作者: M. Salas , B. Tuchweber , K. Kovacs , B.D. Garg
DOI: 10.1016/S0005-8165(76)80146-1
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摘要: In rats, liver steatosis and necrosis were induced by cerous chloride (CeCl3) the evolution of these changes was examined. By electron microscopy, 17 hours after CeCl3 treatment, dilation, disorganization degranulation rough endoplasmic reticulum (RER) noted with an increase in number density lysosome-like bodies. addition, nuclear chromatin showed a marked focal density, membrane appeared to be interrupted. At 24 hours, RER markedly dilated degranulated, free ribosomes aggregated cytoplasm. The Golgi cisternae empty. There size lipid droplets, depletion glycogen. 48 massive proliferation smooth (SER) vesicles occurred. Large droplets scattered throughout cytoplasm, while mitochondria displayed mild changes. 8th day, returned normal; no abnormalities detected other cell organelles. Biochemically, total hepatic ATP levels fell significantly 12th hour, dropping minimum 48th hour. gradually depleted glycogen within first triglycerides increased rapidly, reaching peak at 96 hours. Exogenous administration adenine, (adenosine triphosphate), or tryptophan completely prevented CeCl3-induced mortality; fat accumulation decreased. Glucose, dl-methionine, choline had protective effect. It appears that defect hepatocellular lipoprotein synthesis and/or release may responsible for accumulation.