Morphologic evidence that disruption of the Golgi apparatus in PFHR 9-tumor cells causes disturbance in the traffic through this organelle.

PFHR 9 is a murine teratocarcinoma-derived tumor which produces basement membrane components. Electron microscopy of the tumor cells disclosed a disorganization of the Golgi complex whose saccules, instead of being flattened, round up into 0.13 micron-wide spherical vesicles (SV). Their shape does not permit the normal stacking of parallel cisternae, and thus these SV become intermingled with transport vesicles (TV) which measure 44 nm in diameter. The cytoplasm of these tumor cells contains numerous multivesicular bodies (MVB) of varying size (ranging from 0.3 to 2.6 micron), which occupy 7% of the cellular volume. These MBV are packed with very many small vesicles similar in all aspects to the TV, and also contain a few larger vesicles which resemble the altered Golgi saccules (SV). Since these MVB display morphologic evidence for gradual lysis of their contents and strongly react with the cytochemical method for acid phosphatase, it is assumed that MVB are autophagic vacuoles which result from the accumulation of TV. This seems to be a unique example of a disease of the Golgi stack, with consequent accumulation and disposal of this material via autophagic vacuoles.

Effects of sodium and calcium concentration on the barium chloride-induced electrical and contractile responses of the guinea pig vas deferens.

1. The mechanism of 10 mM barium chloride-induced electrical and contractile responses of the guinea pig vas deferens was investigated using calcium channel blockers and by modifying the Na+ and Ca2+ concentrations of the nutritional solution. Isometric contraction and membrane depolarization were measured simultaneously by the sucrose-gap technique. 2. In the absence of added Ca2+ there was a decay of the contractile but not of the depolarizing effect, which was independent of the frequency of 10 mM barium chloride administration. However, both barium-induced contraction and depolarization were reduced and the former more rapidly in a Ca2+-free solution (0.5 mM EGTA). 3. In low-Na+ solution (16 mM) there was a 3-fold increase in depolarization and no change in contraction, but in a low-Na+ Ca2+-free solution (0.5 mM EGTA), only contraction was reduced. 4. Nifedipine blocked both barium-induced contraction and depolarization in a dose-dependent manner when the organs were bathed in regular nutrient solution. In contrast, in low-Na+ solution only 50% of the depolarization was blocked by 10(-6) M nifedipine, which completely inhibited contraction. Both barium-induced contraction and depolarization in low-Na+ Ca2+-free solution were blocked by 10(-3) M LaCl3. 5. These data indicate that in the presence of calcium, barium mobilizes extracellular calcium through voltage-dependent channels and the contraction is due to the entry of calcium. In contrast, in the absence of added Ca2+ or in Ca2+-free solutions (0.5 mM EGTA), barium enters through the voltage-dependent channel and the contraction is reduced because the intracellular stores of calcium are limited.