PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Butylated Hydroxytoluene”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1979

Inhibition of promutagen activation by the antioxidants butylated hydroxyanisole and butylated hydroxytoluene.

Butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) exhibited antimutagenic activity in the Salmonella typhimurium reversion test. Both BHA and BHT reduced reversion induced by chemicals requiring metabolic activation for effectiveness. However, they did not affect reversion induced by direct-acting mutagens. These results suggested that BHA and BHT may inhibit the metabolic activation processes and demonstrated that the S. typhimurium reversion test may be used to identify inhibitors of the neoplastic process.

Animals↗
PubMed1978

Inactivation of cytomegalovirus and Semliki Forest virus by butylated hydroxytoluene.

Butylated hydroxytoluene (BHT) is an antioxidant that is widely used in foods because it prevents spoilage by delaying degradation of lipid components. This hydrophobic compound inactivated human and murine cytomegalovirus (CMV) and Semliki Forest virus (SFV). Both human and murine CMV were inactivated more than 90% by 40 microgram of BHT/ml after incubation for 1 hr at 37 C. Under the same conditions, SVF was inactivated about 75%, whereas poliovirus, which does not contain lipid membrane as a part of its structure, was not inactivated at all. Vaccinia virus was less sensitive to BHT than was CMV or SFV.

Animals↗
PubMed1985

Treatment of recurrent herpes simplex labialis with topical butylated hydroxytoluene.

Butylated hydroxytoluene (BHT) is a hydrophobic compound with in vitro activity against many enveloped viruses, including herpes simplex virus. The effect of topical therapy with 15% BHT in mineral oil on the course of recurrent herpes simplex labialis was examined in 30 patients in a double-blind, placebo-controlled pilot study in which treatment was initiated by the physician. Sixteen patients received BHT and 14 received the placebo mineral oil vehicle. The time from lesion onset to dry crust formation was slightly shorter among BHT recipients than among placebo recipients (2.0 and 2.4 days; P = 0.01). Duration of the vesicle-ulcer stages was likewise shorter (1.2 and 2.0 days; P = 0.09), and lesion virus excretion appeared to be less in the subjects who received BHT than in the controls, but these differences were not significant. There was no clinical or laboratory evidence of toxicity.

Administration, Topical↗
PubMedDate not supplied

Reduction of 2-acetylaminofluorene-induced unscheduled DNA synthesis in human and rat hepatocytes by butylated hydroxytoluene.

Butylated hydroxytoluene (BHT) protected against DNA damage induced in rat hepatocytes by 2-acetylaminofluorene (2AAF) or N-hydroxy 2AAF as shown by a marked reduction of unscheduled DNA synthesis. BHT also inhibited 2AAF-induced DNA damage (as shown by reduced repair) in human hepatocytes. In addition, rats pre-treated with BHT in the diet (0.5% w/w for 10 days) provided hepatocytes which exhibited less unscheduled DNA synthesis than did hepatocytes from control rats when these cells were exposed to either 2AAF or N-hydroxy 2AAF. The results indicate both direct (in vitro) and indirect (by pre-treatment in vivo) inhibitory effects of BHT on the genotoxicity of 2AAF in liver cells, in accord with the reported anti-tumorigenicity in the liver. This effect contracts with a BHT-mediated increase in the efflux of 2AAF-derived mutagens from liver cells which may contribute to enhanced extrahepatic carcinogenesis.

2-Acetylaminofluorene↗
PubMed1978

Stimulation of DNA synthesis in mouse and rat lung following administration and butylated hydroxytoluene.

Butylated hydroxytoluene (BHT) is a widely used antioxidant in food. It has recently been reported that intraperitoneal injection of BHT to female mice produced, within 3-5 days, a hypertrophy, hyperplasia, and general disorganisation of the cellular components of the lung (Marion and Mitchell, 1972). In male mice it was shown that this effect of BHT was associated with a marked stimulation of DNA synthesis in the lung (Witschi and Saheb, 1974). Measuring the incorporation of thymidine-2-14C into DNA in lung confirmed the results reported in mice. 500 mg of BHT per kg, i.p., resulted in a 20-40 fold increase in thymidine incorporation in both male and female mice after 4 days. In similar experiments in the rat, however, a two-fold increase was observed in female rats, no effect could be demonstrated in male rats. In experiments in male and female mice using p.o. administration of BHT similar results have been obtained as following i.p. administration.

Animals↗
PubMed1990

Comparison of lung injury induced in 4 strains of mice by butylated hydroxytoluene.

