Deoxycholate, an Endogenous Cytotoxin/Genotoxin, Induces the Autophagic Stress-Survival Pathway: Implications for Colon Carcinogenesis
Figure 1
Transmission electron micrographs of control NCM-460 colonic
epithelial cells (a) and cells treated with 0.4 mM DOC for 1 (b), 2 (c), and 3 (d)
hours. Note the increase in number and size of autophagolysosomes after DOC
treatment. (a) Arrow indicates the presence of small, electron-dense lysosomes;
X4,400); (b) arrow indicates a large autophagolysosome with adjacent smaller
autophagolysosomes in the process of fusing with the larger autophagolysosome
(X7,100); (c) a large number of autophagic vacuoles containing cellular debris in
various stages of degradation are present (X7,100); (d) arrow indicates the
presence of a mitochondrion (M) within an autophagic vacuole (X15,000). (All cells were pretreated with protease inhibitors to retard the degradation
process within lysosomes (see Section 2); this allowed the
identification of cellular organelles that were difficult to observe in the absence of
the protease inhibitors.) (Uranyl acetate, lead citrate counterstains.)
