TBHQ

Catalog No.S4990 Batch:S499005

Print

Technical Data

Formula

C10H14O2

Molecular Weight 166.22 CAS No. 1948-33-0
Solubility (25°C)* In vitro DMSO 33 mg/mL (198.53 mM)
Ethanol 33 mg/mL (198.53 mM)
Water 4 mg/mL (24.06 mM)
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description 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.
Targets
Nrf2 [1]
In vitro 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].
In vivo 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].

Protocol (from reference)

Cell Assay:

[1]

  • Cell lines

    HeLa cells

  • Concentrations

    0-15 μM

  • Incubation Time

    1 h

  • Method

    HeLa cells are grown until confluent and loaded with 100 µM DCF in loading medium (DMEM with 1% FBS) for 30 min. Cells are washed and then treated with tBHQ (0-15 μM in DMSO) for 1 h. DCF fluorescence is followed in a fluorometer at 488-nm excitation and 520-nm emission.

Animal Study:

[2]

  • Animal Models

    male C57BL/6 mice

  • Dosages

    ratio of 1% (w/w) with the animal food powder

  • Administration

    oral

Selleck's TBHQ has been cited by 19 publications

Inhibition of insulin degrading enzyme suppresses osteoclast hyperactivity via enhancing Nrf2-dependent antioxidant response in glucocorticoid-induced osteonecrosis of the femoral head [ Mol Med, 2024, 30(1):111] PubMed: 39085816
BATF is involved in the malignant phenotype and epithelial-mesenchymal transition of colon cancer cells via ERK/PD-L1 signaling [ Histol Histopathol, 2024, 27:18823] PubMed: 39439410
DDRGK1 Enhances Osteosarcoma Chemoresistance via Inhibiting KEAP1-Mediated NRF2 Ubiquitination [ Adv Sci (Weinh), 2023, 10(14):e2204438] PubMed: 36965071
STING Suppresses Mitochondrial VDAC2 to Govern RCC Growth Independent of Innate Immunity [ Adv Sci (Weinh), 2023, 10(3):e2203718] PubMed: 36445063
Fighting cancer by triggering non-canonical mitochondrial permeability transition-driven necrosis through reactive oxygen species induction [ Free Radic Biol Med, 2023, 202:35-45] PubMed: 36963639
NRF2 is a critical regulator and therapeutic target of metal implant particle-incurred bone damage [ Biomaterials, 2022, 288:121742] PubMed: 36030105
AADAC protects colorectal cancer liver colonization from ferroptosis through SLC7A11-dependent inhibition of lipid peroxidation [ J Exp Clin Cancer Res, 2022, 41(1):284] PubMed: 36163032
Dihydrotanshinone I inhibits ovarian tumor growth by activating oxidative stress through Keap1-mediated Nrf2 ubiquitination degradation [ Free Radic Biol Med, 2022, 180:220-235] PubMed: 35074488
Vitamin D3 protects against nitrogen mustard-induced apoptosis of the bronchial epithelial cells via activating the VDR/Nrf2/Sirt3 pathway [ Toxicol Lett, 2022, 354:14-23] PubMed: 34757179
TBHQ attenuates ferroptosis against 5-fluorouracil-induced intestinal epithelial cell injury and intestinal mucositis via activation of Nrf2 [ Cell Mol Biol Lett, 2021, 26(1):48] PubMed: 34794379

RETURN POLICY
Selleck Chemical’s Unconditional Return Policy ensures a smooth online shopping experience for our customers. If you are in any way unsatisfied with your purchase, you may return any item(s) within 7 days of receiving it. In the event of product quality issues, either protocol related or product related problems, you may return any item(s) within 365 days from the original purchase date. Please follow the instructions below when returning products.

SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.