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Chemical Compound Review

CHEMBL192451     4-methoxy-2-tert-butyl-phenol

Synonyms: CCRIS 3746, AG-D-45687, ACMC-209a8y, CHEBI:76358, ANW-17552, ...
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Psychiatry related information on BUTYLATED HYDROXYANISOLE

  • After hatching, swim-up, and the onset of vigorous feeding behavior (2 weeks pest swim-up), duplicate groups of 60 AFB1-treated and sham-treated fry were started on a test diet containing 0.6% (6000 ppm) BHA, and the other duplicate groups of treated and untreated fry were fed the control Oregon Test Diet (OTD) [5].
  • Information gleaned from the BHA and EDB studies with multiple animal species facilitated regulatory decision-making regarding the potential toxicity/carcinogenicity of these compounds to man [6].
  • In the maintenance of shelf-stability, nutritional and organoleptic properties of ground melon 'egusi'-Colocynthis citrullus L., vacuum-packaged samples were found to be better than unpackaged samples and samples treated with 0.2% butylated hydroxyanisole (BHA) and 0.02% BHA + 0.045% sodium metabisulphite [7].

High impact information on BUTYLATED HYDROXYANISOLE


Chemical compound and disease context of BUTYLATED HYDROXYANISOLE

  • Rats were fed either a 2(3)-tert-butyl-4-hydroxyanisole (0.5% w/w)- or ethoxyquin (0.5% w/w)-containing diet with or without ciprofibrate (10 mg/kg of body weight) for 60 weeks [12].
  • While non-hepatocarcinogens exerted no such effects, their influence being limited to inducing lesions in their own respective target organs such as urinary bladder cancers in the EHBN case and glandular stomach adenocarcinomas with MNNG, BHA demonstrated inhibition potential in both experiments [13].
  • Inhibition of prostaglandin H synthase by ASA in cultures treated with TBHQ decreased the oxidation ratio significantly, confirming the significance of this enzyme system in the mechanism of toxicity of BHA [14].
  • We have tested this hypothesis by examining the ability of butylated hydroxyanisole (BHA), ethoxyquin, and other antioxidants to prevent thyroiditis in Obese strain (OS) chickens, a strain that develops severe disease by 4 weeks of age [15].
  • However, the incidence and multiplicity of papillomas in the group given BHA + DHEA + RNs were again elevated [16].




  • The data showed that BHA feeding resulted in altered properties of liver microsomes, including a decrease in BP metabolite binding to DNA [21].
  • Incubation of BP with liver microsomes from mice that received BHA 2,4, or 8 hours before being killed resulted in less binding of BP metabolites to added DNA than occurred with control microsomes [3].
  • Whereas the 2 antioxidants BHA and TC inhibited the incidence of both liver and pancreatic lesions, CA, itself giving rise to considerable numbers of enzyme-altered foci, enhanced carcinogenesis in the liver while inhibiting carcinogenesis in the pancreas [22].
  • However, BHA has multiple biologic actions so that its inhibitory effect on MAM acetate-induced neoplasia of the large intestine may entail some other mechanism [23].
  • Incubation of BP and calf thymus DNA with liver microsomes from BHA-fed mice showed about half the binding of BP metabolites to DNA as compared to that of controls [21].

Associations of BUTYLATED HYDROXYANISOLE with other chemical compounds



  • Activation of ERK2 by BHA was rapid and transient, whereas the JNK1 activation was relatively delayed and persistent [28].
  • Amongst class Pi transferase subunits, the constitutive hepatic level of mRNA for Gstp1 and Gstp2 was not substantially affected in the KO mice, but their induction by BHA was dependent on Nrf2; this was more obvious in female mutant mice than in male mice [29].
  • We next examined the phosphorylation of the MAPKs, and found that BHA significantly increased the phosphorylation levels of ERK1/2 and JNK1/2 [30].
  • Semi-quantitative RT-PCR study and microarray analysis revealed that HO-1 and NQO1 were transcriptionally activated in primary-cultured rat hepatocytes and a substantial transcriptional activation, including HO-1 occurred in primary-cultured human hepatocytes after BHA treatment [31].
  • Non-significant modulation of catalase activity by BHA was also noted [32].

