Pub Date : 1981-01-01DOI: 10.1016/0015-6264(81)90352-7
J.L. Greger, M.A. Johnson
Male, weanling Sprague-Dawley rats were fed a diet containing 206 μg tin (as stannous chloride)/g feed for 21 days. The rats fed the test diet lost significantly more zinc in their faeces and retained significantly lower levels of zinc in their tibias and kidneys than rats fed the control diet (which contained 1 μg tin/g). The rats fed the tin-supplemented diet retained significantly higher levels of tin in their kidneys and tibias and significantly lower levels of copper in their kidneys than the control animals.
{"title":"Effect of dietary tin on zinc, copper and iron utilization by rats","authors":"J.L. Greger, M.A. Johnson","doi":"10.1016/0015-6264(81)90352-7","DOIUrl":"10.1016/0015-6264(81)90352-7","url":null,"abstract":"<div><p>Male, weanling Sprague-Dawley rats were fed a diet containing 206 μg tin (as stannous chloride)/g feed for 21 days. The rats fed the test diet lost significantly more zinc in their faeces and retained significantly lower levels of zinc in their tibias and kidneys than rats fed the control diet (which contained 1 μg tin/g). The rats fed the tin-supplemented diet retained significantly higher levels of tin in their kidneys and tibias and significantly lower levels of copper in their kidneys than the control animals.</p></div>","PeriodicalId":12197,"journal":{"name":"Food and cosmetics toxicology","volume":"19 ","pages":"Pages 163-166"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0015-6264(81)90352-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18299019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1981-01-01DOI: 10.1016/0015-6264(81)90334-5
{"title":"The cause of MBK neuropathy?","authors":"","doi":"10.1016/0015-6264(81)90334-5","DOIUrl":"https://doi.org/10.1016/0015-6264(81)90334-5","url":null,"abstract":"","PeriodicalId":12197,"journal":{"name":"Food and cosmetics toxicology","volume":"19 ","pages":"Page 133"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0015-6264(81)90334-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136778845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1981-01-01DOI: 10.1016/0015-6264(81)90367-9
{"title":"Immunopathology. Sixth international convocation on immunology","authors":"","doi":"10.1016/0015-6264(81)90367-9","DOIUrl":"https://doi.org/10.1016/0015-6264(81)90367-9","url":null,"abstract":"","PeriodicalId":12197,"journal":{"name":"Food and cosmetics toxicology","volume":"19 ","pages":"Pages 265-266"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0015-6264(81)90367-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136819158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1981-01-01DOI: 10.1016/0015-6264(81)90326-6
{"title":"Metabolism of aspartate and aspartame","authors":"","doi":"10.1016/0015-6264(81)90326-6","DOIUrl":"https://doi.org/10.1016/0015-6264(81)90326-6","url":null,"abstract":"","PeriodicalId":12197,"journal":{"name":"Food and cosmetics toxicology","volume":"19 ","pages":"Page 129"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0015-6264(81)90326-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136819165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1981-01-01DOI: 10.1016/0015-6264(81)90318-7
{"title":"Diagnostic Electron Microscopy of Tumours","authors":"","doi":"10.1016/0015-6264(81)90318-7","DOIUrl":"https://doi.org/10.1016/0015-6264(81)90318-7","url":null,"abstract":"","PeriodicalId":12197,"journal":{"name":"Food and cosmetics toxicology","volume":"19 ","pages":"Page 120"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0015-6264(81)90318-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136819290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1981-01-01DOI: 10.1016/0015-6264(81)90361-8
A.F. Gunnison, L. Dulak, G. Chiang, J. Zaccardi, T.J. Farruggella
Toxicity resulting from exposure to sulphite originating both endogenously and exogenously was investigated in normal rats and in rats made sulphite-oxidase-deficient by molybdenum deficiency abetted by administration of tungstate. The sulphite-oxidase-deficient rats were outwardly as healthy as controls and exhibited normal weight gain and maintenance over the 9-wk test period. The systemic sulphite exposures of normal and deficient rats resulting from various sulphite treatments could be compared by determining the concentrations of tissue S-sulphonate (RS-SO3−) metabolites formed. In general, relatively low intakes of exogenous sulphite (0–3·5 mmol/kg/day) by sulphite-oxidase-deficient rats produced systemic sulphite exposures equivalent to those produced by the ingestion by normal rats of highly sulphited diets (intakes of 13–25 mmol/kg/day). The advantages of the sulphite-oxidase-deficient rat compared to the normal rat as a model for human exposure are discussed. Using these two animal models, it was demonstrated that anaemia and thiamine deficiency, which have been produced previously in sulphite-feeding studies, result solely from the action of high concentrations of sulphite in the diet and/or gut and are not attributable to systemic sulphite exposure. Likewise, prothrombin time and erythrocyte concentrations of glutathione were not affected by high systemic sulphite concentrations in these experiments.
