Effect of tumour necrosis factor alpha on rat blastocyst growth and glucose metabolism

J Reprod Fertil. 1994 May;101(1):199-206. doi: 10.1530/jrf.0.1010199.

Abstract

Tumour necrosis factor alpha (TNF-alpha) synthesis has recently been described in the uterus during the preimplantation phase of pregnancy. The present study was undertaken to determine whether preimplantation embryos are a potential target for TNF-alpha in rats. First, the expression of TNF-alpha receptors by blastocysts was demonstrated by ligand binding assay with human 125I-labelled TNF-alpha and reverse transcription-amplification for the p60 receptor form. The functionality of these receptors was then assessed by incubating blastocysts with 3 nmol mouse TNF-alpha l-1 in vitro and determining their morphology and the number of cells after 24 h. At that concentration, cell proliferation in blastocysts was inhibited by TNF-alpha but this was not accompanied by any change in the morphology of the embryos. Similar results were obtained when lower doses of TNF-alpha (30 and 300 pmol l-1) were tested. The rate of glucose consumption of rat blastocysts exposed to 3 nmol TNF-alpha l-1 was not altered when they were incubated with the cytokine for 4 h, but the rate of glucose incorporation decreased over the same period. Our data indicate that rat blastocysts are responsive to physiological concentration of TNF-alpha and that this cytokine has the potential to influence the preimplantation development of rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blastocyst / chemistry
  • Blastocyst / metabolism
  • Blastocyst / physiology*
  • Cell Division / drug effects
  • Cells, Cultured
  • Embryonic and Fetal Development / drug effects*
  • Glucose / metabolism*
  • RNA, Messenger / analysis
  • Rats
  • Rats, Wistar
  • Receptors, Tumor Necrosis Factor / analysis
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • RNA, Messenger
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Glucose