Analytical, diagnostic and therapeutic context of BUTYLATED HYDROXYANISOLE


  1. Dose response in butylated hydroxyanisole induction of forestomach carcinogenesis in F344 rats. Ito, N., Fukushima, S., Tamano, S., Hirose, M., Hagiwara, A. J. Natl. Cancer Inst. (1986) [Pubmed]
  2. Effects of butylated hydroxyanisole, butylated hydroxytoluene, and NaCl on gastric carcinogenesis initiated with N-methyl-N'-nitro-N-nitrosoguanidine in F344 rats. Shirai, T., Fukushima, S., Ohshima, M., Masuda, A., Ito, N. J. Natl. Cancer Inst. (1984) [Pubmed]
  3. Effects of administration to mice of butylated hydroxyanisole by oral intubation on benzo[a]pyrene-induced pulmonary adenoma formation and metabolism of benzo[a]pyrene. Speier, J.L., Lam, L.K., Wattenberg, L.W. J. Natl. Cancer Inst. (1978) [Pubmed]
  4. Inhibition of promutagen activation by the antioxidants butylated hydroxyanisole and butylated hydroxytoluene. McKee, R.H., Tometsko, A.M. J. Natl. Cancer Inst. (1979) [Pubmed]
  5. Long-term, high-dose dietary exposure of rainbow trout to butylated hydroxyanisole is non-carcinogenic. Hendricks, J.D., Arbogast, D.N., Pereira, C.B., Bailey, G.S. Cancer Lett. (1994) [Pubmed]
  6. Forestomach lesions induced by butylated hydroxyanisole and ethylene dibromide: a scientific and regulatory perspective. Moch, R.W. Toxicologic pathology. (1988) [Pubmed]
  7. Effect of sample pretreatments on the storability of ground melon 'egusi'-Colocynthis citrillus L. Adegoke, G.O., Ndife, J. Plant foods for human nutrition (Dordrecht, Netherlands) (1993) [Pubmed]
  8. Dual signaling of the Fas receptor: initiation of both apoptotic and necrotic cell death pathways. Vercammen, D., Brouckaert, G., Denecker, G., Van de Craen, M., Declercq, W., Fiers, W., Vandenabeele, P. J. Exp. Med. (1998) [Pubmed]
  9. Mutagens from heated Chinese and U.S. cooking oils. Shields, P.G., Xu, G.X., Blot, W.J., Fraumeni, J.F., Trivers, G.E., Pellizzari, E.D., Qu, Y.H., Gao, Y.T., Harris, C.C. J. Natl. Cancer Inst. (1995) [Pubmed]
  10. Polyunsaturated fatty acid-induced cytotoxicity against tumor cells and its relationship to lipid peroxidation. Bégin, M.E., Ells, G., Horrobin, D.F. J. Natl. Cancer Inst. (1988) [Pubmed]
  11. Comparison of lesions induced in the Syrian golden hamster by diethylnitrosamine, dimethylhydrazine, and dibutylnitrosamine: influence of subsequent butylated hydroxyanisole treatment. Moore, M.A., Thamavit, W., Ito, N. J. Natl. Cancer Inst. (1987) [Pubmed]
  12. Inhibitory effect of antioxidants ethoxyquin and 2(3)-tert-butyl-4-hydroxyanisole on hepatic tumorigenesis in rats fed ciprofibrate, a peroxisome proliferator. Rao, M.S., Lalwani, N.D., Watanabe, T.K., Reddy, J.K. Cancer Res. (1984) [Pubmed]
  13. Correlation between medium-term liver bioassay system data and results of long-term testing in rats. Ogiso, T., Tatematsu, M., Tamano, S., Hasegawa, R., Ito, N. Carcinogenesis (1990) [Pubmed]
  14. Induction of oxidative DNA damages and enhancement of cell proliferation in human lymphocytes in vitro by butylated hydroxyanisole. Schilderman, P.A., Rhijnsburger, E., Zwingmann, I., Kleinjans, J.C. Carcinogenesis (1995) [Pubmed]
  15. Antioxidants delay the onset of thyroiditis in obese strain chickens. Bagchi, N., Brown, T.R., Herdegen, D.M., Dhar, A., Sundick, R.S. Endocrinology (1990) [Pubmed]
  16. Inhibition by dehydroepiandrosterone of butylated hydroxyanisole (BHA) promotion of rat-bladder carcinogenesis and enhancement of BHA-induced forestomach hyperplasia. Shibata, M.A., Shirai, T., Asakawa, E., Hirose, M., Fukushima, S. Int. J. Cancer (1993) [Pubmed]
  17. Cytokine suppression of protease activation in wild-type p53-dependent and p53-independent apoptosis. Lotem, J., Sachs, L. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  18. Induction of cell proliferation in the forestomach of F344 rats following subchronic administration of styrene 7,8-oxide and butylated hydroxyanisole. Cantoreggi, S., Dietrich, D.R., Lutz, W.K. Cancer Res. (1993) [Pubmed]
  19. Rapid regression of squamous cell hyperplasia and slow regression of basal cell hyperplasia in the forestomach of F344 rats treated with N-methyl-N'-nitro-N-nitrosoguanidine and/or butylated hydroxyanisole. Tatematsu, M., Ogawa, K., Mutai, M., Aoki, T., Hoshiya, T., Ito, N. Cancer Res. (1991) [Pubmed]
