Effects of Zinc and N-Acetylcysteine in Damage Caused by Lead Exposure in Young Rats

Biol Trace Elem Res. 2017 Dec;180(2):275-284. doi: 10.1007/s12011-017-1009-z. Epub 2017 Apr 7.

Abstract

This study investigated the toxicity of rats exposed to lead acetate (AcPb) during the second phase of brain development (8-12 days postnatal) in hematological and cerebral parameters. Moreover, the preventive effect of zinc chloride (ZnCl2) and N-acetylcysteine (NAC) was investigated. Pups were injected subcutaneously with saline (0.9% NaCl solution), ZnCl2 (27 mg/kg/day), NAC (5 mg/kg/day) or ZnCl2 plus NAC for 5 days (3rd-7th postnatal days), and with saline (0.9% NaCl solution) or AcPb (7 mg/kg/day) in the five subsequent days (8th-12th postnatal days). Animals were sacrificed 21 days after the last AcPb exposure. Pups exposed to AcPb presented inhibition of blood porphobilinogen-synthase (PBG-synthase) activity without changes in hemoglobin content. ZnCl2 pre-exposure partially prevented PBG-synthase inhibition. Regarding neurotoxicity biomarkers, animals exposed to AcPb presented a decrease in cerebrum acetylcholinesterase (AChE) activity and an increase in Pb accumulation in blood and cerebrum. These changes were prevented by pre-treatment with ZnCl2, NAC, and ZnCl2 plus NAC. AcPb exposure caused no alteration in behavioral tasks. In short, results show that AcPb inhibited the activity of two important enzymatic biomarkers up to 21 days after the end of the exposure. Moreover, ZnCl2 and NAC prevented the alterations induced by AcPb.

Keywords: AChE; Cerebral; Hematological; Lead; NAC; PBG-synthase; Pups; Zinc.

Publication types

  • Comparative Study

MeSH terms

  • Acetylcholinesterase / metabolism
  • Acetylcysteine / administration & dosage
  • Acetylcysteine / therapeutic use*
  • Animals
  • Animals, Newborn
  • Biomarkers / blood
  • Biomarkers / metabolism
  • Blood-Brain Barrier / drug effects
  • Blood-Brain Barrier / metabolism
  • Cerebrum / drug effects*
  • Cerebrum / enzymology
  • Cerebrum / metabolism
  • Chlorides / administration & dosage
  • Chlorides / metabolism
  • Chlorides / pharmacokinetics
  • Chlorides / therapeutic use*
  • Drug Therapy, Combination
  • Environmental Pollutants / blood
  • Environmental Pollutants / metabolism
  • Environmental Pollutants / toxicity
  • GPI-Linked Proteins / antagonists & inhibitors
  • GPI-Linked Proteins / metabolism
  • Injections, Subcutaneous
  • Lead / blood
  • Lead / metabolism
  • Lead / toxicity
  • Lead Poisoning, Nervous System / blood
  • Lead Poisoning, Nervous System / metabolism
  • Lead Poisoning, Nervous System / prevention & control*
  • Nerve Tissue Proteins / antagonists & inhibitors
  • Nerve Tissue Proteins / metabolism
  • Neurons / drug effects*
  • Neurons / enzymology
  • Neurons / metabolism
  • Neuroprotective Agents / administration & dosage
  • Neuroprotective Agents / metabolism
  • Neuroprotective Agents / pharmacokinetics
  • Neuroprotective Agents / therapeutic use*
  • Organometallic Compounds / administration & dosage
  • Porphobilinogen Synthase / antagonists & inhibitors
  • Porphobilinogen Synthase / blood
  • Random Allocation
  • Rats, Wistar
  • Tissue Distribution / drug effects
  • Toxicokinetics
  • Zinc Compounds / administration & dosage
  • Zinc Compounds / metabolism
  • Zinc Compounds / pharmacokinetics
  • Zinc Compounds / therapeutic use*

Substances

  • Biomarkers
  • Chlorides
  • Environmental Pollutants
  • GPI-Linked Proteins
  • Nerve Tissue Proteins
  • Neuroprotective Agents
  • Organometallic Compounds
  • Zinc Compounds
  • Lead
  • zinc chloride
  • Acetylcholinesterase
  • Ache protein, rat
  • Porphobilinogen Synthase
  • lead acetate
  • Acetylcysteine