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Sexual dimorphism in the regulation of cell turnover during liver hyperplasia.

Abstract
A sexual dimorphism occurs in liver cell proliferation following partial hepatectomy, female liver regenerating faster than male, while a continuous excess of choline to females shifts their growth pattern toward that of males (L. Tessitore, P. Pani and M.U. Dianzani, Carcinogenesis, 13 (1992) 1929). In this study we have investigated (a) if the same sexual modulation occurs in a different type of liver growth, hyperplasia induced by a direct mitogen and (b) if the pre-administration of choline to females is able to modulate this dimorphism. Liver hyperplasia induced by lead nitrate, a potent mitogen, has also shown a peculiar sexual dimorphism in all phases of the proliferative process. In contrast with liver regeneration after partial hepatectomy, the mitogenic action of lead nitrate was less effective and was delayed in females as compared with males, by evaluating liver weight, protein accumulation, DNA synthesis and mitotic index. These results were also confirmed by the trend of liver regression by apoptosis. The apoptotic index was higher in males than in females. A prolonged administration of an excess of choline has partially filled these sexual differences, since choline has moved, in females, all the observed parameters (liver weight, protein accumulation, DNA synthesis, mitotic and apoptotic indexes) to values closer to those observed in males.
AuthorsL Tessitore, E Sesca, P Pani, M U Dianzani
JournalChemico-biological interactions (Chem Biol Interact) Vol. 97 Issue 1 Pg. 1-10 (Jun 30 1995) ISSN: 0009-2797 [Print] Ireland
PMID7767937 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Nitrates
  • Proteins
  • Lead
  • lead nitrate
  • DNA
  • Choline
Topics
  • Animals
  • Apoptosis (drug effects)
  • Body Weight (drug effects)
  • Choline (metabolism)
  • DNA (biosynthesis)
  • Female
  • Lead
  • Liver Regeneration
  • Male
  • Mitosis (drug effects)
  • Nitrates
  • Proteins (metabolism)
  • Rats

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