Effect Of Tert-butylhydroquinone Research Articles

Effect of tert-butylhydroquinone on biodiesel properties during extreme oxidation conditions

The use of alternative sources for fuel production has been gaining attention in the past years. Thus, the role of biodiesel seems to be crucial, as it can contribute to the sustainable economic growth of developing countries. The main raw materials for biodiesel production are vegetable oils, obtaining fatty acid methyl (or ethyl) esters through transesterification with methanol (or ethanol). The properties of these natural feedstocks can influence the quality of biodiesel. Specifically, its oxidative stability is usually low, not complying with the lower limit established by standards. As a consequence, some properties of biodiesel (especially viscosity and acid number) can vary during storage due to oxidation. In order to avoid these undesirable effects, antioxidant addition, as well as the selection of stable oils, is necessary. Among them, tert-butylhydroquinone (TBHQ) is one of the most popular additives. The aim of this work was to assess the evolution of some properties of biodiesel from different sources (cardoon, waste cooking, rapeseed and high-oleic safflower oil) during extreme oxidation conditions, evaluating the effectiveness of TBHQ addition on quality maintenance. As a result, the most unstable samples (cardoon and waste cooking biodiesel) required higher amounts of TBHQ (750 and 450 ppm, respectively) to comply with the standard (induction point = 8 h), whereas high-oleic safflower did not require any addition (induction point = 8.35 h). During extreme oxidation conditions, all the samples kept their viscosity and acid number values when the right amount of TBHQ was added, assuring their quality parameters during storage.

Tert-butylhydroquinone enhanced angiogenesis and astrocyte activation by activating nuclear factor-E2-related factor 2/heme oxygenase-1 after focal cerebral ischemia in mice

Angiogenesis after cerebral ischemia plays a pivotal role in neurological recovery and represents a therapeutic target. The angiogenic effect of nuclear factor E2-related factor 2 (Nrf2) was identified in recent years. However, the effects of tert-butylhydroquinone, an Nrf2 inducer, on angiogenesis and astrocyte activation after stroke remain unclear. In this study, we investigated whether tert-butylhydroquinone enhanced angiogenesis and astrocyte activation through Nrf2 pathway. Wild-type (Nrf2+/+) and Nrf2-deficient (Nrf2−/−) mice were subjected to permanent distal middle cerebral artery occlusion (dMCAO). We established 6 experimental groups (sham Nrf2+/+ group, vehicle Nrf2+/+ group, tBHQ Nrf2+/+ group; sham Nrf2−/− group, vehicle Nrf2−/− group, and tBHQ Nrf2−/− group). The infarct volume, neurological function, microvessel density (MVD), astrocytic endfeet covered ratio and the expression of Nrf2, HO-1 and VEGF in the ischemic brain were measured at different time points. Compared with that observed in the vehicle Nrf2+/+ group, tBHQ significantly reduced the infarct volume, enhanced post-stroke angiogenesis and astrocytic endfeet covered ratio in the peri-infarct area. The Nrf2/HO-1/VEGF pathway was activated by tBHQ in the angiogenesis process. However, in Nrf2−/− mice, Nrf2 deficiency blocked the effects of tBHQ on angiogenesis process and neurological recovery as well as abolished the mediation of proangiogenic factors. These results suggested that tBHQ enhanced angiogenesis and astrocyte activation through activating Nrf2 pathway after cerebral ischemia.

Effect of tert-Butylhydroquinone on the expression of nuclear factor erythroid 2-related factor 2, heme oxygenase-1 and phosphatidylinositol 3-kinase in high glucose cultured retinal Müller cells

