Title of article :
Protective effect of curcumin against heavy metals-induced liver damage
Author/Authors :
Garcيa-Niٌo، نويسنده , , Wylly Ramsés and Pedraza-Chaverrي، نويسنده , , José، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2014
Pages :
20
From page :
182
To page :
201
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 :
Nrf2 , Hepatoprotective , Curcumin , Mitochondrial dysfunction , Heavy metals , oxidative stress
Journal title :
Food and Chemical Toxicology
Serial Year :
2014
Journal title :
Food and Chemical Toxicology
Record number :
2126980
Link To Document :
بازگشت