ISSN:
0003-276X
Keywords:
Life and Medical Sciences
;
Cell & Developmental Biology
Source:
Wiley InterScience Backfile Collection 1832-2000
Topics:
Medicine
Notes:
Female mice of the Taconic Swiss stock were fed one of the three diets described below then injected subcutaneously with 0.035 cm3CCl4/100 gm body weight in a mineral oil solution. One group was fed an adequate commercial laboratory ration, then mice were killed 12, 24 and 48 hours after CCl4; another a cholinedeficient, high-fat, low-protein diet for 14 days, then injected with CCl4, and killed 12, 24 and 48 hours later; and another group, a choline-supplemented (2 gm choline chloride/100 gm diet), high-fat, low-protein diet for 14 days, then injected with CCl4 and killed 24 hours later.In the group fed the normal diet, the polyhalogen produced within 24 hours the expected centrolobular necrosis and glycogen depletion, involving one-third to one-half of the lobular areas. In fatty livers produced by feeding the choline-deficient diet, necrosis at 24 hours post injection was limited in a majority of instances to a zone one or two cells thick immediately surrounding the central vein. Despite this decreased necrosis in fatty livers centrolobular glycogen depletion still involved one-third to one-half of lobules and there was an infiltration of inflammatory cells immediately adjacent to the central vein. The hepatic necrosis at 12 and 48 hours paralleled that in the normal dietary group.Feeding of the choline-supplemented, high-fat, low-protein diet for two weeks produced an extremely limited parenchymal liposis. In such relatively non-fatty livers CCl4 produced hepatic necrosis comparable to that in mice receiving normal diets. The extent of protection from the necrogenic actions of CCl4 was clearly associated with extensive intracytoplasmic liposis of hepatic parenchyma.
Additional Material:
1 Tab.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1002/ar.1091650308
