizona was analyzed for mutagenic potential using the Salmonella/microsome mutagenicity assay before and after treatment with the ammonia procedure. Crude acetonitrile: water (1 + 1) extracts of high-pressure/ambient temperature (HP/AT) ammonia decontaminated, HP/AT plus low pressure/high temperature (LP/HT), and non-ammoniated fumonisin contaminated corn were tested for mutagenic potentials. Relatively pure (approx. 90%) fumonisin B1 standard was also tested for comparison purposes. The results of this experiment indicate that there was no mutagenic potential for the fumonisin B1 standard at the concentrations tested (100 micrograms/plate). Also, neither the naturally-contaminated corn nor the ammonia decontaminated samples elicited a positive mutagenic response. Fumonisin B1 levels, as determined by HPLC methods, were reduced by an average of 79% via the ammonia decontamination process. It is encouraging to note that, while further work is necessary to increase the efficacy of the ammonia process to reduce fumonisin levels, the ammonia process did reduce fumonisin levels and no mutagenic potentials were apparent in the treated corn.

Ammonia↗
PubMed1992

Rapid facile solid-phase immunobead assay for screening ciguatoxic fish in the market place.

The precision of the solid-phase immunobead assay (Ciguatect) to detect toxins associated with ciguatera poisoning have been evaluated through analysis of toxic and non-toxic fish obtained from fishing areas around the Hawaiian Islands. The Ciguatect test kit has been optimized for application to field/marketplace screening of ciguatoxic fish. Twelve parrot, surgeon, and amberjack fish fillet and fish extract test portions containing various concentrations of toxins were distributed to participating laboratories for analysis. The presence or absence of ciguatera-related toxins is determined by binding the toxins to a membrane attached to a plastic strip and exposing the toxin ladened membrane to a monoclonal antibody-colored latex bead complex which has a high specificity for ciguatera-related toxins. The intensity of the color on the membrane denotes the presence of the toxins in the fish or fish extract. Toxic components in the fish were confirmed by extraction, column purification, and toxicity testing using the brine shrimp (Artemia sp.) assay. Okadaic acid was used to standardize both the S-PIA and brine shrimp assays. For determination of ciguatoxin and related polyether toxins in parrot, surgeon, and amberjack fish fillets, the relative standard deviations for repeatability (RSDR) were 13.5, 9.0 and 4.3%, respectively, and the relative standard deviations for reproducibility (RSDR) were 44.4, 29.7 and 14.3%, respectively, for concentrations ranging from 1-4 ng/test strip. For determination of ciguatoxin and related polyether toxins in parrot, surgeon, and amberjack fish extracts, the RSDR were 5.8, 4.8, and 3.7%, respectively, and the RSDR were 11.9, 9.9, and 7.6%, respectively, for concentrations ranging from 3-5 ng/test strip.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Foodborne toxins of marine origin: ciguatera.

Ciguatera poisoning has long been recognized as a serious problem in the tropical and subtropical regions of the world. Due to international and interstate commerce and tourist travel the phenomenon is spreading to other parts of the globe. Various species of fish (surgeonfish, snapper, grouper, barracuda, jack, amberjack among others) have been implicated in this type of poisoning. These fish accumulate toxins in their flesh and viscera through the consumption of smaller fish that have been previously contaminated by feeding on toxic dinoflagellates. The most probable source of ciguatera is thought to be the benthic microorganism, Gambierdiscus toxicus, which produces both CTX and MTX, but other species of dinoflagellates such as Prorocentrum lima may also contribute with secondary toxins associated with the disease. Potentially ciguatoxic dinoflagellates have been isolated, cultured under laboratory conditions and dinoflagellate growth requirements as well as some factors affecting toxin production have been determined. Also, data from their ecological environment have been accumulated in an attempt to reveal a relationship with the epidemiology of ciguatera outbreaks. Several bioassays have been employed to determine the ciguatoxicity of fish. Cats have been used due to their sensitivity, but regurgitation has made dosage information difficult to obtain. Mongooses have also been used but they often carry parasitic and other type of diseases which complicate the bioassay. Mice have been used more commonly; they offer a more reliable model, can be easily housed, readily are dosed in several ways, and manifest diverse symptoms similar to human intoxications; but the amount of toxic extract needed, time consumed, complicated extraction techniques, and instrumentation involved limit the use of this assay commercially. Other bioassays have been explored including the brine shrimp, chicken, mosquito, crayfish nerve cord, guinea pig ileum, guinea pig atrium, and other histological preparations. All require elaborate time-consuming procedures, are not reproducible, lack specificity, and are semiquantitative at best. The techniques that appear to represent the major advance in identifying and detecting ciguatoxic fish are immunochemical methods: radioimmunoassay (RIA), competitive enzyme immunoassay (EIA), and enzyme-linked immunosorbent assay (ELISA). Of these, the enzyme immunoassay stick test is the simplest, fastest, most specific, more sensitive, and does not require complicated instrumentation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Aflatoxin control--how a regulatory agency managed risk from an unavoidable natural toxicant in food and feed.