Objective To observe the effect of tert-Butylhydroquinone (tBHQ) on the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase (HO)-1 and phosphatidylinositol 3-kinase (PI3K) in high glucose cultured retinal Muller cells; and to investigate the anti-oxidative stress and anti-apoptotic effects of tBHQ. Methods Retinal Muller cells were divided into normal glucose group (5.5 mmol/L, N group), high glucose group (45 mmol/L, HG group) and tBHQ intervention group (HG+tBHQ group). After retinal Muller cells were cultured with high glucose for 48 hours, the pretreatment with tBHQ (20 μmol/L) induced the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1. The Muller cells were identified by immunofluorescence staining. The expressions of Nrf2, HO-1, PI3K, B-cell lymphoma-2 (Bcl-2) and Bax were detected by Western blot and real-time fluorescence quantitative PCR. Flow cytometry was used to detect the apoptosis of retinal Muller cells in rats. Results Muller cytoplasm and nucleus GS showed strong positive, large cell body, abundant cytoplasm, uniform green fluorescence; nuclear DAPI staining round or oval, clear boundary. The expression of Nrf2 protein (t=4.114, P=0.006), HO-1 protein (t=9.275, P=0.000), Nrf2 mRNA (t=7.292, P=0.000) and HO-1 mRNA (t=15.014, P=0.000) in the HG group were higher than those in the N group. The expressions of Nrf2 protein (t=7.847, P=0.000) , HO-1 protein (t=7.947, P=0.000), PI3K protein (t=5.397, P=0.002), Bcl-2 protein (t=6.825, P=0.000), Nrf2 mRNA (t=18.046, P=0.000), HO-1 mRNA (t=39.458, P=0.000), PI3K mRNA (t=4.979, P=0.003) and Bcl-2 mRNA (t=9.535, P=0.000) in the HG+tBHQ group were significantly higher than those in the HG group. The protein and mRNA expressions of Bax protein in the HG+tBHQ group were significantly lower than those in the HG group (t=14.998, 16.520; P=0.000, 0.000). Flow cytometry showed that the apoptosis rate of Muller cells in the HG group was significantly higher than that in the N group (t=39.905, P=0.000). The apoptosis rate of Muller cells in the HG+tBHQ group was significantly lower than that in the HG group (t=21.083, P=0.000). Conclusion tBHQ can inhibit the apoptosis of retinal Muller cells by up-regulating the expression of Nrf2, HO-1 and PI3K. Key words: Hydroquinones; NF-E2-related factor 2; Heme oxygenase (decyclizing); Phosphatidylinositol 3-kinase; Muller cell

Effect of tert-butylhydroquinone on DJ-1/Nrf2 pathway during renal ischemia-reperfusion in diabetic rats

Objective To evaluate the effect of tert-butylhydroquinone (t-BHQ) on DJ-1/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway during renal ischemia-reperfusion (I/R) in diabetic rats. Methods Forty SPF healthy adult male Sprague-Dawley rats, weighing 200-220 g, were divided into 4 groups (n=10 each) using a random number table method: control group (group C), diabetes mellitus group (group D), diabetes mellitus plus renal I/R group (I/R group) and t-BHQ group (group T). Diabetes mellitus was induced by intraperitoneal streptozotocin 60 mg/kg and confirmed by fasting blood glucose level>16.7 mmol/L 72 h later.t-BHQ 50 mg/kg was intraperitoneally injected in 3 times at an interval of 8 h starting from 24 h before surgery in group T, while the equal volume of normal saline was given instead in D and I/R groups.Blood samples were collected from the apex of the heart at 24 h of reperfusion for determination of serum creatinine (Cr), cystatin C (Cys C) and β2-microglobulin (β2-MG) concentrations.The rats were then sacrificed, and kidneys were removed for determination of pathological changes of kidneys (with a light microscope) and for detection of the expression of DJ-1, Nrf2 and heme oxygenase-1 (HO-1) in renal tissues (by Western blot). Results Compared with group C, the concentrations of serum Cr, Cys C and β2-MG and pathological scores were significantly increased, and the expression of DJ-1, Nrf2 and HO-1 was up-regulated in D, I/R and T groups (P<0.05). Compared with group D and group I/R, the concentrations of serum Cr, Cys C and β2-MG and pathological scores were significantly decreased, and the expression of DJ-1, Nrf2 and HO-1 was up-regulated in group T (P<0.05). Conclusion t-BHQ can attenuate renal I/R injury by activating DJ-1/Nrf2 pathway in diabetic rats. Key words: Diabetes mellitus; Kidney; Reperfusion injury; Transcription factors; t-BHQ; DJ-1

TBHQ and peanut skin inhibit accumulation of PAHs and oxygenated PAHs in peanuts during frying

The effects of tert-butylhydroquinone (TBHQ) and peanut skins on the concentrations of polycyclic aromatic hydrocarbons (PAHs) and oxygenated PAHs (OPAHs) in fried peanuts were investigated. Sixteen PAHs and five OPAHs were quantified using gas chromatography-mass spectrometry (GC-MS). Addition of TBHQ to the frying oil reduced the total PAH and total OPAH concentrations by up to 71.75% and 74.80%, respectively. After frying, average PAH and OPAH levels were respectively 22.63% and 79.22% lower in peanuts with skins versus those without skins. The concentration of benzo[a]anthracene (BaA) was significantly correlated with that of benzo[a]anthracene-7,12-dine (BaAQ) in the fried peanuts. These results may be helpful for production of good quality fried peanuts with a low PAH content, as well as providing guidance for reducing PAHs in other fried foods.

