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DOI:10.1080/15287397709529612 - Corpus ID: 8778877
@article{Garthoff1977BiochemicalAC, title={Biochemical and cytogenetic effects in rats caused by short-term ingestion of Aroclor 1254 or Firemaster BP6.}, author={Larry H. Garthoff and Leonard Friedman and Theodore M. Farber and K K Locke and Thomas Joseph Sobotka and Sidney Green and N E Hurley and Edmund L. Peters and G. E. Story and F. M. Moreland and Catherine H Graham and J. E. Keys and M. Joan Taylor and John V. Scalera and Joan Rothlein and E M Marks and F E Cerra and Stephen Rodi and E M Sp*rn}, journal={Journal of toxicology and environmental health}, year={1977}, volume={3 4}, pages={ 769-96 }, url={https://api.semanticscholar.org/CorpusID:8778877}}
- L. Garthoff, L. Friedman, E. Sp*rn
- Published in Journal of Toxicology and… 1 November 1977
- Biology, Environmental Science, Medicine
Some apparent differences in biochemical responses determined at sacrifice may have been partly due to the fact that, for the 3 wk study, rats were exposed to FM 48 hr longer than to ARO, and thus the comparison of ARO and FM toxiclties should be considered tentative.
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Kidney being the main excretory organ comes into direct contact of the toxicants present in the blood and thus shows high rate of toxicity related functional alterations, and Bruckner et al.
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A system for the long term culture of adult rat hepatocytes which for several weeks maintain differentiated functions, like fatty acid and TG synthesis and their export to the culture medium is described.
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The appearance of numerous, new proteins excreted by the PBB-dosed rats demonstrates the utility of 2DE for the sensitive detection of possible health effects from toxicant exposure.
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H hepatic mitochondria from ARO rats that experienced a significant loss of body weight were suppressed and more permeable to ions than AF and PF controls, which may have predisposed the ARO Rats toward urea formation rather than glucose synthesis and nitrogen retention.
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The acute toxicity of PBB in laboratory animals is low, but a variety of subacute effects have been reported, including induction of microsomal enzymes, enlargement and histopathological changes of the liver, fetotoxicity, and immunosuppression are among the more significant.
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Aroclor 1254 was found to potentiate the toxicity of carbon tetrachloride in the rat and residues were found in all tissues analyzed, with the greatest concentration in the fat.
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The BUN, serum proteins, liver ALA-synthetase and hematologic values were similar in all groups, and the livers in the 1254- and 1242-treated rabbits were significantly enlarged compared to the 1221-treated and control animals.
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Rats fed diets containing 0.1 percent of three polychlorinated biphenyls (PCBs) for six weeks show a progressive enlargement of the liver, attributed to proliferation of the smooth endoplasmic reticulum, development of large membranous concentric arrays, and increase in lipid droplets within the cytoplasm of the affected liver cells.
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An epoxy-resin paint has been used in the laboratory to coat galvanized batteries employed for trace mineral studies, but on one occasion the paint did not harden before chicks were placed in the battery and within 3 weeks the chicks showed symptoms closely resembling those of the “chick edema” or “toxic fat” syndrome.
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The effect of Aroclor 1254 on the liver was more pronounced than that of A RoClor 1260, and the epithelial component of adenofibrosis consisted of goblet cells and cells that resembled the epithelium which lines the bile ducts.
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