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Biomedical subjects

R S Applebaum

Publications and source records attributed to R S Applebaum.

6 recordsLinked to original sources
PubMed2000

Criteria to determine food allergen priority.

The emergent health issue of food allergens presents an important challenge to the food industry. More than 170 foods have been reported in the scientific literature as causing allergic reactions. Clearly, it would be impossible to deal with the presence of trace amounts of all these in the context of food labeling. If the decision to classify major allergens is based solely on the knowledge and experience of allergists and food scientists in the field, without scientifically defined criteria, it is likely to lead to a proliferation of lists. Such practices may lead to an unnecessary elimination of foods containing important nutrients. This paper defines food allergy, food intolerance, and food anaphylaxis and identifies criteria for classifying food allergens associated with frequent allergic reactions. A practical list of food allergens that may result in potentially life-threatening allergic reactions is provided. A mechanism-based (i.e., immunoglobulin E mediated), acute life-threatening anaphylaxis that is standardized and measurable and reflects the severity of health risk is proposed as the principal inclusion criterion for food allergen labeling. Where available, prevalence in the population and threshold levels of allergens should be used as an additional guide to identify possible future labeling needs.

Allergens↗
PubMed1986

Evaluation of the teratogenic potential of cocoa powder and theobromine in New Zealand White rabbits.

Studies were conducted to determine the teratogenic potential of theobromine (TBR) and cocoa powder (CP) in rabbits. TBR was given either by gavage at dose levels of 0, 25, 75, 125 or 200 mg/kg body weight/day or administered in the diet at 0, 0.0625, 0.125 or 0.1875% (approximately 0, 21, 41 or 63 mg/kg/day, respectively). CP was given at 2.5, 5.0 or 7.5% of the diet (approximately 25, 50 or 75 mg methylxanthines/kg body weight/day). The duration of exposure was from days 6 to 29 of gestation. Significant maternal mortality (40%) and reduced food consumption were observed at 200 mg TBR/kg/day. Mean foetal weights were similar to those of the control group at 25 or 75 mg TBR/kg/day, but decreases in foetal body weight and increases in various malformations and developmental variations were observed in groups given 125 or 200 mg/kg/day. Insufficient litters were available for examination in the 200-mg/kg/day dose group because of maternal toxicity/lethality (repetitive exposure by gavage to 200 mg TBR/kg approached the maternal LD50). In the dietary CP studies, three does died and three aborted, but these deaths and abortions were not treatment related. No maternal deaths occurred during dietary TBR exposure. Maternal weight gain and food consumption, and the mean number of corpora lutea were unaffected by either dietary CP or TBR. Neither foetotoxicity nor teratogenicity was associated with dietary ingestion of CP or TBR. The foetuses exposed to 0.125% or 0.1875% TBR had a significantly higher incidence of incompletely ossified or absent sternebrae, whereas exposure to 0.1875% or 7.5% CP resulted in corresponding effects on metacarpal bones, indicating a delay in osteogenesis. The predominant compound found in serum after TBR ingestion was unchanged TBR, and there was no evidence of bioaccumulation of TBR in serum during gestation. The highest levels of CP or TBR used in these studies was 38 times greater than the maximum consumption level reported for humans in marketing surveys, and corresponds to a consumption of greater than 7.5 lb milk chocolate/day.

Abnormalities, Drug-Induced↗
PubMed1986

Evaluation of the perinatal, postnatal and teratogenic effects of cocoa powder and theobromine in Sprague-Dawley/CD rats.

Studies were conducted to evaluate the effects of cocoa powder (CP) and theobromine (TBR) on perinatal and postnatal parameters and to assess their potential teratogenicity in the rat. In the peri/postnatal study, CP was given at 0, 2.5, 5.0 or 7.5% in the diet throughout gestation and lactation (postnatal day 21). In the teratology study, rats were given diets containing 0, 2.5 or 5.0% CP or 0.0675 or 0.135% TBR on days 6-19 of gestation. The CP-treated dams in the peri/postnatal study consumed significantly more food than did the controls during gestation. Weight gain was increased only in the 5.0 and 7.5% CP groups during lactation. Litter size was reduced slightly at 7.5% CP and pup survival was slightly decreased at 5.0 and 7.5% CP but none of these reductions was statistically significant. However, small but statistically significant decreases in pup body weights were noted in all treatment groups throughout lactation. In the teratology studies, rats given 2.5 or 5.0% CP or 0.0675 or 0.135% TBR consumed significantly more food than did the controls and the CP-treated dams gained significantly more weight. The percentage of pregnant dams and the mean number of corpora lutea were not affected by either CP or TBR. Foetuses exposed to 0.135 TBR had a significantly higher incidence of incompletely ossified or absent sternebrae and pubic bones, indicating a delay in osteogenesis. On the basis of the survival of treated offspring in the peri/postnatal study, these effects were not considered to be deleterious to either growth or survival. The effects are similar to those that have been reported elsewhere and been considered to indicate potential maternal or foetal toxicity that is unrelated to a specific compound/treatment. We conclude that any variations observed in these studies may be attributed to this non-specific maternal toxicity and are not related to the ingestion of either CP or TBR. The major methylxanthine found in the serum after CP or TBR ingestion was unchanged TBR and it did not bioaccumulate during gestation. The levels of CP and TBR used in these studies were more than 50 times greater than the maximum level of consumption by humans as reported in marketing surveys and were equivalent to a consumption of 10 lb of milk chocolate per day. The results indicate that neither CP nor TBR pose any health hazard to the developing foetus.

Abnormalities, Drug-Induced↗
PubMed1982

Responses of dairy cows to dietary aflatoxin: feed intake and yield, toxin content, and quality of milk of cows treated with pure and impure aflatoxin.

Ten fistulated Holstein cows in midlactation were given daily doses of 13 mg of aflatoxin B1 for 7 days. Six received pure aflatoxin B1; three received an impure preparation that contained aflatoxin B1 plus other aflatoxins and metabolites produced by Aspergillus parasiticus in culture. Toxin was administered to each animal twice daily, one-half of the total dose each time, via the rumen orifice. Morning and evening milks were collected and analyzed for aflatoxin M1. Milk production and feed intake were monitored for 5 days before, every day during, and for 8 days after treatment with aflatoxin B1. Milk contained from 1.05 ppb to 10.58 ppb of aflatoxin M1. None was in milk 4 days after administration of toxin had stopped. Somatic cell counts and standard plate counts from milks of two cows were not affected appreciably by administration of toxin. Fluctuations in feed intake and milk production occurred in all animals during the treatment period with a significant decrease in milk production of those cows receiving 13 mg of impure aflatoxin B1 per day. Differences in results when cows received equal amounts of aflatoxin B1 may be attributable to the type of toxin administered (pure versus impure).

Aflatoxin B1↗
PubMed1981

Biogenesis of the C20 polyketide, aflatoxin. A review.

Aflatoxin B2 is a secondary metabolite produced by the ubiquitous molds Aspergillus flavus and Aspergillus parasiticus. The toxin was first characterized in 1963 as the etiological agent responsible for the infamous "Turkey X' disease. Since that time, much information on its chemistry, toxicity and biological activity has accumulated. A significant amount of work has been done to elucidate its biosynthesis. Evidence indicates the polyketide route as its point of origin. The steps involved in the polyketide pathway, the six identified intermediated compounds, and the experimental techniques and analytical instrumentation used to procure information on aflatoxin biogenesis are included in this review.

Acetates↗