The effect of tert-butylhydroquinone (TBHQ) on biodiesel bioremediation in soil samples inoculated with bacterial cells

The study aimed to determine the effect of tert-butyl-hydroquinone (TBHQ) on the activities of dehydrogenases and esterases, free fatty acid level, early plant growth of Sinapis alba, Lepidium sativum, and Sorghum saccharatum, pH, degradation of biodiesel and the rate of FAME assimilation during bioremediation process with two selected bacterial strains (Achromobacter xylosoxidans G21 or Sarcina spp.). Biodiesel with or without TBHQ (210 mg l−1) in 5% (w/w) concentration were introduced into soil. Based on the obtained results, inhibition of esterases and dehydrogenases activity, reduction of FAME assimilation and a marked decrease in FAME degradation was found when TBHQ was added to biodiesel. Obtained results provide evidence that the presence of TBHQ in biofuel impacts the course of bioremediation of soil contaminated with biodiesel. Too high TBHQ concentrations in the fuel may reduce the effectiveness of soil clean-up processes.

Protective Effect of Tert Butyl Hydroquinone on Diazinon-Induced Oxidative Stress in Brain and Heart of Male Rats

Background: The present study was designed to investigate the chronic effects of diazinon on oxidative stress markers in brain and heart of rats and the possible protective effects of tert butyl hydroquinone (TBHQ), as an antioxidant. Objectives: Therefore, the present study was undertaken to evaluate the protective role of TBHQ on oxidative stress induced by diazinon in brain and heart tissues of rats after 7 weeks exposure to sub-lethal dose of diazinon. Materials and Methods: In this experimental study, 28 male Wistar rats which were randomly divided into four groups: diazinon group (10 mg/kg, once a day), TBHQ group (0.028 g/kg of diet, once a day), diazinon + TBHQ group (diazinon, 10 mg/kg, once a day + TBHQ, 0.028 g/kg of diet, once a day) and control group (corn oil, as vehicle of diazinon and TBHQ). The animals were treated with diazinon, TBHQ or corn oil orally using a stomach tube for 7 weeks. Results: At the end of 7th week, total thiol groups, ferric reducing antioxidant power (FRAP) and malondialdehyde (MDA) levels in brain and heart tissues were investigated. A significant increase in MDA levels (P = 0.01) in heart tissue was evident in diazinon group, when compared to control group. Rats of the TBHQ and diazinon + TBHQ groups presented a significant increase in thiol groups (P = 0.01), when compared to control and diazinon groups. In addition, TBHQ administration significantly increased the FRAP level of brain tissue in TBHQ and TBHQ + diazinon groups, when compared with control and diazinon groups, respectively (P = 0.001). Conclusions: The results of the present study showed that TBHQ treatment could improve antioxidant status in brain and heart tissues of rats with chronic toxicity of diazinon. However, it could not ameliorate the lipid peroxidation sufficiently.

Oxidative Conversion Mediates Antiproliferative Effects of tert-Butylhydroquinone: Structure and Activity Relationship Study.

Previous studies have shown that tert-butylhydroquinone (TBHQ), a widely used food antioxidant, has cytotoxic effects at high doses; however, the underlying mechanisms are not well understood. Here, we found that the effects of TBHQ on cell proliferation, cell cycle progression, and apoptosis are mainly mediated by its oxidative conversion to a quinone metabolite tert-butylquinone (TBQ). Co-addition of cupric ion (Cu(2+)) caused accelerated oxidative conversion of TBHQ to TBQ and enhanced the biological activities of TBHQ on cell proliferation, cell cycle progression, and apoptosis in MC38 colon cancer cells. In contrast, co-addition of ethylenediaminetetraacetic acid (EDTA) suppressed TBHQ oxidation and inhibited the biological activities of TBHQ in MC38 cells. For example, after 24 h of treatment in basal medium, low-dose TBHQ (1.88-7.5 μM) had little effect on MC38 cell proliferation, while co-addition of 50 μM Cu(2+) caused 30-70% inhibition of cell proliferation; in contrast, treatment with high-dose TBHQ (15 μM) inhibited 50 ± 4% MC38 proliferation, which was abolished by co-addition of 50 μM EDTA. We further showed that TBQ had more potent actions on cell proliferation and associated cellular responses than TBHQ, supporting a critical role of TBQ formation in the biological activities of TBHQ. Finally, a structure and activity relationship study showed that the fast-oxidized para-hydroquinones had potent antiproliferative effects in MC38 cells, while the slow-oxidized para-hydroquinones had weak or little biological activities. Together, these results suggest that the biological activities of TBHQ and other para-hydroquinones are mainly mediated by their oxidative metabolism to generate more biologically active quinone metabolites.

