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TBHQ (tert-Butylhydroquinone) Sale

(Synonyms: 特丁基对苯二酚; tert-Butylhydroquinone) 目录号 : GC34057

Tert-butylhydroquinone (TBHQ) is an antioxidant compound which is used to prevent lipid peroxidation and shows multiple cytoprotective actions. It is an activator of Nrf2.

TBHQ (tert-Butylhydroquinone) Chemical Structure

Cas No.:1948-33-0

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10mM (in 1mL DMSO)
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产品描述

Tert-butylhydroquinone (TBHQ) is an antioxidant compound which is used to prevent lipid peroxidation and shows multiple cytoprotective actions. It is an activator of Nrf2.

Tert-butylhydroquinone (tBHQ) is a metabolite of the chemical compound butylated hydroxyanisole and induces Nrf2 activation and conveys protection against hydrogen peroxide, 6-hydroxydopamine, the pesticidal deltamethrin, and other toxicants. tBHQ preferentially alters the redox status in the mitochondrial compartment in HeLa cells. HeLa cells treated with tBHQ show a preferential oxidation of mitochondrial thioredoxin-2 (Trx2), while cellular glutathione and cytosolic thioredoxin-1 are not affected[1]. In cultured H9c2 cells and primary cardiac myocytes, TBHQ stimulates Akt phosphorylation and suppresses oxidant-induced apoptosis[2].

TBHQ treatment elicits significant cytoprotective actions in different organs under pathological conditions. Systemic or local intra-cerebroventricular treatment with TBHQ in an ischemic stroke model in rats significantly reduces the infarct size and neurological deficits. Administration of TBHQ in rats suppresses renal damage and oxidative stress after ischemia and reperfusion injury. In mice with type 1 diabetes, chronic treatment with TBHQ significantly reduces the degree of glomerular fibrosis and ameliorates proteinuria. TBHQ treatment prevents left ventricular dilatation and cardiac dysfunction induced by transverse aortic constriction (TAC), and decreases the prevalence of myocardial apoptosis. The beneficial effects of TBHQ are associated with an increase in Akt activation, but not related to activations of Nrf2 or AMP-activated protein kinase. TBHQ-induced Akt activation is accompanied by increased phosphorylation of Bad, glycogen synthase kinase-3β (GSK-3β) and mammalian target of rapamycin (mTOR)[2].

[1] Imhoff BR, et al. Cell Biol Toxicol. 2010, 26(6):541-51. [2] Yongtao Zhang, et al. Sci Rep. 2015, 5: 13005.

Chemical Properties

Cas No. 1948-33-0 SDF
别名 特丁基对苯二酚; tert-Butylhydroquinone
Canonical SMILES OC1=CC=C(O)C=C1C(C)(C)C
分子式 C10H14O2 分子量 166.22
溶解度 DMSO : ≥ 56.66 mg/mL (340.87 mM) 储存条件 Store at RT
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Research Update

Toxicology of tert-Butylhydroquinone (TBHQ)

Food Chem Toxicol 1986 Oct-Nov;24(10-11):1063-5.PMID:3542758DOI:10.1016/0278-6915(86)90289-9.

This paper traces the history of the EEC Scientific Committee for Food's examination of available toxicological data on tert-Butylhydroquinone (TBHQ). Studies of mutagenicity, metabolism, enzyme activities, reproduction and long-term toxicity and carcinogenicity are reviewed. The author concludes that dose level is an important factor in the induction of forestomach tumours. Further long-term toxicity testing of TBHQ is needed to evaluate its genotoxicity. However, since information is not available, an attempt is made to calculate the 'safety' margin between actual intake by man and the conventional no-effect level in dogs and rats.

[Rapid Determination of tert-Butylhydroquinone (TBHQ) in Foods Using Three-Layer Extraction]

Shokuhin Eiseigaku Zasshi 2021;62(4):125-128.PMID:34470941DOI:10.3358/shokueishi.62.125.

A rapid, easy and versatile analytical method based on three-layer extraction was developed for the determination of tert-Butylhydroquinone (TBHQ) in foods. In this method, degreasing with n-hexane, partitioning into acetonitrile, and purification by the salting-out were simultaneously performed after extraction with acetone. It allowed to prepare a test solution without concentrating, transferring, and purification using solid phase extraction column. As a result, TBHQ for a wide variety of 11 foods met the management criteria of the guideline for validity assessment (Ministry of Health, Labour and Welfare of Japan). Thus, the present method could be useful for a rapid determination of TBHQ in foods.

tert-Butylhydroquinone (TBHQ) protects hepatocytes against lipotoxicity via inducing autophagy independently of Nrf2 activation

Biochim Biophys Acta 2014 Jan;1841(1):22-33.PMID:24055888DOI:10.1016/j.bbalip.2013.09.004.

