G2 restriction point within populations of hepatocytes and tongue keratinocytes in young, growing mice

The authors studied the effect of either extracts from liver (LE) or the malignant tumour ES2 (TE) or plasma from intact mice (PI) or tumour-bearing animals (PT) on the mitotic activity of the hepatocytes and tongue keratinocytes in young, growing C3H/s male mice (28+/-1 days old). Animals standardi...

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Bibliographic Details
Published in:Cell biology international 1998, Vol.22 (5), p.359-362
Main Authors: Errecalde, A L, García, A L, Inda, A M, Badrán, A F
Format: Article
Language:English
Subjects:
Aging - physiology
Animals
Cell Cycle - physiology
Cell Division
Colchicine
G2 Phase
Keratinocytes - cytology
Liver - cytology
Liver - growth & development
Liver - physiology
Male
Metaphase
Mice
Mice, Inbred C3H
Mitotic Index
Neoplasms, Experimental - pathology
Neoplasms, Experimental - physiopathology
Tongue - cytology
Tongue - growth & development
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Summary:The authors studied the effect of either extracts from liver (LE) or the malignant tumour ES2 (TE) or plasma from intact mice (PI) or tumour-bearing animals (PT) on the mitotic activity of the hepatocytes and tongue keratinocytes in young, growing C3H/s male mice (28+/-1 days old). Animals standardized for periodicity analysis were injected intraperitoneally with either TE, LE, PI, PT, or saline (S) at 16:00 h with 0.01 ml of sample/g of body weight and were then killed at (time of day/h post-injection) 20:00/04, 00:00/08, and 04:00/12. Colchicine (2 microg/g) was injected 4 h before death. Samples of the liver and tongue from each animal were processed for histology and assessment of mitotic index. The results were expressed as colchicine-arrested metaphases/1000 nuclei. The TE and LE stimulated the mitotic activity of hepatocytes and tongue keratinocytes. Taking into account the time elapsed between the injections and the measurements made in these light-dark synchronized animals, we conclude that the increase in mitotic index observed in those tissues stemmed from a reinitiation of cell-cycle traverse in a subpopulation of G2-arrested, noncycling cells.
ISSN:1065-6995
DOI:10.1006/cbir.1998.0264