Distribution of 2-tert-butyl-1,4-benzoquinone and its precursor, tert-butylhydroquinone, in typical edible oils and oleaginous foods marketed in Hangzhou City, China.

This study aimed to obtain a reliable evaluation about addition of tert-butylhydroquinone (TBHQ), and distribution of TBHQ and 2-tert-butyl-1,4-benzoquinone (TBBQ) contents in typical edible oils and oleaginous foods marketed in Hangzhou City. Briefly, the probability of labeled with addition of TBHQ in foods decreased from 36.45 ± 2.6% to 28.78 ± 3.7% in the period from 2018 to 2020. In the 135 analyzed samples, TBHQ contents were far less than the maximum legal additive amount, and TBBQ contents ranged from below its limit of quantification (LOQ) to 13.54 ± 1.15 mg/kg. The conversion rate from TBHQ to TBBQ in edible oils was 2.94 ± 1.17%, much lower than that in other food categories. Further research determined that the process method and food composition were the main factors for different conversion rates from TBHQ to TBBQ in various food categories. In addition, oil consumption was found to be the primary source of dietary intake of TBHQ and TBBQ.

tert-Butyl-p-benzoquinone induces autophagy by inhibiting the Akt/mTOR signaling pathway in RAW 264.7 cells.

tert-Butyl-p-benzoquinone (TBBQ), a metabolite of tert-butylhydroquinone from food, has cytotoxicity, the underlying mechanism of which is not clear. In this study, the viability of RAW 264.7 cells exposed to TBBQ at concentrations of 0.5-10 µg mL-1 was assayed by MTT. Results suggest that TBBQ decreased the viability in a dose-dependent manner. Monodansylcadaverine (MDC) staining results indicate the occurrence of autophagy induced by TBBQ, which was manifested by activation of LC3-II concurrent with the increased levels of Beclin1 and reduced levels of p62. Elevated lipid peroxide and decreased SOD activity by TBBQ exposure suggest the overproduction of ROS, which may account for the increase in the genotoxic stress protein p53. Both upregulation of p53 and reduction of Akt levels inhibited mTOR, which activated autophagy. Addition of 3-MA counteracted the impact of TBBQ on ATG proteins and cell viability. All of these results suggest that TBBQ induces autophagy of RAW 264.7 cells principally by inhibition of the Akt/mTOR signaling pathway, and they implicate ROS in this regulation.