Exposure to xenobiotic compounds: looking for new biomarkers

Gen Comp Endocrinol. 2003 May;131(3):203-8. doi: 10.1016/s0016-6480(03)00105-9.

Abstract

A variety of antropogenic compounds that have an estrogenic effect, and are known to be present in the environment, shows a significant potential for interference with the health and reproduction of both wildlife and humans. In this review, the effect of estrogenic and antiestrogenic chemicals with widely divergent potencies-nonylphenol (NP), which acts by binding with the estradiol response element, and beta-naphthoflavone (beta-NF), a dioxin-like compound that exerts its toxic action through the aryl hydrocarbon receptor-was compared with that induced by 17beta-estradiol (E(2)) in a marine teleost, the Gobius niger, under controlled laboratory experiments. The capacity of these compounds to affect the levels of estrogen-regulated proteins such as cathepsin D (CAT D)-in humans, a protein associated with the development of breast cancer, and, in oviparous vertebrates, with reproductive success-was assessed. The results of this study showed that both the estradiol and the higher dose of NP induce CAT D gene expression and its associated activity. On the contrary, beta-NF treatments inhibited CAT D gene expression and, at lengthier exposure (96 h), its enzymatic activity. Based on these results, we suggest CAT D as a novel bioindicator of the presence of endocrine-disrupting substances in the environment. The other biomarker assessed in this study is the Heath Shock Protein 70 (HSP70); this protein protects cells against harmful conditions by binding and refolding damaged proteins. Interestingly, HSP70 was found to be affected by all the toxicant compounds employed in the study. The HSP70 gene expression was significantly increased by both NP concentrations and the exposure time of beta-NF, with the E(2) being the most potent inducer. These data indicate that HSP70 may provide a useful early warning biomarker for studies on the presence of exogenous pollutants in the environment.

Publication types

  • Review

MeSH terms

  • Animals
  • Biomarkers*
  • Cathepsin D / biosynthesis
  • Cloning, Molecular
  • Estrogen Antagonists / toxicity*
  • Estrogens, Non-Steroidal / toxicity*
  • Fishes
  • Gene Expression / drug effects
  • HSP70 Heat-Shock Proteins / biosynthesis
  • HSP70 Heat-Shock Proteins / genetics
  • Liver / drug effects
  • Liver / metabolism
  • Male
  • Xenobiotics / toxicity*

Substances

  • Biomarkers
  • Estrogen Antagonists
  • Estrogens, Non-Steroidal
  • HSP70 Heat-Shock Proteins
  • Xenobiotics
  • Cathepsin D