The influence of tert-butyl hydroquinone on retinal nuclear factor E2-related factor 2 and heme oxygenase-1 in type 2 diabetic rats

Objective To observe the effect of tert-butyl hydroquinone (tBHQ) on type 2 diabetic rats retinal nuclear factor E2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1). Methods 60 Sprague Dawley rats were randomly divided into normal control group ( NC group, n=20) and model group (n=40). The rats in model group were intraperitoneal injected with streptozotocin (30 mg/kg) to establishing type 2 diabetic mellitus (DM). There were 35 rats successfully established and they were randomly divided into diabetic group (DM group, 17 rats) and tBHQ group (18 rats). The rats in tBHQ group were fed with high fat and sugar diet with 1% tBHQ. After 4 weeks and 12 weeks of tBHQ intervention, hematoxylin eosin staining of retinal sections, immunohistochemical staining and quantitative polymerase chain reaction (PCR) of Nrf2 and HO-1 were performed. Results In tBHQ control, the retina of rats was normal and individual cells showed slightly edema at 4 weeks; the retinal structure of rats was clear and part of cells showed edema at 12 weeks. At 4 and 12 weeks, the expression of Nrf2 (t=3.115, 3.781) and HO-1 (t=3.485, 3.785) protein in DM group were higher than that in NC group (P<0.05); the expression of Nrf2 (t=2.473, 2.576) and HO-1 (t=2.785, 2.879) protein in tBHQ group were higher than that in DM group (P<0.05). In DM group, the expression of Nrf2 protein at 12 weeks was higher than that at 4 weeks (t=0.276, P<0.05). In tBHQ group, the expression of Nrf2 (t=2.516) and HO-1 (t=2.776) protein at 12 weeks were higher than that at 4 weeks (P<0.05). 4 and 12 weeks, the expression of Nrf2 (t=4.758, 4.285) and HO-1 (t=5.114, 4.514) mRNA in DM group were higher than that in NC group (P<0.05); the expression of Nrf2 (t=5.133, 4.976) and HO-1 (t=4.758, 4.251) mRNA in tBHQ group were higher than that in DM group (P<0.05). In DM gruop, the expression of Nrf2 protein at 12 weeks was higher than that at 4 weeks (t=5.114, P<0.05). In tBHQ group, the expression of Nrf2 (t=4.292) and HO-1 (t=4.974) protein at 12 weeks were higher than that at 4 weeks (P<0.05). Conclusion tBHQ intervention can increased the expression of Nrf2, HO-1 significantly in the retina of type 2 diabetic rats. Key words: Diabetic retinopathy/physiopathology; NF-E2-related factor 2; Heme oxygenase (decyclizing); Animal experimentation

Tert-butylhydroquinone (TBHQ) improves antioxidant status in rat tissues following chronic diazinon intoxication

Considering that the involvement of oxidative stress has been implicated in the toxicity of organophosphate insecticides, the objective of the present study was to investigate antioxidants and oxidative stress markers in the liver and kidney of Wistar rats treated with chronic doses of diazinon. In addition, the effect of Tert-butylhydroquinone (TBHQ), a food-additive antioxidant, on attenuation of diazinon-induced oxidative stress was evaluated. 28 rats were randomly assigned to 1 of 4 treatment groups: diazinon (10 mg/kg BW, once a day; n=7), TBHQ (0.028 g/kg of diet, once a day; n=7), TBHQ + diazinon (diazinon; 10 mg/kg BW, once a day + TBHQ; 0.028 g/kg of diet, once a day; n=7) and control (corn oil, as vehicle of diazinon and TBHQ, n=7). TBHQ, diazinon and corn oil were given to rats orally via gavage for 7 weeks. Total thiol groups, ferric reducing antioxidant power (FRAP) and malondialdehyde (MDA) levels in liver and kidney tissues were investigated at the end of 7th week. Treatment with diazinon significantly increased MDA level, as a marker of lipid peroxidation, in the kidney (p<0.05). Co-administration of TBHQ with diazinon significantly increased total thiol groups and FRAP levels in liver and kidney (p<0.05). However, TBHQ did not reduce lipid peroxidation in the tissues. The results of the present study showed that administration of TBHQ at a dose of 0.028 g/kg of diet, increased antioxidant capacity of tissues of rats treated with diazinon, though this increase was not sufficiently effective to reduce lipid peroxidation caused by diazinon. Higher amounts of TBHQ might be more effective in attenuation of diazinon-induced lipid peroxidation.

