Effects of selenite on metabolic events during the proliferation of canine mammary tumor cells

Increased cytoplasmic and nuclear selenium retention in CMT-13 cells was correlated with cell growth inhibition caused by selenite supplementation. Greater quantities of cytosolic selenium-containing proteins and a nuclear selenium-containing protein were detected as the quantity of selenium within CMT-13 cells increased. One of the antiproliferation effects of selenite on CMT-13 cells is accompanied by decreased rates of macromolecule synthesis, increased cellular macromolecule contents and increased cell size and multiple nuclei, indicating that enhanced cell fusion occurred. Selenite modulated the S and M phases during the cell cycle. Selenite increased the activity of the 114 KD protein kinase only during the S phase. Selenite treatment during the M phase resulted in a disappearance of a 53 KD kinase and the appearance of a 47 KD kinase. The cellular $\rm\sp{32}P$ incorporation into macromolecules increased when inhibition of cell growth was observed by supplementation of selenite. Selenite generally increased the phosphorylation of nuclear phosphoproteins in the S phase, especially the phosphorylation of a 46 KD protein. Selenite inhibited hyperphosphorylation of the 21, 62 and 108 KD proteins during the M phase. Results of this study suggest that perturbations in protein phosphorylation may explain the ability of selenite to alter cell proliferation.

Name thesis:degree_name

Ph.D.

Level thesis:degree_level

Dissertation

Discipline thesis:degree_discipline

Nutritional Sciences

Grantor

University of Illinois at Urbana-Champaign

Year dc:date

1994

Author dc:creator

• Hwang, Kyung Hee

Contributors dc:contributor

• Milner, J.A.

• Biology, Molecular
• Biology, Cell
• Agriculture, Animal Culture and Nutrition

Statement dc:rights

• Copyright 1994 Hwang, Kyung Hee

Language dc:language

eng

Identifier

AAI9503220
(UMI)AAI9503220

OAI identifier oai:identifier

oai:www.ideals.illinois.edu:2142/19090