Summary
L1210 leukemic cells were treated with either vitamin A alcohol or neuraminidase. Ascites cells in vivo and cultures of an L1210 cell line in vitro were used. In untreated cells stained with ruthenium red, the glycoprotein surface coat appears as a thick, uninterrupted, electron-dense band. Positive colloidal iron staining results in deposition of particles in similar continuous fashion. No gaps were detected with both stains. After negative colloidal staining, no particle deposition was seen on the cell surface.
Treatment with vitamin A resulted in the following changes. Ruthenium red staining showed a thinner, discontinuous surface coat. Positive colloidal iron binding was markedly decreased, and particle deposition occurred in sparse clusters separated by extensive gaps. Negative colloidal particle binding was enhanced, with the appearance of patchy clusters separated by gaps.
These results indicate a loss of surface coat material, reduction in negative cell surface charge, and exposure of positive changes induced by vitamin A. The striking similarities between the effects of the vitamin and neuraminidase suggest that release of lysosomal neuraminidase by vitamin A may play a role in the surface changes. A direct effect of the vitamin on the cell coat cannot be disregarded.
Supported by USPHS Grants 1 P01 HD 06323, NICHD, and CA 08518 from the National Cancer Institute. Laboratory facilities are located at the Gerontology Research Center, Baltimore City Hospitals, Baltimore, Md. 21224.
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