作者: K R Bridges
DOI: 10.1016/S0021-9258(18)47862-3
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摘要: Ascorbic acid retards ferritin degradation in K562 erythroleukemia cells leading to an increase the availability of cellular iron (Bridges, K. R., and Hoffman, E. (1986) J. Biol. Chem. 261, 14273-14277). To explore mechanism this effect, influence ascorbate on subcellular distribution was examined. Cellular pulse-labeled with 59Fe for 2 h, after which were hypotonically lysed fractionated 8% Percoll density gradient. Immediately labeling, all cytoplasmic fractions at top When labeling followed by a 24-h period growth, portion shifted lysosome-associated bottom gradient, consistent lysosomal autophagy ferritin. added culture medium during incubation, magnitude shift reduced. This process also examined size-fractionation contents labeled using Sepharose CL-6B column. emerged from column two peaks, indicating existence both monomer aggregates within cytoplasm. After peak disappeared, while new coincident lysosomes again, indicative In cultured 24-h, there marked attenuation fractions. The as controls, but instead, accumulation aggregates. total content ascorbate-treated increased 4-fold over that control. These experiments indicate blocks reducing protein. access cell potentially toxic stored molecule is thereby increased.