A incidence of mammary adenocarcinoma was observed in sulphite-oxidase-deficient rats, all in rats aged less than 5 months, compared to observed in age-matched rats with normal sulphite oxidase. Although this result was not statistically significant, the rarity of spontaneous tumours of this type among rats of this age suggests that these carcinomas may, in fact, have been treatment related. If indicated, further investigation will be undertaken to determine the role of sulphite-oxidase-deficiency, sulphite and/or tungstate, as well as other elements of the model, in the aetiology of these tumours.
{"title":"A sulphite-oxidase-deficient rat model: Subchronic toxicology","authors":"A.F. Gunnison, L. Dulak, G. Chiang, J. Zaccardi, T.J. Farruggella","doi":"10.1016/0015-6264(81)90361-8","DOIUrl":"10.1016/0015-6264(81)90361-8","url":null,"abstract":"<div><p>Toxicity resulting from exposure to sulphite originating both endogenously and exogenously was investigated in normal rats and in rats made sulphite-oxidase-deficient by molybdenum deficiency abetted by administration of tungstate. The sulphite-oxidase-deficient rats were outwardly as healthy as controls and exhibited normal weight gain and maintenance over the 9-wk test period. The systemic sulphite exposures of normal and deficient rats resulting from various sulphite treatments could be compared by determining the concentrations of tissue <em>S</em>-sulphonate (RS-SO<sub>3</sub><sup>−</sup>) metabolites formed. In general, relatively low intakes of exogenous sulphite (0–3·5 mmol/kg/day) by sulphite-oxidase-deficient rats produced systemic sulphite exposures equivalent to those produced by the ingestion by normal rats of highly sulphited diets (intakes of 13–25 mmol/kg/day). The advantages of the sulphite-oxidase-deficient rat compared to the normal rat as a model for human exposure are discussed. Using these two animal models, it was demonstrated that anaemia and thiamine deficiency, which have been produced previously in sulphite-feeding studies, result solely from the action of high concentrations of sulphite in the diet and/or gut and are not attributable to systemic sulphite exposure. Likewise, prothrombin time and erythrocyte concentrations of glutathione were not affected by high systemic sulphite concentrations in these experiments.</p><p>A <span><math><mtext>4</mtext><mtext>149</mtext></math></span> incidence of mammary adenocarcinoma was observed in sulphite-oxidase-deficient rats, all in rats aged less than 5 months, compared to <span><math><mtext>0</mtext><mtext>143</mtext></math></span> observed in age-matched rats with normal sulphite oxidase. Although this result was not statistically significant, the rarity of spontaneous tumours of this type among rats of this age suggests that these carcinomas may, in fact, have been treatment related. If indicated, further investigation will be undertaken to determine the role of sulphite-oxidase-deficiency, sulphite and/or tungstate, as well as other elements of the model, in the aetiology of these tumours.</p></div>","PeriodicalId":12197,"journal":{"name":"Food and cosmetics toxicology","volume":"19 ","pages":"Pages 221-232"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0015-6264(81)90361-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18299027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1981-01-01DOI: 10.1016/0015-6264(81)90501-0
D. Conning
{"title":"Twenty years of toxicology","authors":"D. Conning","doi":"10.1016/0015-6264(81)90501-0","DOIUrl":"https://doi.org/10.1016/0015-6264(81)90501-0","url":null,"abstract":"","PeriodicalId":12197,"journal":{"name":"Food and cosmetics toxicology","volume":"77 1","pages":"529-530"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73811518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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