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1. 2-tert-butylhydroquinone
2. 2-tertiary-butylhydroquinone
3. Mono-tert-butylhydroquinone
4. Monotertiary Butyl Hydroquinone
5. Mtbhq
6. Tbhq
1. 1948-33-0
2. Tbhq
3. 2-tert-butylhydroquinone
4. 2-tert-butylbenzene-1,4-diol
5. T-butylhydroquinone
6. Mtbhq
7. T-butyl Hydroquinone
8. 2-t-butylhydroquinone
9. Mono-tert-butylhydroquinone
10. 2-tert-butyl-1,4-benzenediol
11. Sustane
12. Mono-tertiarybutylhydroquinone
13. Tert-butyl-1,4-benzenediol
14. Tenox Tbhq
15. Tertiary-butylhydroquinone
16. 1,4-benzenediol, 2-(1,1-dimethylethyl)-
17. Hydroquinone, Tert-butyl-
18. Banox 20ba
19. 2-(1,1-dimethylethyl)-1,4-benzenediol
20. 2-tert-butyl(1,4)hydroquinone
21. 2-tertiary-butylhydroquinone
22. T-bhq
23. 2-(tert-butyl)benzene-1,4-diol
24. Tertiary Butylhydroquinone
25. Tert-butylhydrochinone
26. 2-t-butyl-1,4-benzenediol
27. Butylhydroquinone, Tert-
28. Eastman Mtbhq
29. Nsc 4972
30. Mfcd00002344
31. 1,4-benzenediol (1,1-dimethylethyl)-
32. Chebi:78886
33. Tert-butyl-hydroquinone
34. Nsc4972
35. Nsc-4972
36. 2-(1,1-dimethylethyl)benzene-1,4-diol
37. Ncgc00013051-05
38. E319
39. Dsstox_cid_220
40. C12674942b
41. Dsstox_rid_75441
42. Dsstox_gsid_20220
43. Hydroquinone, T-butyl-
44. Eyk
45. Cas-1948-33-0
46. Monotertiary Butyl Hydroquinone
47. Ccris 1447
48. Hsdb 838
49. Butylhydroquinone, T-
50. Tenox 20
51. Tert-butyl Hydroquinone
52. Einecs 217-752-2
53. Brn 0637923
54. 2-(tert-butyl)benzene-1,4-diol(may Occur To Produce Black Solid)
