Literature DB >> 4002234

A 13-week feeding study of butylated hydroxyanisole: the subsequent regression of the induced lesions in male Fischer 344 rat forestomach epithelium.

F Iverson, E Lok, E Nera, K Karpinski, D B Clayson.   

Abstract

Feeding butylated hydroxyanisole (BHA) to male Fischer 344 rats at concentrations of 2, 0.5, 0.25, 0.1 and 0% for 13 weeks led to proliferative lesions developing in the forestomach epithelium of the 2%-treated rats but not in other groups. The [methyl-3H]thymidine labelling index was raised in the 2%- and 0.5%-treated groups and showed an apparent no observable effect level at 0.25%. Within 1 week after withdrawal of BHA the labelling indexes in all treated groups returned to near the values in the controls. The induced mucosal lesions, however, reverted more slowly and even after 9 weeks on the basal diet, the stratified squamous epithelium along the lesser curvature, was still slightly thicker than the control. There were multilayered basal cell processes in the lamina propria with connections to the basal cell layer. The possible significance of these results to the ultimate development of cancer is discussed.

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Year:  1985        PMID: 4002234     DOI: 10.1016/0300-483x(85)90127-1

Source DB:  PubMed          Journal:  Toxicology        ISSN: 0300-483X            Impact factor:   4.221


  4 in total

1.  Types and amounts of carcinogens as potential human cancer hazards.

Authors:  J H Weisburger; G M Williams
Journal:  Cell Biol Toxicol       Date:  1989-12       Impact factor: 6.691

Review 2.  Needs for biological risk assessment in interspecies extrapolation.

Authors:  D B Clayson
Journal:  Environ Health Perspect       Date:  1988-04       Impact factor: 9.031

3.  Comparison of reversibility of rat forestomach lesions induced by genotoxic and non-genotoxic carcinogens.

Authors:  M Kagawa; K Hakoi; A Yamamoto; M Futakuchi; M Hirose
Journal:  Jpn J Cancer Res       Date:  1993-11

4.  Reversibility of carcinogen-induced rat forestomach basal cell hyperplasia is due to squamous cell differentiation.

Authors:  K Ogawa; T Hoshiya; T Kato; T Shirai; M Tatematsu
Journal:  Jpn J Cancer Res       Date:  1992-07
  4 in total

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