Tert-butylhydroquinone (
tBHQ) has been commonly used as a synthetic food
antioxidant to prevent
oils and
fats from oxidative deterioration and rancidity due to its potent anti-lipid peroxidation activity. In North America, the maximum level of
tBHQ allowed in fat products is 0.02% with an acceptable daily intake of 0-0.7 mg/kg
body weight. Extensive studies have demonstrated that
tBHQ exhibit
anti-carcinogenic effect. The ability of
tBHQ to induce phase II
xenobiotic metabolizing
enzymes through an Nrf2-dependent pathway is thought to be responsible for the observed protective effect of
tBHQ. It has been proposed that
tBHQ enhances Nrf2-mediated transcription by promoting
reactive oxygen species-mediated dissociation of Nrf2-Keap1, Nrf2 stabilization,
phosphatidylinositol 3-kinase (PI3K)/Akt activity, and MAPK pathway activation. In contrast to the beneficial effects of
tBHQ, a number of studies have shown that chronic exposure to
tBHQ may induce carcinogenicity. However, the precise mechanisms of
tBHQ carcinogenicity are not well understood. The toxicity or carcinogenicity of
tBHQ has been attributed to the formation of reactive GSH-conjugates, generation of reactive species,
CYP1A1 induction,
caspase activation and reduced GSH/
ATP levels. This review provides an account of recent mechanisms proposed for both chemoprotective and carcinogenic effect of
tBHQ.