The control by the Food and Drug Administration (FDA) of aflatoxin, a relatively recently discovered, unavoidable natural contaminant produced by specific molds that invade a number of basic food and feedstuffs, provides an example of the varying forces that affect risk assessment and management by a regulatory Agency. This is the story of how the FDA responded to the initial discovery of a potential carcinogenic hazard to humans in a domestic commodity, to the developing information concerning the nature of the hazard, to the economic and political pressures that are created by the impact of natural forces on regulatory controls, and to the restraints of laws within which the Agency must work. This story covers four periods: the years of discovery and action decisions on the basis of meager knowledge and the fear of cancer; the years of tinkering on paper with the regulatory process, the years of digestion of the accumulating knowledge, and the application of that knowledge to actions forced by natural events; and an audit of the current status of knowledge about the hazard from aflatoxin, and proposals for regulatory control based on that knowledge.

Aflatoxins↗
PubMed1986

Evaluation of chicken embryo, brine shrimp, and bacterial bioassays for saxitoxin.

The chicken embryo, brine shrimp (Artemia salina) and selected bacteria (Staphylococcus epidermidis, Micrococcus flavus, and Bacillus subtilis) were evaluated as alternative test systems for the determination of paralytic shellfish poisoning toxicity (saxitoxin). Dose levels ranging from 0.045 to 0.3 microgram were administered to the developing embryo through the air cell at either 0 or 96 h following incubation. Embryos dosed 96 h after incubation were the most sensitive, with 100% mortality at the 0.11-microgram dose level 24 h following exposure. Embryo mortality was 42% at to 0.3-microgram dose level when the toxin was administered at 0 h. Some embryonic malformations were observed in the 0-h treatment group. Brine-shrimp larvae were sensitive to saxitoxin at a dose level of 5 micrograms. A dose response based on mortality was apparent only 48 h after dosing. Limited growth inhibition was observed with the bacteria tested at concentrations between 0.0035 and 0.35 microgram and 0.35 microgram/well.

Animals↗
PubMed1980

In vivo and in vitro metabolism of [14C]penicillic acid.

In vivo and in vitro studies of the metabolism of [14C]penicillic acid showed a significant uptake of penicillic acid by red blood cells and a significant increase in radioactivity associated with the membrane fraction with time (1-4 hr); however, the majority of the red blood cell activity was intracellular. The 14C-radioactivity concentration in liver fractions (1.5 percent of the administered dose 2 hr following administration) was high in the RNA-DNA and protein fractions. The level of the 14C activity associated with these fractions increased with time (24 hr). Preliminary studies of the in vivo metabolism of [14C]penicillic acid by rats showed that a significant amount of radioactivity was excreted in the urine (82 percent of the administered dose after 7 days), of which strongly acidic urinary metabolites accounted for 23 percent; weakly to moderately acidic, 60 percent; strongly basic, 2 percent; and neutral, 15 percent. Isolation and identification studies of the neutral urinary fraction indicated that the major metabolites are non-ionic macromolecules (Mr < 5000). Biliary metabolites (10 percent of the administered dose 2 hr following administration) were 28 percent strongly acidic and 72 percent weakly to moderately acidic.

Absorption↗
PubMed1978

Biliary excretion of [14C]penicillic acid by rats.

Adult male rats were given [14C]penicillic acid by oral intubation, and the biliary excretion of the compound was monitored. The significance of bile as an excretory route was confirmed and compared by using open and recycle cannulation of the bile duct. The biological half-retention life of [14C]penicillic acid in the bile was 3.63 h.

Animals↗
PubMed1978

Preliminary report of the distribution of [14C]penicillic acid in rats: autoradiographic technique.

