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Lead exposure induces metabolic reprogramming in rat models.

Monica Shirley Mani1, Manjunath B Joshi2, Rashmi R Shetty3

  • 1Department of Radiation Biology and Toxicology, Manipal School of Life Sciences, Manipal Academy of Higher Education, Manipal, Karnataka, India.

Toxicology Letters
|September 19, 2020
PubMed
Summary

High lead exposure in rats significantly alters metabolism, causing reduced body weight, impaired cognition, and changes in key metabolites linked to oxidative stress. This study provides a novel dose-dependent model for lead toxicity research.

Keywords:
BiomarkersBlood lead levelsExposureLeadMetabolismOxidative stressPathwayToxicity

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Area of Science:

  • Environmental Toxicology
  • Metabolomics
  • Neurotoxicology

Background:

  • Lead is a pervasive environmental toxin impacting public health across all age groups.
  • Individual susceptibility to lead toxicity varies due to genetic and metabolic factors.
  • Understanding dose-dependent effects is crucial for public health risk assessment.

Purpose of the Study:

  • To investigate the dose-dependent systemic metabolic changes induced by lead exposure in a rat model.
  • To identify specific biomarkers of lead toxicity through comprehensive metabolite profiling.
  • To elucidate the impact of lead on cognitive function and organ histopathology.

Main Methods:

  • Rats were administered low (10 mg/kg), moderate (50 mg/kg), or high (100 mg/kg) doses of lead for one month.
  • Biochemical, hematological, and spatial learning/memory tests were performed.
  • Histopathological examination of liver and kidney tissues was conducted.
  • Liquid chromatography-mass spectrometry (LC-MS) was used for serum metabolite profiling, followed by pathway enrichment analysis.

Main Results:

  • High lead exposure (H-Pb) resulted in decreased body weight, feed efficiency, total protein, and δ-aminolevulinate dehydratase (ALAD) activity.
  • Elevated blood lead levels, creatinine, blood urea nitrogen (BUN), RBC, and WBC counts were observed in the H-Pb group.
  • H-Pb exposure impaired spatial learning and memory, evidenced by increased latency.
  • Histopathological changes were noted in the liver and kidneys.
  • Significant reductions in Butyryl-L-carnitine and Ganglioside GD2 were observed in the H-Pb group.
  • Metabolite analysis indicated pathways associated with oxidative stress were significantly modulated.

Conclusions:

  • Lead exposure exerts dose-dependent systemic effects, impacting metabolism, hematology, cognition, and organ health.
  • Specific metabolites, including Butyryl-L-carnitine and Ganglioside GD2, are sensitive biomarkers of lead toxicity.
  • This study establishes a novel in vivo model for dose-dependent lead exposure and serum metabolite profiling, highlighting oxidative stress as a key mechanism.