55. Ai3-61039
56. Sustane Tbhq
57. Tenox Tbho
58. Unii-c12674942b
59. Tenox Tbhqtbhq
60. T-butyl-hydroquinone
61. Tert-butylhydroquinon
62. 2-t-butyl Hydroquinone
63. Tert.-butyl Hydroquinone
64. 2-tert-butyl-hydroquinone
65. Tbhq [inci]
66. Tbhq [fcc]
67. Ec 217-752-2
68. Ncistruc1_000241
69. Ncistruc2_000017
70. Schembl26745
71. Tert-butylhydroquinone, 97%
72. Mls002222348
73. Butylhydroquinone,tert-
74. Mono-tertiarybuytl Hydroquinone
75. Chembl242080
76. Ins No.319
77. Dtxsid6020220
78. Ins-319
79. Nci4972
80. Hydroquinone,tertiary Butyl
81. Wln: Qr Dq Bx1&1&1
82. Kuc109743n
83. T-butylhydroquinone [hsdb]
84. Zinc388085
85. 1,4-dihydroxy-2-tert-butylbenzene
86. 2-tert-butyl-1,4-dihydroxybenzene
87. Tert-butylhydroquinone [ii]
88. Tox21_110006
89. Tox21_110007
90. Tox21_202309
91. Tox21_300081
92. Bdbm50065387
93. Ccg-37948
94. Ncgc00013051
95. S4990
96. Stk372011
97. Akos003627061
98. Cs-5774
99. Db07726
100. Ncgc00013051-01
101. Ncgc00013051-02
102. Ncgc00013051-03
103. Ncgc00013051-04
104. Ncgc00013051-06
105. Ncgc00013051-07
106. Ncgc00013051-08
107. Ncgc00013051-09
108. Ncgc00013051-10
109. Ncgc00090788-01
110. Ncgc00090788-02
111. Ncgc00090788-03
112. Ncgc00090788-04
113. Ncgc00254178-01
114. Ncgc00259858-01
115. Ac-10579
116. Bs-15862
117. Nci60_004196
118. Smr001253806
119. Sy001798
120. Tertiary Butylhydroquinone [mart.]
121. Hydroquinone,tertiary Butyl [vandf]
122. Ksc-241-078-1
123. Tert-butylhydroquinone, Analytical Standard
124. Db-019879
125. Hy-100489
126. B0833
127. E-319
128. Ft-0652102
129. 2-(1,1-dimethylethyl)-1,4-benzenediol, 9ci
130. D70420
131. Q662443
132. W-107698
133. Brd-k36452089-001-01-8
134. Brd-k36452089-001-02-6
135. F0001-0696
136. Z1945707490
| Molecular Weight | 166.22 g/mol |
|---|---|
| Molecular Formula | C10H14O2 |
| XLogP3 | 2.8 |
| Hydrogen Bond Donor Count | 2 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 1 |
| Exact Mass | 166.099379685 g/mol |
| Monoisotopic Mass | 166.099379685 g/mol |
| Topological Polar Surface Area | 40.5 Ų |
| Heavy Atom Count | 12 |
| Formal Charge | 0 |
| Complexity | 148 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
/EXPL THER/ /The objective was/ to investigate the protective effect of tert-butylhydroquinone on bone marrow cells in rats from cytotoxicity induced by benzene in vitro. The bone marrow cells in rats were divided into two groups randomizedly. Cells of the control group were stimulated by 0, 5, 10, 15, 20 mmol/L benzene for 2, 4, 6 hours respectively. Cells of the tBHQ-pretreated group were treated by 100 umol/L tBHQ for 12 hours followed by the same conditions as the control group. The DNA damage was detected by single cell gel electrophoresis assay (SCGE) and cell apoptosis was examined by flow cytometry. The activities of NAD (P) H: quinone oxidoreductase (NQO1) in bone marrow cells of rats were also measured before benzene treatment in two groups. In the control group, the DNA damage and the apoptosis of bone marrow cells was increased with the growing concentration and time of benzene treatment. The DNA migration and the lengths of DNA migration of the bone marrow cells in the rats under 5, 10, 15, 20 mmol/L benzene treatment in the tBHQ-pretreated group were significantly lower than those in control group at the same time point (p<0.05). The apoptosis of the bone marrow cells in the rats stimulated by 15, 20 mmol/L benzene for 2 hours and 10, 15, 20 mmol/L benzene for 4 hours as well as 5, 10, 15, 20 mmol/L benzene for 6 hours were also significantly lower than those in control group (p<0.05). The activities of NQO1 in the bone marrow cells in the rats were increased after tBHQ treatment (p<0.01) (1.62 +/- 0.16 min(-1).mg(-1) vs. the control group: 0.95 +/- 0.08 min(-1).mg(-1)). Benzene can induce the DNA damage and the apoptosis of bone marrow cells in rats in a time dependent and dose dependent manner to some extent. tBHQ can protect the bone marrow cells in rats from the cytotoxicity induced by benzene, which can be partly explained by the increase of the NQO1 activity induced by tBHQ.
PMID:16600132 Zhao ZW et al; Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 24 (3): 143-6 (2006)
/EXPL THER/ ... In this study, we evaluated whether tBHQ pretreatment prevented renal damage induced by ischemia and reperfusion (I/R). Four groups of rats were studied: (a) control-sham (CT), (b) tBHQ-sham (tBHQ), (c) I/R and (d) tBHQ + I/R. Intraperitoneal (i.p.) injections of tBHQ (50 mg/kg) were given to the tBHQ and tBHQ + I/R groups and 3% ethanol/isotonic saline solution to the CT and I/R groups. Animals were killed 24 hours after I/R. tBHQ attenuated I/R-induced renal dysfunction, structural damage, oxidative/nitrosative stress, glutathione depletion and the decrease in several antioxidant enzymes. The renoprotective effect of tBHQ on I/R injury was associated with the attenuation in oxidative/nitrosative stress and the preservation of antioxidant enzymes.