The distribution of [14C]penicillic acid in rats was determined by autoradiographic technique. Adult male rats were given [14C]penicillic acid orally and IV. According to autoradiographic analyses 24 hours later, high levels of radioactivity were in liver, heart, kidneys, lungs, and caudal part of the intestine. The significance of bile as an excretory route for penicillic acid was confirmed by the results from IV administration of the compound.

Administration, Oral↗
PubMed1977

The absorption, distribution, and excretion of 14C-penicillic acid by rats.

Adult male and female rats were given 14C-penicillic acid (labeled in the 1, 3, and 5 positions by fermentation with acetate-1-14C) by oral intubation and were sacrificed at 1, 2, 4, 24, 48, 72, and 168 hours following administration of the labeled compound. Approximately 98 p. 100 of the 14C-radioactivity given was absorbed from the gastrointestinal tract of the rats during the first 48 hours. After 7 days, 82 p. 100 was recovered in the urine and 13 p. 100 in the feces. Less than 1 p. 100 of the total radioactivity was recovered as 14CO2 from the expired air; most of this amount was recovered within the first 72 hours after administration. Various tissues were, analyzed for 14C-radioactivity throughout the 7-day-period; no significant retention of radioactivity was apparent in any of the tissues examined. The level of 14C-penicillic acid reached a maximum in the blood and tissues 2-4 hours after administration. Red blood cells contained the highest concentration of 14C-radioactivity. Liver, bladder, kidneys, heart, and bile also showed a high level of 14C-radioactivity concentration. The estimated biological half-life of penicillic acid was 18.7 and 17.1 hours for the male and female, respectively. The estimated biological half-retention time from the point of administration by the red blood cells, liver, and kidney of the male and female rats was 24.2 and 14.0; 19.8 and 17.8; and 21.3 and 19.0 hours, respectively. Recovery studies indicated no unchanged penicillic acid in the urine.

Animals↗
PubMed1976

Collaborative study of the Food Chemicals Codex method for the determination of the neutralizing value of sodium aluminum phosphate.

Fifteen laboratories participated in a collaborative study to evaluate the Food Chemicals Codex method for the determination of the neutralizing value of sodium aluminum phosphate. The AOAC method for determining the neutralizing value of sodium acid pyrophosphate, sec. 8.010, was also included in the study. The precisions of the Food chemicals Codex method, based on the between-replicate standard deviation and on one collaborator making one determination, are 1.16 and 3.66, respectively. The Food Chemicals Codex method for the determination of the neutralizing value of sodium aluminum phosphate has been adopted as official first action.

Aluminum↗
PubMedDate not supplied

Changes in the avian cochlea after single high-dose gentamicin.

PURPOSE: Define the time course of functional and anatomical damage and subsequent recovery (by regeneration) of hair cells in the chicken inner ear after a single high-dose of gentamicin. MATERIALS AND METHODS: Broiler chicks were given a single intraperitoneal dose (200 mg/kg) of gentamicin (n = 39) or saline (n = 39). Functional status was evaluated with auditory brainstem response (ABR) thresholds before injection and before sacrifice at 2, 5, 9, 16, 21, 28, and 70 days postinjection. The cochleae were then examined with scanning electron microscopy (SEM) to assess the extent of damage along the cochlea and absolute hair cell numbers in the basal 15% of the cochlea (high-frequency region). RESULTS: Considerable variability between animals was seen for both ABR and SEM changes. Damage was maximal at 5 days postinjection with an average ABR threshold shift of 12 dB (range -10 to 50 dB) and basal cochlear damage of 28% (range 12%-57%). Hair cell counts were significantly decreased in the basal 15% of the cochlea at 5 days. Hair cell regeneration resulted in rapid anatomical and functional recovery, but evidence of hair cell disorganization persisted at 70 days despite improved thresholds. CONCLUSION: A single high dose of gentamicin produces a significant but variable anatomical and functional insult in the chick cochlea. Hair cell regeneration results in rapid but incomplete recovery.

Analysis of Variance↗
PubMedDate not supplied

Rationales for the establishment of limits and regulations for mycotoxins.

