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Biomedical subjects

F Berglund

Publications and source records attributed to F Berglund.

At least 37 records · Page 2Linked to original sources

Food additives.

The use of additives to food fulfils many purposes, as shown by the index issued by the Codex Committee on Food Additives: Acids, bases and salts; Preservatives, Antioxidants and antioxidant synergists; Anticaking agents; Colours; Emulfifiers; Thickening agents; Flour-treatment agents; Extraction solvents; Carrier solvents; Flavours (synthetic); Flavour enhancers; Non-nutritive sweeteners; Processing aids; Enzyme preparations. Many additives occur naturally in foods, but this does not exclude toxicity at higher levels. Some food additives are nutrients, or even essential nutritents, e.g. NaCl. Examples are known of food additives causing toxicity in man even when used according to regulations, e.g. cobalt in beer. In other instances, poisoning has been due to carry-over, e.g. by nitrate in cheese whey - when used for artificial feed for infants. Poisonings also occur as the result of the permitted substance being added at too high levels, by accident or carelessness, e.g. nitrite in fish. Finally, there are examples of hypersensitivity to food additives, e.g. to tartrazine and other food colours. The toxicological evaluation, based on animal feeding studies, may be complicated by impurities, e.g. orthotoluene-sulfonamide in saccharin; by transformation or disappearance of the additive in food processing in storage, e.g. bisulfite in raisins; by reaction products with food constituents, e.g. formation of ethylurethane from diethyl pyrocarbonate; by metabolic transformation products, e.g. formation in the gut of cyclohexylamine from cyclamate. Metabolic end products may differ in experimental animals and in man: guanylic acid and inosinic acid are metabolized to allantoin in the rat but to uric acid in man. The magnitude of the safety margin in man of the Acceptable Daily Intake (ADI) is not identical to the "safety factor" used when calculating the ADI. The symptoms of Chinese Restaurant Syndrome, although not hazardous, furthermore illustrate that the whole ADI cannot always be ingested as a single dose on an empty stomach with impunity.

Animals↗

Effect of trimethoprim-sulfamethoxazole on the renal excretion of creatinine in man.

Treatment with the chemotherapeutic combination of 160 mg. trimethoprim plus 800 mg. sulfamethoxazole twice daily increased the serum creatinine level by an average of 2 mg. per 1. in 21 patients. The effect was clearly reversible. The chemical analysis of creatinine was not affected by the addition of trimethoprim, sulfamethoxazole or their metabolites. In 2 subjects given the drug combination for 12 days renal excretion and 24-hour clearances of creatinine decreased but iothalamate 131I clearance was unchanged. Consequently, the rise in serum creatinine does not indicate any decrease in the glomerular filtration rate. The serum creatinine started to rise within 4 hours after oral administration of a single dose. The rise in serum creatinine could be produced with trimethoprim alone but not with sulfamethoxazole alone. When the plasma creatinine was raised to 100 mg. per l. in healthy subjects (by giving creatinine orally), trimethoprim increased the creatinine levels 10 times as much as at normal plasma levels. The effect was interpreted as a competitive inhibition of the mechanism for tubular secretion of creatinine through the base-secreting pathway.

Creatinine↗

Electrocardiogram and renal concentrating capacity in rats fed a diet containing rapeseed oil.

The functional effects of a diet containing rapeseed oil (40% of total energy intake) were studied in rats, starting at age 28 days. There were no effects on the electrocardiogram in spite of morphological changes in the myocardium. In 10 female rats the urine osmolality following 16 hours of dehydration was approximately 20% lower than in 10 control rats during the 9th, 10th and 20th week of the experiment. It is suggested that erucic acid in the rapeseed oil inhibits beta-oxidation of fatty acids in the kidney, thereby depriving the kidney of energy involved in sodium transport.

Animals↗

Problems of toxicants in marine food products. 1. Marine biotoxins.

The expansion of marine fisheries into tropical waters, which is now occurring, will increase the risks of widespread poisonings because of the abundance of biotoxins in warm-water organisms. However, toxic marine organisms are not only a health hazard but also a possible source of new pharmaceutical products.A classification of marine intoxicants is given in this paper with special reference to the oral biotoxins which will be of primary concern in the expansion of warm-water fisheries. The biotoxins are both invertebrate (e.g., molluscs, arthropods) and vertebrate (mostly fishes) in origin. Biotoxications of vertebrate origin may be caused by the muscles, the gonads or the blood of certain fishes or by special poison glands not equipped with traumagenic devices. (Venomous fishes, having poison glands and traumagenic spines, etc., are of no direct concern as oral intoxicants.)The ichthyosarcotoxic fishes, in which the flesh is poisonous, appear to constitute the most significant health hazard. A list of fishes reported as causing ciguatera poisoning (one of the most serious and widespread forms of ichthyosarcotoxism) is included in this paper.

Animals↗

Cyclamates.

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Carcinogens↗