Cadmium induced-oxidative stress in pituitary gland is reversed by removing the contamination source

Hum Exp Toxicol. 2010 Oct;29(10):873-80. doi: 10.1177/0960327110362703. Epub 2010 Mar 2.

Abstract

Cadmium (Cd(2+)) is one of the most important environmental contaminants and acts as an endocrine disruptor. Previously, we have demonstrated that the simultaneous administration of Cd(2+) and melatonin (Mel) in drinking water impaired metal-induced oxidative stress in rat anterior pituitary gland. The aim of this study was to investigate if a treatment started after the toxic manifestations of Cd( 2+) became evident could reverse the effects of the metal. Animals exposed to Cd(2+) (5 parts per million [ppm], 30 days) were treated with Mel or without the metal during the next 1 or 2 months. Cd(2+) exposure increased the expression of heme oxygenase-1 (HO-1), a biomarker of oxidative stress, and an a posteriori Mel treatment reversed oxidative stress induced by Cd(2+). This effect was also observed 1 month after metal removal. The Cd(2+)-induced increase in metallothionein-1 (MT-1) and nitric oxide synthase 1 (NOS1) expression were also reversed by metal removal. In addition, serum prolactin and luteinizing hormone levels affected by Cd( 2+) exposure were normalized. Considering that the manifestations of Cd(2+) intoxication become evident only after a certain period of metal accumulation, these results show that metal removal is enough to reverse Cd(2+) effects in anterior pituitary gland and bring to light the relevance of moving away the individual from the contamination source.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers / metabolism
  • Cadmium Chloride / toxicity*
  • Environmental Pollutants / toxicity*
  • Gene Expression / drug effects
  • Heme Oxygenase (Decyclizing) / genetics
  • Heme Oxygenase (Decyclizing) / metabolism
  • Luteinizing Hormone / blood
  • Male
  • Melatonin / pharmacology*
  • Metallothionein / genetics
  • Metallothionein / metabolism
  • Nitric Oxide Synthase / genetics
  • Nitric Oxide Synthase / metabolism
  • Nitric Oxide Synthase Type I
  • Oxidative Stress / drug effects*
  • Pituitary Gland, Anterior / drug effects*
  • Prolactin / blood
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Recovery of Function / drug effects*

Substances

  • Biomarkers
  • Environmental Pollutants
  • Mt2A protein, rat
  • RNA, Messenger
  • Prolactin
  • Luteinizing Hormone
  • Metallothionein
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type I
  • Nos1 protein, rat
  • Heme Oxygenase (Decyclizing)
  • Hmox1 protein, rat
  • Cadmium Chloride
  • Melatonin