Regeneration of glutathione by α-lipoic acid via Nrf2/ARE signaling pathway alleviates cadmium-induced HepG2 cell toxicity

Environ Toxicol Pharmacol. 2017 Apr:51:30-37. doi: 10.1016/j.etap.2017.02.022. Epub 2017 Feb 27.

Abstract

Alpha-lipoic acid (α-LA) is an important antioxidant that is capable of regenerating other antioxidants, such as glutathione (GSH). However, the underlying molecular mechanism by which α-LA regenerates GSH remains poorly understood. The current study aimed to investigate whether α-LA regenerates GSH by activation of Nrf2 to alleviate cadmium-induced cytotoxicity in HepG2 cells. In the present study, we found that cadmium induced cell death by depletion of GSH through inactivation of Nrf2. Addition of α-LA to cadmium-treated cells reactivated Nrf2 and regenerated GSH through elevating the Nrf2-downstream genes γ-glutamate-cysteine ligase (γ-GCL) and GR, both of which are key enzymes for GSH synthesis. However, blocking Nrf2 with brusatol in the cells co-treated with α-LA and cadmium reduced the mRNA and the protein levels of γ-GCL and GR, thus suppressed GSH regeneration by α-LA. Our results indicated that α-LA activated Nrf2 signaling pathway, which upregulated the transcription of the enzymes for GSH synthesis and therefore GSH contents to alleviate cadmium-induced cytotoxicity in HepG2 cells.

Keywords: Cadmium; Glutathione; Nrf2; Regeneration; α-Lipoic acid.

MeSH terms

  • Antioxidant Response Elements / drug effects*
  • Antioxidant Response Elements / genetics
  • Antioxidant Response Elements / physiology
  • Antioxidants / pharmacology*
  • Cadmium / toxicity*
  • Cell Culture Techniques
  • Cell Survival / drug effects
  • Environmental Pollutants / toxicity*
  • Glutamate-Cysteine Ligase / genetics
  • Glutathione / metabolism*
  • Glutathione Reductase / genetics
  • Hep G2 Cells
  • Humans
  • NF-E2-Related Factor 2 / genetics
  • NF-E2-Related Factor 2 / metabolism*
  • Oxidative Stress / drug effects
  • Signal Transduction
  • Thioctic Acid / pharmacology*

Substances

  • Antioxidants
  • Environmental Pollutants
  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • Cadmium
  • Thioctic Acid
  • Glutathione Reductase
  • Glutamate-Cysteine Ligase
  • Glutathione