Analyses for hormonal substances in food producing animals by Jack F Kay

By Jack F Kay

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In the study report there is insufficient information to evaluate whether an adequate number of cells was treated, there is no dose-response (significant increases were seen in cultures treated with 10À11, 10À10, 10À7 and 10À6 M 17b-oestradiol but not with 10À8 and 10À9 M) and there is no evidence that the protocol ensured the independence of the individual mutant colonies picked for assessing the mutation spectra. The mutation induction data appears to be based on separate experiments, combined into a single results table, making it impossible to determine the data obtained in each separate experiment and thus to see how the reported increases relate to control (or spontaneous) values.

The use of generally lower doses for the main study largely avoided these confounding problems and provided only sketchy evidence for any significant impact on reproductive development and function as a result of in utero or postnatal exposures to MGA, TBA or zeranol. e. the problem was present prior to initiation of treatment, as cryptorchidism is not uncommon in rabbits) or that the final stage of inguinal testicular descent had been compromised. The latter is well established to be an androgen-dependent process, but the very limited data available for testosterone concentrations show no indications of suppression.

Concurrent cytotoxicity data are not given, but assuming the concentrations are similar to those measured in the mutation assay, then an increase in aberrations was only seen at toxicity concentrations in excess of the internationally acceptable limits. Nearly all the damage was due to ‘‘chromosome pulverisation’’, an effect attributed by the authors to asynchronous division within multinucleate cells, and not therefore The Use of Hormomally Active Substances 25 due to clastogenicity. Aneuploidy and polyploidy were also induced.

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