Proliferation and apoptosis of human placental cells exposed to aromatic hydrocarbons

Ginekol Pol. 2017;88(12):686-691. doi: 10.5603/GP.a2017.0122.

Abstract

Objectives: The objective of this study is to assess the effect of elevated urinary levels of aromatic hydrocarbons (AH) on the proliferation and apoptosis of human placental trophoblast cells obtained in the course of normal pregnancy in an AH-polluted region.

Material and methods: Tissue material was obtained for study purposes from 50 afterbirths from Płock as the study group and 50 afterbirths from Kutno as the control group. The extent and intensity of reactions were analyzed. The levels of phenol and 1-hydroxypyrene in the excreted urine of pregnant (in labor) patients were determined by gas chromatography and colorimetry. The proliferative activity of trophoblast cells was assessed using MPM-2 antibodies against phosphoprotein synthesized upon mitotic induction and Ki-67 antigen while the intensity of apoptosis in trophoblast cells was assessed using p53 and bcl-2 oncoproteins involved in apoptosis-regulating mechanisms. The immunohistochemical reactions were assessed for their extent and intensity.

Results: The levels of phenol and 1-hydroxypyrene excreted in the urine were statistically significantly higher in patients from Płock region. The proliferative activity of trophoblast cells was statistically significantly higher in the study group (p < 0.05). The activity of oncoprotein bcl-2 was significantly higher in the study group while the activity of p53 was sig¬nificantly higher in the control group. Pregnancy in an aromatic hydrocarbon-polluted environment has a significantly negative impact on placental tissue. Ad¬aptation mechanisms are induced as manifested by increased proliferative activity within the trophoblast and extensive inhibition of apoptosis in the study group.

Keywords: 1-hydroxypiren; aromatic hydrocarbons; human placenta; phenol.

MeSH terms

  • Air Pollutants / toxicity
  • Apoptosis / drug effects*
  • Cell Proliferation / drug effects*
  • Environmental Exposure*
  • Female
  • Humans
  • Ki-67 Antigen / metabolism
  • Kinesins / metabolism
  • Phenol / toxicity*
  • Phenol / urine
  • Placenta / drug effects
  • Placenta / metabolism*
  • Pregnancy
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Pyrenes / toxicity*
  • Pyrenes / urine
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Air Pollutants
  • BCL2 protein, human
  • Ki-67 Antigen
  • Proto-Oncogene Proteins c-bcl-2
  • Pyrenes
  • Tumor Suppressor Protein p53
  • Phenol
  • KIF20B protein, human
  • Kinesins
  • 1-hydroxypyrene