The transcriptional response to oxidative stress during vertebrate development: effects of tert-butylhydroquinone and 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Oxidative stress is an important mechanism of chemical toxicity, contributing to teratogenesis and to cardiovascular and neurodegenerative diseases. Developing animals may be especially sensitive to chemicals causing oxidative stress. The developmental expression and inducibility of anti-oxidant defenses through activation of NF-E2-related factor 2 (NRF2) affect susceptibility to oxidants, but the embryonic response to oxidants is not well understood. To assess the response to chemically mediated oxidative stress and how it may vary during development, zebrafish embryos, eleutheroembryos, or larvae at 1, 2, 3, 4, 5, and 6 days post fertilization (dpf) were exposed to DMSO (0.1%), tert-butylhydroquinone (tBHQ; 10 µM) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 2 nM) for 6 hr. Transcript abundance was assessed by real-time qRT-PCR and microarray. qRT-PCR showed strong (4- to 5-fold) induction of gstp1 by tBHQ as early as 1 dpf. tBHQ also induced gclc (2 dpf), but not sod1, nqo1, or cyp1a. TCDD induced cyp1a but none of the other genes. Microarray analysis showed that 1477 probes were significantly different among the DMSO-, tBHQ-, and TCDD-treated eleutheroembryos at 4 dpf. There was substantial overlap between genes induced in developing zebrafish and a set of marker genes induced by oxidative stress in mammals. Genes induced by tBHQ in 4-dpf zebrafish included those involved in glutathione synthesis and utilization, signal transduction, and DNA damage/stress response. The strong induction of hsp70 determined by microarray was confirmed by qRT-PCR and by use of transgenic zebrafish expressing enhanced green fluorescent protein (EGFP) under control of the hsp70 promoter. Genes strongly down-regulated by tBHQ included mitfa, providing a molecular explanation for the loss of pigmentation in tBHQ-exposed embryos. These data show that zebrafish embryos are responsive to oxidative stress as early as 1 dpf, that responsiveness varies with development in a gene-specific manner, and that the oxidative stress response is substantially conserved in vertebrate animals.

Preparation and characterization of methylic and ethylic biodiesel from cottonseed oil and effect of tert-butylhydroquinone on its oxidative stability

This work reports the preparation and characterization of methylic and ethylic biodiesel from cottonseed oil. Biodiesel was prepared by a transesterification process involving the reaction of the oil with methanol or ethanol using KOH as catalyst. The conversion of triglycerides to the corresponding methyl and ethyl ester was 91.5 and 88.5 (wt%). All the physical–chemical properties of the obtained biodiesels met the minimum or maximum limits of the EN 14214 except oxidation stability. The addition of the synthetic antioxidant tert-butylhydroquinone at the concentration of 300mgkg−1 was sufficient to obtain acceptable oxidation stability values (>6h). Thermogravimetric analysis was also performed and similar profiles were verified for both ethylic and methylic biodiesels. Therefore, this work demonstrates the feasibility of using the ethanolic route to produce cottonseed oil biodiesel.

Protective effects of tert-butylhydroquinone on sodium arsenite-induced cytotoxicity and oxidative injuries