Although 50 countries have enacted or proposed regulations for control of alfatoxins in food or feed, and 15 of these countries also have regulations for permitted levels of contamination by other mycotoxins, very few countries have formally presented the rationale for the need to regulate, or for the selection of a particular maximum tolerated level. After several successive inquiries, information concerning the rationale for regulation was obtained from 21 countries. Most of the responses concerned limits for aflatoxin in food, and most of these were based on a vague, unsupported statement of the carcinogenic risk for humans. There was a general consensus that exposure to a potential human carcinogen that could not be totally avoided should be limited to the lowest practical level; the definition of practicality depended on whether the country was an importer or producer of the potentially contaminated commodity. A claim to a hazard evaluation was made by six countries (Canada, Belgium, India, United Kingdom, United States, Switzerland) without providing specifics; and one country, South Africa, referred to a risk determination. The most comprehensive rationale for any mycotoxin regulation was provided by the United States in support of limits for aflatoxin in specific animal feedstuffs. The responses provided no rationale for setting limits for other mycotoxins; but scholarly risk assessments for zearalenone and ochratoxin A have been published by Canadian government scientists, and a symposium presentation provides the information that in Norway patulin is regulated for quality control purposes only. It is apparent that, in most countries, either the scientific basis for regulation of mycotoxins is nonexistent, or the science has not been fully utilized.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗
PubMedDate not supplied

Perspectives on mycotoxin decontamination procedures.

Unquestionably, prevention is the best method for controlling mycotoxin contamination. Should the contamination occur, however, the hazard associated with the toxin must be removed if the product is to be used for food or feed purposes. Decontamination procedures currently used are based on (a) physical, chemical, or biological removal, or (c) physical or chemical inactivation. Ammoniation of corn, peanuts, cottonseed, and meals to alter the toxic and carcinogenic effects of aflatoxin contamination has been the subject of intense research effort by scientists in various government agencies and universities worldwide. Engineers have devised workable systems of treatment of whole seeds, kernels, or meals; chemists have identified and characterized products formed from the reaction of aflatoxin B1 with ammonia with and without a meal matrix; biochemists have studied the biological effects of these compounds in model systems; and nutritionists have studied animal responses to rations containing ammoniated or non-ammoniated components. This review describes these studies as well as other potentially useful decontamination processes. The results of aflatoxin/ammonia decontamination research demonstrate the efficiency and safety of ammoniation as a practical solution to aflatoxin detoxification in foods and animal feeds.

Aflatoxins↗
PubMedDate not supplied

Efficacy and permanency of ammonia treatment in reducing aflatoxin levels in corn.

Naturally contaminated yellow corn containing 12500 ng/g of aflatoxin B1 (AFB1) was ground and blended with non-contaminated corn to obtain various levels of AFB1 (7500, 6300, 400, 354, and 17 ng AFB1/g). All samples were exposed to ammonia treatment under various conditions for 60 min. Treatment variables included ammonia concentration, moisture level of the corn, temperature, and pressure applied. The moisture content of the corn (8%) was adjusted to 12% and 16%, respectively. Four ammonia treatments were conducted for each moisture level: (a) 1.5% and 2.0% gaseous NH3 at 40-45 degrees C and 55 psi; (b) aqueous NH4OH (2.0% as NH3) at 121 degrees C and 17 psi; (c) sequential treatment of (a) and (b); and (d) aqueous NH4OH (2.0% as NH3) at 25 degrees C and 55 psi. For the treatment with 2% gaseous NH3, the reduction in levels of AFB1 in samples containing 12% moisture ranged from 52.7 to 67.7%, while in samples containing 16% moisture, the reduction ranged from 79.4 to 93.1%. Treatment with NH4OH alone at elevated temperatures (b) or following gaseous NH3 treatment (c) resulted in a reduction of the AFB1 content by greater than 99%. Treatment with NH4OH at 25 degrees C (d) showed a lower efficiency in reducing AFB1 levels. The permanency of the process, i.e. reversion of inactivated AFB1 to the parent compound, was studied by exposing the ammonia-treated corn to HCl (pH = 2.0 at 37 degrees C for 2 h) to simulate stomach acidity. The results showed no significant reversion of aflatoxin (reversibility less than 0.05%). These findings suggest that at high temperature aqueous NH4OH or gaseous NH3 can be used effectively to reduce AFB1 in corn. The present study also revealed that the moisture level of the product and holding temperature were the crucial factors that influenced the efficacy of aflatoxin decontamination by ammoniation.

Aflatoxins↗