PMID:21607921 Guerrero-Beltran CE et al; J Nephrol 25(1):84-9 (2012)
/EXPL THER/ Cis-diamminedichloroplatinum II (CDDP)-induced nephrotoxicity is associated with the overproduction of reactive oxygen species. ... The purpose of this study was to investigate the ability of tBHQ to prevent the nephrotoxic effect of CDDP in rats as well as the mechanisms involved. Thirty-six Wistar rats divided in the following groups were used: control, tBHQ (12.5 mg/kg), CDDP (7.5 mg/kg) and tBHQ+CDDP. Twenty-four hr urine was collected at the beginning and at the end of the experiment and the rats were sacrificed 72 hr after CDDP-administration. Histological studies were performed and markers of renal function and oxidative/nitrosative stress were measured. In addition, the activity of the following antioxidant enzymes was measured: glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GR) and glutathione-S-transferase (GST). CDDP-induced renal dysfunction, structural damage and oxidative/nitrosative were prevented by tBHQ. In addition, tBHQ completely prevented the CDDP-induced fall in GPx and GST activities. In conclusion, the present study indicates that the antioxidant activity of tBHQ is associated with its nephroprotective effect against CDDP-induced acute kidney injury in rats.
PMID:21802473 Perez-Rojas JM et al; Food Chem Toxicol 49 (10): 2631-7 (2011)
/EXPL THER/ The present study was aimed at determining the role of paraquat (PQ) in the activation of the NF-E2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway and the possible neuroprotective effects of tert-butylhydroquinone (tBHQ) pretreatment on PQ-induced neurodegeneration in vivo and in vitro. 7 mg/kg PQ treatment of male C57BL/6 mice caused decreased spontaneous locomotor activity, decreased tyrosine hydroxylase (TH)-positive neurons, increased terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end-labeling (TUNEL)-positive cells in the substantia nigra, as well as increased protein levels of both nuclear Nrf2 and HO-1. In PQ-treated mice, pretreatment with 1% tBHQ (w/w) significantly attenuated impairments in behavioral performance, decreased TH-positive neurons, and increased TUNEL-positive cells in the substantia nigra, as well as increased protein expression of both nuclear Nrf2 and HO-1. Pretreatment with 40 uM tBHQ protected PC12 cells against 100 and 300 uM PQ-mediated cytotoxicity. The dual-luciferase reporter gene also revealed that the transcriptional activation of HO-1 gene expression of the antioxidant responsive element via Nrf2 occurred as a consequence of 100 and 300 uM PQ exposure. Collectively, these results clearly indicated for the first time that the Nrf2/HO-1 pathway in the substantia nigra was activated by PQ, and pretreatment with tBHQ conferred neuroprotection against PQ-induced Parkinsonism presumably by increasing Nrf2 and HO-1 expression.
PMID:22983789 Li H et al; Arch Toxicol 86 (11): 1729-40 (2012)
For more Therapeutic Uses (Complete) data for T-BUTYLHYDROQUINONE (7 total), please visit the HSDB record page.
Enzyme Inhibitors
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)
Antioxidants
Naturally occurring or synthetic substances that inhibit or retard oxidation reactions. They counteract the damaging effects of oxidation in animal tissues. (See all compounds classified as Antioxidants.)
TBHQ is readily metabolized. In mouse studies, metabolism primarily involved oxidation at the tert-butyl group, followed by formation of the glucuronide conjugate and excretion in the urine, or by excretion of the free acid in feces. In rats, 80-90% of the (14)C-radiolabel was excreted in urine or feces within 96 hours, mostly as the free acid in feces with smaller amounts in urine, and less than 0.3% in expired air. More than 43 metabolites were present in the urine and feces of mice and rats. In several studies with rats and dogs, TBHQ by the oral route was shown to be well absorbed and rapidly excreted, mainly in the urine. Primary urinary metabolites in both species are the 4-O-sulfate conjugate and the 4-O-glucuronide. Excretion seems to be essentially complete after 4 days.
