Document VGvyY0YQvqL6Nj9qRKR857GpZ

Industrial Hygiene Digest June, 1957 735 Tolerance for Residues of Ethylene Oxide. Anon. Federal Register 2, 931 (Feb. 14, 1957). A tolerance o( 50 ppm U established lor residues ol ethylene oxide in or on whole spices, under the Federal Food, Drug, and Cosmetic Act. -- Chem. Absts. 736 Toxic Liver Injury, The Metabolism ot Dimcthylnitroso Amine. F. N. Magee. Biochem. J. o4, 677-68Z (1956). The metabolism, distribution in the body, and excretion of dlmethylnltroso amine were studied alter its administration to rats, mice, and rabbits. It has been shown previously that this compound is a selective liver poison in these species, and that it can produce malig nant primary liver tumors in the rat. The evidence suggests that dlmethylnltroso amine is rapidly metabolised, and that the liver is the main, probably the only organ concerned. The compound is distributed uniformly in most tissues ot the body, and there is reason to believe that it penetrates into the intracellular space. There is no selective concentration in the liver. SKF 52SA (2 -dlethyUminoethyl dlphenylpropylacetate hydrochloride) inhibits the metabolism ot dlmethylnltroso amine in the mouse, but only when given in large doses. The tlndtngs are dis cussed in relation to the pathogenesis ot the acute liver necrosis caused by dlmethylnltroso amine. -- Chem. Absts. 737 Acute Changes In the Liver atter Administration of Thioaeetamlde. D. N. Gupta. J. Pathol. Bacteriol. 72, 163-192 (195h). Thioaeetamlde produces consistent liver necrosis after 24 hours in rats when a dose of 200 mg. per kg. or more is given by various routes. The first change apparent after six hours is the loss of glycogen and of basophilic bodies in the centrolobulax liver cells. The central veins and the adjacent sinusoids dilate and edema channels appear which connect the central veins with each other. Necrosis develops in the.centroLobular cells and spreads along the edema channels; by 24 hours it is well established. In 42-48 hours, the necrotic liver cells were cleared away by mononuclear cells which move Into the necrotic none at about 12 hours. Regeneration extends from the periportal none and healing Is com plete after a week. The histological sequence of events to acute thioacetamide intoxication is non-specific, since it resembles that of many other liver injuries. The centrolobular necrosis is probably due to a number of factors. -- Author's summary (Biol. Absts,) 738 Biochemical Changes tn Liver in Acute Thioacetamide Intoxication. C. H. Gallagher. D. N. Gupta, J. D. Judah, and K. R. Rees. J. Pathol Bacteriol. 72, 193-201 (1956). The observed inhibitions in enzyme systems in liver are due to the accumulation . of calcium in the affected liver cell. Administration of antihistamines protects against the action of thioacetamide. Adrenalectomy did hot protect against thioacetamide Intoxication. The evidence so far obtained suggests that the primary lesion in the liver call is a loss of the semi-permeable properties of the cell wall with the entry of calcium ions. It is likely that the loss of this semi-permeable property Is due to a direct attack on the cell wall rather than to a secondary effect resulting from a failure of the metabolic activity of the cell. Authors' summary (BioL Absts.) 739 Tolerance for Residues of Sodium 2, 2-Dlchloropropiouate^ Anon. Federal Register li, 637 (jau. 31, 1957). A tolerance is established under the Federal Food, Drug, and Cosmetic Act tor residues of sodium 2, 2-dichloropropionate as 2, 2-dlchloroproplonlc acid of 35 ppm In or on cottonseed oil and 5 ppm in or on sugar beets and sugar-beet tops. -- Chem. Absts. 11 206 1038 11.