Saturated fatty acids (SFAs) induce hepatocyte cell death, wherein oxidative stress is mechanistically involved. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a master transcriptional regulator of cellular antioxidant defense enzymes. Therefore, Nrf2 activation is regarded as an effective strategy against oxidative stress-triggered cellular damage. In this study, tert-Butylhydroquinone (TBHQ), a widely used Nrf2 activator, was initially employed to investigate the potential protective role of Nrf2 activation in SFA-induced hepatoxicity. As expected, SFA-induced hepatocyte cell death was prevented by TBHQ in both AML-12 mouse hepatocytes and HepG2 human hepatoma cells. However, the protective effect of TBHQ is Nrf2-independent, because the siRNA-mediated Nrf2 silencing did not abrogate tBHQ-conferred protection. Alternatively, our results revealed that autophagy activation was critically involved in the protective effect of TBHQ on lipotoxicity. TBHQ induced autophagy activation and autophagy inhibitors abolished TBHQ's protection. The induction of autophagy by TBHQ exposure was demonstrated by the increased accumulation of LC3 puncta, LC3-II conversion, and autophagic flux (LC3-II conversion in the presence of proteolysis inhibitors). Subsequent mechanistic investigation discovered that TBHQ exposure activated AMP-activated protein kinase (AMPK) and siRNA-mediated AMPK gene silencing abolished tBHQ-induced autophagy activation, indicating that AMPK is critically involved in tBHQ-triggered autophagy induction. Furthermore, our study provided evidence that tBHQ-induced autophagy activation is required for its Nrf2-activating property. Collectively, our data uncover a novel mechanism for TBHQ in protecting hepatocytes against SFA-induced lipotoxicity. tBHQ-triggered autophagy induction contributes not only to its hepatoprotective effect, but also to its Nrf2-activating property.

Endothelial cell metabolic memory causes cardiovascular dysfunction in diabetes

Cardiovasc Res 2022 Jan 7;118(1):196-211.PMID:33483741DOI:10.1093/cvr/cvab013.

Aims: The aim of this study was to identify the molecular mechanism for hyperglycaemia-induced metabolic memory in endothelial cells (ECs), and to show its critical importance to development of cardiovascular dysfunction in diabetes. Methods and results: Hyperglycaemia induces increased nuclear factor-κB (NF-κB) signalling, up-regulation of miR-27a-3p, down-regulation of nuclear factor erythroid-2 related factor 2 (NRF2) expression, increased transforming growth factor-β (TGF-β) signalling, down-regulation of miR-29, and induction of endothelial-to-mesenchymal transition (EndMT), all of which are memorized by ECs and not erased when switched to a low glucose condition, thereby causing perivascular fibrosis and cardiac dysfunction. Similar metabolic memory effects are found for production of nitric oxide (NO), generation of reactive oxygen species (ROS), and the mitochondrial oxygen consumption rate in two different types of ECs. The observed metabolic memory effects in ECs are blocked by NRF2 activator tert-Butylhydroquinone and a miR-27a-3p inhibitor. In vivo, the NRF2 activator and miR-27a-3p inhibitor block cardiac perivascular fibrosis and restore cardiovascular function by decreasing NF-κB signalling, down-regulating miR-27a-3p, up-regulating NRF2 expression, reducing TGF-β signalling, and inhibiting EndMT during insulin treatment of diabetes in streptozotocin-induced diabetic mice, whereas insulin alone does not improve cardiac function. Conclusions: Our data indicate that disruption of hyperglycaemia-induced EC metabolic memory is required for restoring cardiac function during treatment of diabetes, and identify a novel molecular signalling pathway of NF-κB/miR-27a-3p/NRF2/ROS/TGF-β/EndMT involved in metabolic memory.

TBHQ attenuates ferroptosis against 5-fluorouracil-induced intestinal epithelial cell injury and intestinal mucositis via activation of Nrf2

Cell Mol Biol Lett 2021 Nov 18;26(1):48.PMID:34794379DOI:10.1186/s11658-021-00294-5.

Background: Intestinal mucositis is a common side effect of chemotherapy and radiotherapy. Very few drugs can efficiently ameliorate it. Tertiary butylhydroquinone (TBHQ) is a widely used food preservative with known immunomodulatory activity. Whether it has an effect on intestinal mucositis remains unknown. In this study, we investigated the role and mechanism of action of TBHQ on 5-fluorouracil-induced (5-FU-induced) human intestinal epithelial cell (HIEC) injury and intestinal mucositis in mice. Methods: We established a cell model of HIEC injury and a mouse model of intestinal mucositis via treatment with 5-FU. Cell death, Cell Counting Kit-8, and lactate dehydrogenase (LDH) release were assessed for the HIECs. Diarrhea, body weight, intestinal length, mucosal damage, and the levels of IL-6, TNF-α, IL-1β, glutathione, reactive oxygen species, and malondialdehyde were determined for the mice. Additionally, we performed immunohistochemical analysis, immunofluorescence, western blotting, quantitative real-time PCR, and ELISA to examine the effects of TBHQ. Finally, HIECs were transfected with an Nrf2 gene silencer to verify its role in ferroptosis. All data were analyzed using one-way analysis of variance or paired t-tests. Results: TBHQ markedly decreased LDH release and cell death and improved the proliferative ability of 5-FU-treated HIECs. The TBHQ-treated mice showed reduced weight loss, a lower diarrhea score, and longer colons than the 5-FU-treated mice. The in vivo expressions of IL-1β, IL-6, and TNF-α were suppressed by TBHQ treatment. Ferroptosis was shown to be involved in 5-FU-induced intestinal mucositis, and TBHQ markedly hampered its activation. Mechanistically, TBHQ activated Nrf2 effectively and selective Nrf2 knockdown significantly reduced the anti-ferroptotic functions of TBHQ in 5-FU-treated HIECs. Conclusions: TBHQ attenuates ferroptosis in 5-FU-induced intestinal mucositis, making it a potential novel protective agent against intestinal mucositis.