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Gas explosion is a recurrent event in coal mining that cause severe spleen damage. This study aimed to investigate the role and mechanism of oxidative stress in gas explosion-induced spleen injury. 120 male Sprague–Dawley (SD) rats were randomly divided into a control group (NC), a gas explosion-induced spleen injury model group (Model), an Nrf2 inhibitor group (Model + ATRA), and an Nrf2 induction group (Model + TBHQ). After explosion, the rats of the inhibitor group and induction group were immediately given intraperitoneal injection of all-trans-retinoicacid (ATRA, 5 mg/kg) or tertiary butylhydro-quinone (TBHQ, 1 mg/kg) once. Then, the rats were anesthetized with blood taken from the abdominal aorta at 24 h, 72 h and 7 days. The results showed that gas explosion reduced the spleen index. The expression of oxidative stress-related genes and proteins Nrf2, HO-1, COX2 and GPX4 were increased significantly ( P  < 0.05) after gas explosion. Compared with the model group, TBHQ improved the spleen index, and reduced inflammation. Moreover, the expression of inflammatory factor IL-6 and ROS was decreased ( P  < 0.05), HMOX1 and the expression of oxidative stress-related genes and proteins were increased ( P  < 0.05), but the opposite results were observed in the inhibitor group. Taken together, we firstly found that TBHQ may regulate the degree of oxidative stress in spleen injury induced by gas explosion through the Nrf2/HO-1 signaling pathway.

A new method applying sensitive and selective liquid chromatography coupled with mass spectrometry (LC/MS/MS) for analyzing tertiary-butylhydroquinone (TBHQ) and its metabolites in rat serum was validated. Using an extracted ion chromatogram (EIC) of m/z 149, free TBHQ was observed in rat serum after dosing TBHQ at 350 mg/kg to male and female Sprague-Dawley (SD) rats. Four major metabolites of TBHQ were identified--a TBHQ-sulfate, two TBHQ-sulfate-derived substances and a TBHQ-glucuronide through MSn spectra. Besides its simplicity, the sample treatment allows one to obtain a very good recovery of analysts, namely around 95%. This result suggests that the method described here is useful for the analysis of TBHQ and its metabolites in rat serum. Moreover, the metabolism of TBHQ was investigated using the method. After oral administration, TBHQ appear to be more completely absorbed and bio-transformed by males than females, which may result in higher acute oral toxicity of TBHQ for males than females.

The current ANS Panel statement is a refined exposure assessment of tertiary‐butyl hydroquinone (TBHQ, E 319) when used as a food additive. TBHQ (E 319) is authorised as a food additive in the EU with an acceptable daily intake (ADI) of 0.7 mg/kg body weight (bw), as established by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) in 1998 and confirmed by EFSA in 2004. In 2004, the EFSA Scientific Panel on Food Additives, Flavourings, Processing Aids and Materials in Contact with Food (AFC) adopted an opinion on the safety in use of TBHQ (E 319) in fats and oils used for human consumption. In that opinion, the Panel concluded that the exposure in adults did not exceed the ADI, however, if TBHQ (E 319) was to be used in infant formulae, the exposure in infants could exceed the ADI. Following this conclusion, EFSA performed a refined exposure assessment for TBHQ (E 319) based on individual food consumption data available within the EFSA Comprehensive European Food Consumption Database, on newly submitted data on the actual usage levels of TBHQ (E 319) and analytical data provided by the food industry and Member States. EFSA ANS Panel concluded that, using the maximum permitted levels, exposure estimates exceed the ADI of 0.7 mg/kg bw per day at the high level for toddlers and children, however, in the refined exposure scenarios, the ADI was not exceeded in any of the population groups.