Saccharin Metabolism in Macaca mulatta

Pitkin, Roy M.; Dw, Andersen; Reynolds, W. Ann; Lj, Filer

doi:10.3181/00379727-137-35671

Cited by 20 publications

(7 citation statements)

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“…Saccharin is not metabolized to any significant extent (67)(68)(69)(70)(71), if at all (72-76); it is nucleophilic (64) and does not bind to rat liver or bladder DNA (77), but it does suppress primary humoral antibody production in the rat (78). At dosages of 5% and above, several pharmacokinetic changes are also induced in the rat (79).…”

Section: Discussionmentioning

confidence: 94%

Two-Generation Saccharin Bioassays

Arnold¹

1983

Environmental Health Perspectives

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Section: Discussionmentioning

confidence: 94%

Two-Generation Saccharin Bioassays

Arnold¹

1983

Environmental Health Perspectives

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“…Most evidence suggests that saccharin is hardly metabolized in the rat or monkey (Pitkin et al, 1971;Kennedy et al, 1972;Matthews et al, 1973;Lethco & Wallace, 1975) and not at all in man (Byard et al, 1974;Golberg, 1974 (Kennedy et al, 1976). Nevertheless, saccharin is not entirely biologically inert; it is, for example, the most effective inhibitor, among a variety of structural analogues tested, of phosphotransferase and phosphohydrolase activities of glucose-6-phosphatase (Lygre, 1974).…”

Section: Discussionmentioning

confidence: 99%

Response of the rat to saccharin with particular reference to the urinary bladder

Chowaniec¹,

Hicks²

1979

Br J Cancer

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Summary.-Male and female Wistar rats were administered sodium saccharin for life (2 yr) either in the drinking water or diet. The maximum palatable dose of saccharin in the drinking water was found to be 2 g/kg/day and, even then, there was some voluntary restriction of fluid intake in the males. By contrast, double this dose -namely 4 g/kg/day, was palatable in the diet. A control group of rats of both sexes received saccharin-free diet and drinking water. Mild urothelial hyperplasias developed from 85 weeks in rats of both sexes receiving saccharin either in the drinking water or diet; the incidence was statistically significant in both the bladders and kidneys of rats receiving the higher dose of saccharin in the diet, but in the kidneys only of rats receiving the lower dose of saccharin in the drinking water. Telangiectasia of the vasa recta was significant in saccharin-treated rats of both sexes at both doses. A very low incidence of bladder tumours, exclusively in males receiving the higher saccharin dose in the diet was seen from 95 weeks. No consistent relationship between bladder epithelial hyperplasias and crystalluria could be demonstrated, although all 3 bladder tumours were associated with some form of mineralisation. Results suggest a particular susceptibility of males to saccharin treatment. The possibility that saccharin may promote, or enhance, the development of latent tumour cells already present in the experimental population, rather than initiate carcinogenesis per se is considered.

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“…Saccharin is not metabolized to any significant extent (67)(68)(69)(70)(71), if at all (72)(73)(74)(75)(76); it is nucleophilic (64) and does not bind to rat liver or bladder DNA (77), but it does suppress primary humoral antibody production in the rat (78). At dosages of 5% and above, several pharmacokinetic changes are also induced in the rat (79).…”

Section: Discussionmentioning

confidence: 99%

Two-generation saccharin bioassays.

Arnold¹

1983

Environ Health Perspect

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The controversy regarding the safety of saccharin for human consumption started shortly after its discovery over 100 years ago and has yet to subside appreciably. The consumption of saccharin, particularly in North America, began to escalate when the U.S. Food and Drug Administration set new standards of identity which allowed foods containing artificial sweeteners to be promoted as "nonnutritive" or "noncaloric" sweeteners for use by the general public. In 1969, when cyclamates were banned, at least 10 single-generation feeding studies were undertaken with saccharin to more accurately assess the potential toxicological consequences resulting from the anticipated increase in its consumption. None of these studies resulted in any overt regulatory action. Subsequently, the introduction of the two-generation chronic toxicity/carcinogenicity bioassay added a new tool to the toxicologist's arsenal. Three two-generation studies using saccharin have since been conducted. The results from these studies clearly show that when rats were exposed to diets containing 5 or 7.5% sodium saccharin from the time of conception to death, an increased frequency of urinary bladder cancers was found, predominantly in the males. While some study results suggested that impurities in commercial saccharin or the presence of urinary tract calculi may have been responsible for the observed bladder tumors, it now appears that these possibilities are highly unlikely. The mechanism by which saccharin elicited the bladder tumors using the two-generation experiment has not been ascertained.

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Saccharin Metabolism in Macaca mulatta

Cited by 20 publications

References 0 publications

Two-Generation Saccharin Bioassays

Two-Generation Saccharin Bioassays

Response of the rat to saccharin with particular reference to the urinary bladder

Two-generation saccharin bioassays.

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