EPA/Office of Prevention, Pesticides, and Toxic Substances; Memorandum: Reassessment of One Exemption from the Requirement of a Tolerance For tertiary-Butylhydroquinone (CAS Reg. No. 1948-33-0) p. 12-3 (2006). Available from, as of October 12, 2016: https://www3.epa.gov/
The dominant metabolic pathway of the presumably carcinogenic food antioxidant 2(3)-tert-butyl-4-hydroxyanisole includes O-demethylation to 2-tert-butyl(1,4)hydroquinone and subsequent peroxidation to 2-tert-butyl(1,4)paraquinone. ...
PMID:8384088 Schilderman P A EL et al; Carcinogenesis (OXF) 14 (3): 347-53 (1993)
The tert-butylsemiquinone anion radical is formed from tert-butylhydroquinone and from tert-butylquinone in rat liver microsomes.
PMID:1325685 Bergmann B et al; Toxicology 74 (2-3): 127-33 (1992)
After ip administration of 3-tert-butyl-4-hydroxyanisole to rats two previously undocumented metabolites 2-tert-butyl-5-methylthiohydroquinone and 2-tert-butyl-6-methylthiohydroquinone were identified in the urine. In addition to these metabolites 3-tert-butyl-4,5-dihydroxyanisole was also detected in the urine hydrolyzed by beta-glucuronidase/sulfatase. Administration of tert-butylhydroquinone, an O-demethylated metabolite of 3-tert-butyl-4-hydroxyanisole, also resulted in the formation of the S-containing metabolites, 2-tert-butyl-5-methylthiohydroquinone and 2-tert-butyl-6-methylthiohydroquinone. After incubation of tert-butylhydroquinone with rat liver microsomes in the presence of glutathione, two metabolites were isolated and purified by HPLC. The metabolites were identified as 2-tert-butyl-5-(glutathione-S-yl)hydroquinone and 2-tert-butyl-6-(glutathione-S-yl)hydroquinone.The formation of tert-butyl hydroquinone-glutathione conjugates required NADPH molecular oxygen and glutathione. Cytochrome p450 inhibitors such as SKF 525-A and metyrapone markedly inhibited the formation of tert-butylhydroquinone-glutathione conjugates in vitro. tert-Butylhydroquinone is converted by cytochrome p450-mediated monooxygenases to a reactive metabolite 2-tert-butyl-p-benzoquinone which then conjugates with glutathione to form tert-butylhydroquinone-glutathione conjugates. Glutathione S-transferase activities do not seen to play a role in glutathione conjugation reaction of 2-tert-butyl-p-benzoquinone because cytosol fraction from rat liver homogenates did not enhance the microsome-mediated production of tert-butylhydroquinone-glutathione conjugates.
PMID:1687007 Tajima K et al; Drug Metab Dispos 19 (6): 1028-33 (1991)
... In this study, tert-butylhydroquinone (tBHQ), a widely used Nrf2 activator, was initially employed to investigate the potential protective role of Nrf2 activation in saturated fatty acid (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.
PMID:24055888 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3884638 Li S et al; Biochim Biophys Acta 1841 (1): 22-33 (2014)
/An/ outbreak of H7N9 influenza in China /was/ of high concern to public health. H7 hemagglutinin (HA) plays a critical role in influenza entry and thus HA presents an attractive target for antivirals. Previous studies have suggested that the small molecule tert-butyl hydroquinone (TBHQ) inhibits the entry of influenza H3 HA by binding to the stem loop of HA and stabilizing the neutral pH conformation of HA, thereby disrupting the membrane fusion step. Based on amino acid sequence, structure and immunogenicity, H7 is a related Group 2 HA. In this work we show, using a pseudovirus entry assay, that TBHQ inhibits H7 HA-mediated entry, as well as H3 HA-mediated entry, with an IC50 ~ 6 uM. Using NMR, we show that TBHQ binds to the H7 stem loop region. STD NMR experiments indicate that the aromatic ring of TBHQ makes extensive contact with the H7 HA surface. Limited proteolysis experiments indicate that TBHQ inhibits influenza entry by stabilizing the H7 HA neutral pH conformation. Together, this work suggests that the stem loop region of H7 HA is an attractive target for therapeutic intervention and that TBHQ, which is a widely used food preservative, is a promising lead compound.
PMID:24194835 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3806803 Antanasijevic A et al; PLoS One 8 (10): e76363 (2013)
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