Objective To study the protective effects of tert-butylhydroquinone(tBHQ) on sodium arsenite (NaAsO2)-induced cytotoxicity and oxidative injuries. Methods Chang liver cells were pretreated with tBHQ[0(control), 5, 25 μmol/L]for 24 h, and then co-treated with tBHQ(5 μmol/L) together with NaAsO2[0(control),30, 40, 50, 60 μmol/L] for another 24 h, and Alamar blue reduction rates were used to evaluate cell viability,the results were expressed as the relative ratio of Alamar blue reduction rates between the experimental group and the control group. On the other hand, Chang liver cells were pretreated with tBHQ[0(control), 5, 25 μmol/L] for24 h,and then co-treated with tBHQ(5 μmol/L) together with NaAsO2[0(control), 40, 50 μmol/L] for another 24 h,and the levels of cellular reactive oxygen species(ROS) were detected by staining cells with 2',7'-dichlorofluorescin diacetate(DCFH-DA), the results were expressed as the relative ratio of mean fluorescence intensity between the experimental group and the control group. Results Cell viability decreased dramatically by treatment with NaAsO2(30, 40, 50, 60 μmol/L), while relieved to some extent by pretreatment with 5, 25 μmol/L tBHQ, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant(F =566.57, 55.09, 14.50,all P ＜ 0.05) ; the cell viability of NaAsO2(30, 40, 50, 60 μmol/L) pretreated with tBHQ(5, 25 mol/L) were 0.75 ±0.02, 0.70 ± 0.04, 0.59 ± 0.03, 0.43 ± 0.03 and 0.75 ± 0.02, 0.73 ± 0.03, 0.65 ± 0.02, 0.50 ± 0.02, respectively,all significantly higher than corresponding NaAsO2 alone groups(0.70 ± 0.03, 0.64 ± 0.03, 0.43 ± 0.03, 0.33 ±0.01, all P ＜ 0.05), the cell viability of NaAsO2(50, 60 μmol/L) pretreated with 25 μmol/L tBHQ was higher than corresponding 5 μmol/L tBHQ pretreatment groups(all P ＜ 0.05). On the other hand, 40, 50 μmol/L of NaAsO2 significantly induced hepatocellular ROS generation, while tBHQ(5, 25 μ mol/L) pretreatment significantly decreased NaAsO2-induced intracellular ROS levels, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant (F =181.78, 60.55, 4.93, all P ＜ 0.05) ; the ROS levels of NaAsO2(40, 50 μ mol/L) pretreated with tBHQ(5, 25 μmol/L) were 1.87 ± 0.09, 1.80 ± 0.07 and 1.36 ± 0.11, 1.44 ± 0.12,all significantly decreased than corresponding NaAsO2 alone groups(2.30 ± 0.18, 2.18 ± 0.17, all P ＜ 0.05),the ROS levels of NaAsO2(40, 50 μmol/L) pretreated with 25 μmol/L tBHQ decreased than corresponding 5 μmol/L tBHQ pretreatment groups (all P ＜ 0.05). Conclusion tBHQ has a certain antagonism on arsenic induced cytotoxicity and oxidative injuries. Key words: Arsenites; Tert-butylhydroquinone; Reactive oxygen species

Effects of Tert-Butylhydroquinone on Intestinal Inflammatory Response and Apoptosis following Traumatic Brain Injury in Mice

Traumatic brain injury (TBI) can induce intestinal inflammatory response and mucosal injury. Antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown in our previous studies to prevent oxidative stress and inflammatory response in gut after TBI. The objective of this study was to test whether tert-butylhydroquinone (tBHQ), an Nrf2 inducer, can protect against TBI-induced intestinal inflammatory response and mucosal injury in mice. Adult male ICR mice were randomly divided into three groups: (1) sham + vehicle group, (2) TBI + vehicle group, and (3) TBI + tBHQ group (n = 12 per group). Closed head injury was adopted using Hall's weight-dropping method. Intestinal mucosa apoptosis and inflammatory-related factors, such as nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1), were investigated at 24 h after TBI. As a result, we found that oral treatment with 1% tBHQ prior to TBI for one week markedly decreased NF-κB activation, inflammatory cytokines production, and ICAM-1 expression in the gut. Administration of tBHQ also significantly attenuated TBI-induced intestinal mucosal apoptosis. The results of the present study suggest that tBHQ administration could suppress the intestinal inflammation and reduce the mucosal damage following TBI.

Effect of tert-Butylhydroquinone(TBHQ) on the Formation of Nitrosamines in the Reaction of Secondary Amines with Nitrite.

tert-Butylhydroquinone (TBHQ), an antioxidant for edible fats and oil, inhibited nitrosamine formation in the reaction of secondary amines with nitrite under acidic conditions. The inhibitory effect may be due to the loss of nitrite available for nitrosation. TBHQ was oxidized with nitrite into 2-tert-butyl-p-benzoquinone (TBQ), which was active in enhancing nitrosamine formation in the presence of an adequate amount of available nitrite. TBQ readily reacted with secondary amines to form 1 : 1 secondary amine-TBQ adducts whose structures were established to be 2-tert-butyl-5 (and 6)-amino-p-benzoquinones. The adducts may be nitrosated to be transformed into the nitrosamines, or they may catalytically enhance the nitrosamine formation.