Protective effects of blueberries (Vaccinium corymbosum L.) extract against cadmium-induced hepatotoxicity in mice

Environ Toxicol Pharmacol. 2014 May;37(3):1015-27. doi: 10.1016/j.etap.2014.03.017. Epub 2014 Mar 30.


The oxidative status and morphological changes of mouse liver exposed to cadmium chloride (Cd(II)) and therapeutic potential of blueberry (Vaccinium corymbosum L.) extract against Cd(II)-induced hepatic injury were investigated. A variety of parameters were evaluated, including lipid peroxidation (LPO), protein carbonyl (PCO) level, DNA fragment, as well as antioxidative defense system (i.e., superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH)). Elemental analysis and evaluation of morphological changes and NO levels were also performed. Exposure to Cd(II) led to increased LPO and PCO as well as DNA fragment and a reduction of SOD and CAT activities, however, the content of GSH elevated probably due to biological adaptive-response. In contrast, co-treatment of anthocyanin (Ay) inhibited the increased oxidative parameters as well as restored the activities of antioxidative defense system in a dose-dependent manner. Ay administration regained these morphological changes caused by intoxication of Cd(II) to nearly normal levels. Moreover, the accumulation of Cd(II) in liver may be one of the reasons for Cd(II) toxicity and Ay can chelate with Cd(II) to reduce Cd(II) burden. The influence of Cd(II) on the Zn and Ca levels can also be adjusted by the co-administration of Ay. Exposure to Cd(II) led to an increase of NO and Ay reduced NO contents probably by directly scavenging. Potential mechanisms for the protective effect of Ay have been proposed, including its anti-oxidative and anti-inflammatory effect along with the metal-chelating capacity. These results suggest that blueberry extract may be valuable as a therapeutic agent in combating Cd(II)-induced tissue injury.

Keywords: Anthocyanin; Blueberry; Cadmium; Hepatotoxicity; Oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Anthocyanins / pharmacology
  • Anthocyanins / therapeutic use*
  • Anti-Inflammatory Agents / pharmacology
  • Anti-Inflammatory Agents / therapeutic use*
  • Antioxidants / pharmacology
  • Antioxidants / therapeutic use*
  • Aspartate Aminotransferases / blood
  • Cadmium / toxicity
  • Catalase / metabolism
  • Chelating Agents / pharmacology
  • Chelating Agents / therapeutic use*
  • Chemical and Drug Induced Liver Injury / drug therapy*
  • Chemical and Drug Induced Liver Injury / etiology
  • Chemical and Drug Induced Liver Injury / metabolism
  • Chemical and Drug Induced Liver Injury / pathology
  • DNA Fragmentation / drug effects
  • Glutathione / metabolism
  • Lipid Peroxidation / drug effects
  • Liver / drug effects
  • Liver / metabolism
  • Liver / pathology
  • Male
  • Mice
  • Phytotherapy
  • Plant Extracts / pharmacology
  • Plant Extracts / therapeutic use
  • Protein Carbonylation / drug effects
  • Superoxide Dismutase / metabolism
  • Vaccinium*


  • Anthocyanins
  • Anti-Inflammatory Agents
  • Antioxidants
  • Chelating Agents
  • Plant Extracts
  • Cadmium
  • Catalase
  • Superoxide Dismutase
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • Glutathione