  20. Dose-response relationships for the binding of benzo(a)pyrene metabolites to DNA and protein in lung, liver, and forestomach of control and butylated hydroxyanisole-treated mice. Adriaenssens, P.I., White, C.M., Anderson, M.W. Cancer Res. (1983) [Pubmed]
  21. Alterations in microsomal metabolism of benzo[a]pyrene in mice fed butylated hydroxyanisole. Speier, J.L., Wattenberg, L.W. J. Natl. Cancer Inst. (1975) [Pubmed]
  22. Differential modification of development of preneoplastic lesions in the Syrian golden hamster initiated with a single dose of 2,2'-dioxo-N-nitrosodipropylamine: influence of subsequent butylated hydroxyanisole, alpha-tocopherol, or carbazole. Moore, M.A., Tsuda, H., Thamavit, W., Masui, T., Ito, N. J. Natl. Cancer Inst. (1987) [Pubmed]
  23. Inhibitory effects of butylated hydroxyanisole on methylazoxymethanol acetate-induced neoplasia of the large intestine and on nicotinamide adenine dinucleotide-dependent alcohol dehydrogenase activity in mice. Wattenberg, L.W., Sparnins, V.L. J. Natl. Cancer Inst. (1979) [Pubmed]
  24. Modulation of azaserine-induced pancreatic foci by phenolic antioxidants in rats. Roebuck, B.D., MacMillan, D.L., Bush, D.M., Kensler, T.W. J. Natl. Cancer Inst. (1984) [Pubmed]
  25. Superoxide-mediated modification of low density lipoprotein by arterial smooth muscle cells. Heinecke, J.W., Baker, L., Rosen, H., Chait, A. J. Clin. Invest. (1986) [Pubmed]
  26. Histologic and autoradiographic studies on the forestomach of hamsters treated with 2-tert-butylated hydroxyanisole, 3-tert-butylated hydroxyanisole, crude butylated hydroxyanisole, or butylated hydroxytoluene. Hirose, M., Masuda, A., Kurata, Y., Ikawa, E., Mera, Y., Ito, N. J. Natl. Cancer Inst. (1986) [Pubmed]
  27. Induction of DT-diaphorase by anticarcinogenic sulfur compounds in mice. Benson, A.M., Barretto, P.B., Stanley, J.S. J. Natl. Cancer Inst. (1986) [Pubmed]
  28. Butylated hydroxyanisole and its metabolite tert-butylhydroquinone differentially regulate mitogen-activated protein kinases. The role of oxidative stress in the activation of mitogen-activated protein kinases by phenolic antioxidants. Yu, R., Tan, T.H., Kong, A.T. J. Biol. Chem. (1997) [Pubmed]
  29. Loss of the Nrf2 transcription factor causes a marked reduction in constitutive and inducible expression of the glutathione S-transferase Gsta1, Gsta2, Gstm1, Gstm2, Gstm3 and Gstm4 genes in the livers of male and female mice. Chanas, S.A., Jiang, Q., McMahon, M., McWalter, G.K., McLellan, L.I., Elcombe, C.R., Henderson, C.J., Wolf, C.R., Moffat, G.J., Itoh, K., Yamamoto, M., Hayes, J.D. Biochem. J. (2002) [Pubmed]
  30. Butylated hydroxyanisole regulates ARE-mediated gene expression via Nrf2 coupled with ERK and JNK signaling pathway in HepG2 cells. Yuan, X., Xu, C., Pan, Z., Keum, Y.S., Kim, J.H., Shen, G., Yu, S., Oo, K.T., Ma, J., Kong, A.N. Mol. Carcinog. (2006) [Pubmed]
  31. Induction of Heme Oxygenase-1 (HO-1) and NAD[P]H: Quinone Oxidoreductase 1 (NQO1) by a Phenolic Antioxidant, Butylated Hydroxyanisole (BHA) and Its Metabolite, tert-Butylhydroquinone (tBHQ) in Primary-Cultured Human and Rat Hepatocytes. Keum, Y.S., Han, Y.H., Liew, C., Kim, J.H., Xu, C., Yuan, X., Shakarjian, M.P., Chong, S., Kong, A.N. Pharm. Res. (2006) [Pubmed]
  32. Augmentation of chrysotile-induced oxidative stress by BHA in mice lungs. Ahmad, I., Krishnamurthi, K., Arif, J.M., Ashquin, M., Mahmood, N., Athar, M., Rahman, Q. Food Chem. Toxicol. (1995) [Pubmed]
  33. Neoplastic effects of oral administration of (+/-)-trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene and their inhibition by butylated hydroxyanisole. Wattenberg, L.W., Jerina, D.M., Lam, L.K., Yagi, H. J. Natl. Cancer Inst. (1979) [Pubmed]
  34. Antioxidant treatment of thymic organ cultures decreases NF-kappa B and TCF1(alpha) transcription factor activities and inhibits alpha beta T cell development. Ivanov, V., Merkenschlager, M., Ceredig, R. J. Immunol. (1993) [Pubmed]
  35. Induction of c-fos and c-jun gene expression by phenolic antioxidants. Choi, H.S., Moore, D.D. Mol. Endocrinol. (1993) [Pubmed]
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