Protective effect of curcumin against heavy metals-induced liver damage

Food Chem Toxicol. 2014 Jul:69:182-201. doi: 10.1016/j.fct.2014.04.016. Epub 2014 Apr 18.

Abstract

Occupational or environmental exposures to heavy metals produce several adverse health effects. The common mechanism determining their toxicity and carcinogenicity is the generation of oxidative stress that leads to hepatic damage. In addition, oxidative stress induced by metal exposure leads to the activation of the nuclear factor (erythroid-derived 2)-like 2/Kelch-like ECH-associated protein 1/antioxidant response elements (Nrf2/Keap1/ARE) pathway. Since antioxidant and chelating agents are generally used for the treatment of heavy metals poisoning, this review is focused on the protective role of curcumin against liver injury induced by heavy metals. Curcumin has shown, in clinical and preclinical studies, numerous biological activities including therapeutic efficacy against various human diseases and anti-hepatotoxic effects against environmental or occupational toxins. Curcumin reduces the hepatotoxicity induced by arsenic, cadmium, chromium, copper, lead and mercury, prevents histological injury, lipid peroxidation and glutathione (GSH) depletion, maintains the liver antioxidant enzyme status and protects against mitochondrial dysfunction. The preventive effect of curcumin on the noxious effects induced by heavy metals has been attributed to its scavenging and chelating properties, and/or to the ability to induce the Nrf2/Keap1/ARE pathway. However, additional research is needed in order to propose curcumin as a potential protective agent against liver damage induced by heavy metals.

Keywords: Curcumin; Heavy metals; Hepatoprotective; Mitochondrial dysfunction; Nrf2; Oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Arsenic / toxicity
  • Cadmium / toxicity
  • Copper / toxicity
  • Curcumin / pharmacology*
  • Humans
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Kelch-Like ECH-Associated Protein 1
  • Lead / toxicity
  • Liver / drug effects*
  • Liver / metabolism
  • Liver / pathology
  • Mercury / toxicity
  • Metals, Heavy / toxicity*
  • NF-E2-Related Factor 2 / metabolism
  • Oxidative Stress / drug effects
  • Protective Agents / pharmacology*

Substances

  • Intracellular Signaling Peptides and Proteins
  • KEAP1 protein, human
  • Kelch-Like ECH-Associated Protein 1
  • Metals, Heavy
  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • Protective Agents
  • Cadmium
  • Lead
  • Copper
  • Mercury
  • Curcumin
  • Arsenic