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[Heme oxygenase 1 expression in foundry workers].

P Mozzoni1, G De Palma, E Scotti

  • 1Universita di Parma, Dipartimento di Clinica Medica, Nefrologia e Scienze della Prevenzione, Parma. paola.mozzoni@unipr.it

Giornale Italiano Di Medicina Del Lavoro Ed Ergonomia
|October 26, 2005
PubMed
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Foundry workers exposed to polycyclic aromatic hydrocarbons (PAHs) showed increased heme oxygenase 1 (HO-1) gene expression. This induction was linked to genetic variations in GSTP1, suggesting a role in oxidative stress response.

Area of Science:

  • Environmental Health
  • Occupational Medicine
  • Molecular Epidemiology

Background:

  • Heme oxygenase 1 (HO-1) is a key enzyme in oxidative stress response, catalyzing heme breakdown and exhibiting inducible expression.
  • Occupational exposure to polycyclic aromatic hydrocarbons (PAHs) is a concern in industrial settings like foundries, potentially inducing oxidative stress.
  • Metabolic gene polymorphisms, including those in CYP1A1, CYP1B1, GSTM1, GSTP1, and EPHX, may influence individual susceptibility to environmental toxicants.

Purpose of the Study:

  • To investigate the relationship between polycyclic aromatic hydrocarbon (PAH) exposure and heme oxygenase 1 (HO-1) gene expression in foundry workers.
  • To assess the role of specific metabolic gene polymorphisms (CYP1A1, CYP1B1, GSTM1, GSTP1, EPHX) in modulating HO-1 gene expression in response to occupational exposure.
  • To determine if genetic variations, particularly in GSTP1, influence the correlation between PAH exposure markers and HO-1 induction.

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Main Methods:

  • Study population comprised 37 foundry workers.
  • Blood and urine samples collected at the beginning and end of work shifts, during two different seasons (February and June).
  • Urinary 1-hydroxypyrene (1-OHP) measured as a biomarker for PAH exposure.
  • HO-1 gene expression analyzed, with induction quantified by normalizing end-shift (ES) values to baseline (BS) values (HO-1 ES/BS).

Main Results:

  • HO-1 gene expression (HO-1 ES/BS) was significantly higher at the June sampling (T2) compared to February (T1).
  • HO-1 gene induction correlated positively with urinary 1-OHP levels, particularly evident in the June samples and combined data.
  • Subjects with at least one variant allele for GSTP1 exhibited significantly higher HO-1 induction compared to those with the wild-type GSTP1AA genotype.
  • A positive correlation between HO-1 expression and 1-OHP levels was observed exclusively in subjects with variant GSTP1 alleles.

Conclusions:

  • PAH exposure, indicated by urinary 1-OHP, is correlated with HO-1 gene induction in foundry workers.
  • The observed correlation between PAH exposure and HO-1 induction is significantly influenced by the presence of variant alleles in the GSTP1 gene.
  • Individuals with variant GSTP1 alleles may experience greater oxidative stress and consequently higher HO-1 expression at equivalent PAH exposure levels, potentially due to reduced detoxification capacity.