Beer consumption reduces cerebral oxidation caused by aluminum toxicity by normalizing gene expression of tumor necrotic factor alpha and several antioxidant enzymes

Food Chem Toxicol. 2008 Mar;46(3):1111-8. doi: 10.1016/j.fct.2007.11.006. Epub 2007 Nov 17.


Aluminum (Al)-induced neurotoxicity is well known and different salts of aluminum have been reported to accelerate oxidative damage to biomolecules. The present study has examined whether silicon consumed in the form of silicic acid or beer could potentially inhibit aluminum toxicity in the brain. Male mice were administered with Al(NO(3))(3) orally at a dose of 450 mg/kg/day in drinking water for 3 month. Experimental mice were given Al(NO(3))(3) along with 50 mg/L of silicic acid or with 0.5 ml/day of beer. Al brain levels in the Al group were four times higher than those of control mice while silicic acid and beer group values were 40% lower than those of the Al group. We have observed that beer prevented accumulation of lipid damage significantly, which resulted from aluminum intake. Decline in the expression of mRNA of endogenous antioxidant enzymes associated with aluminum administration was also inhibited by beer and silicic acid. The tumor necrosis factor alpha (TNFalpha) RNA expression was normalized in silicic acid and beer groups. Very high and significant correlations were found for the different parameters tested suggesting that moderate consumption of beer, due to its silicon content, effectively protects against the neurotoxic effects of aluminum.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aluminum / toxicity*
  • Animals
  • Base Sequence
  • Beer*
  • Brain / drug effects*
  • Brain / metabolism
  • DNA Primers
  • Enzymes / genetics*
  • Gene Expression / drug effects*
  • Male
  • Mice
  • Thiobarbituric Acid Reactive Substances / metabolism
  • Tumor Necrosis Factor-alpha / genetics*


  • DNA Primers
  • Enzymes
  • Thiobarbituric Acid Reactive Substances
  • Tumor Necrosis Factor-alpha
  • Aluminum