Butylated hydroxytoluene (BHT) is a phenolic antioxidant which induces lung injury in all strains of mice which have been tested, but not in any other species. The mortality of mice treated with BHT is also highly strain-dependent, with LD50s ranging from 138 to 1739 mg/kg. Despite this wide range of toxic doses, the relationship between lung damage and dose has not been well studied. The data presented here demonstrate that BALB/c, ICR and C57BL/6NHsd mice, with LD50s of 1739, 1243 and 917 respectively, exhibit similar time courses of repair (as assessed by the incorporation of radiolabelled thymidine into DNA) and pulmonary fibrosis (as assessed by lung hydroxyproline content) when given a single 400 mg/kg dose of BHT. SSIn mice, with an LD50 of approximately 350 mg/kg, also exhibited a similar time course of repair when given a single dose of 300 mg/kg BHT, although fibrosis did not develop in these animals. These data indicate that all strains of mice develop similar levels of lung injury at equivalent doses and that the extent of lung damage produced in mice does not correlate with the lethal dose.

Animals↗
PubMed1992

Review of the mutagenicity/genotoxicity of butylated hydroxytoluene.

Butylated hydroxytoluene (BHT) is an effective, widely used, low cost antioxidant. A host of studies examining the potential of BHT to cause point mutations have been published. They include in vitro studies on various bacterial species and strains and on various types of mammalian cell lines as well as in vivo studies on Drosophila melanogaster, silk worms and also the mouse specific locus test (involving long-term exposure). Together these studies convincingly show the absence of a potential for BHT to cause point mutations. A great number of studies on many cell types and species have also been carried out to examine the potential of BHT to cause chromosome aberrations. In vitro studies have been published using plant cells and the WI-38, CHL, CHO, and V79 mammalian cell lines. In vivo studies have been carried out on somatic and/or germ cells of Drosophila melanogaster, rats and mice. Nearly all studies, especially those using validated test systems, indicate that BHT lacks clastogenic potential. In vitro studies on bacterial, yeast and various mammalian cell lines including DON, CHO, CHL cells and primary hepatocytes demonstrate the absence of interactions with or damage to DNA. Taking all the existing data into account, the weight of evidence suggests that BHT does not represent a relevant mutagenic/genotoxic risk to man.

Animals↗
PubMed1985

Decrease in the protein kinase C-catalyzed phosphorylation of an endogenous lung protein (Mr 36,000) following treatment of mice with the tumor-modulatory agent butylated hydroxytoluene.

Butylated hydroxytoluene (BHT) causes transient lung damage in mice, and it can either inhibit or enhance carcinogen induction of tumors in internal organs, such as urethan-induced lung adenomas. Since protein kinase C (Pk-C) may mediate the action of one class of tumor-modulatory agents, the phorbol esters which promote skin tumorigenesis, we are examining the hypothesis that Pk-C is involved in the modulatory effects of BHT on internal organs. Endogenous phosphorylation of a Mr 36,000 cytosolic protein (p36) with a pI of 5.7 was demonstrable in extracts from lung and spleen but not from brain or heart. Phosphorylation required the presence of both Ca2+ and phosphatidylserine, and phosphate was incorporated into seryl and threonyl residues but not into tyrosyl residues. This reaction thus has the characteristics of Pk-C-dependent catalysis. A single i.p. injection of BHT (400 mg/kg body weight) decreased p36 phosphorylation severalfold in both BALB/cByJ and A/J mice. This decrease correlated with the extent of BHT-induced lung damage with regard to both the time course following BHT administration and the dose dependence of BHT. All of the pulmonary effects of BHT are abolished if the mice are pretreated with cedrene, an inducer of drug-detoxifying enzymes. Such treatment with cedrene prevented any BHT-induced decrease in p36 phosphorylation. A decrease in Pk-C specific activity, as measured using histone as an exogenous substrate, which resulted upon BHT treatment may provide a mechanism for decreased p36 phosphorylation. The specificity of this toxicity-related effect of BHT is emphasized by the fact that urethan injection did not detectably affect the phosphorylation of any lung proteins. Both p36 phosphorylation and Pk-C specific activity increased as a function of postnatal age. Thus the extent of p36 phosphorylation was inversely related to the extent of lung cell proliferation in two different physiological states, postnatal growth and regenerative repair following BHT-induced toxic injury. A single BHT injection is sufficient to cause lung toxicity, tumor prophylaxis, or cocarcinogenesis, while tumor promotion requires chronic treatment. P36 phosphorylation also decreased when mice were given multiple BHT injections over a period of 5 weeks. These results are consistent with a hypothesis that decreased Pk-C-dependent phosphorylation of p36 is involved in lung tumor modulation by BHT.

Animals↗
PubMed1978

Cytotoxicity of butylated hydroxytoluene and butylated hydroxyanisole in cultured heart cells.

Butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA) at concentrations of 100 ppm (0.45 and 0.55 mM, respectively) produced a marked leakage of lactic dehydrogenase (LDH) from cultured myocardial and endotheloid cells into the culture medium. At this concentration both BHT and BHA markedly depressed the beating rate of cultured heart cells with maximum inhibition occurring within 1 h after antioxidant exposure. Morphologically the appearance of cells in the presence of 100 ppm BHT and BHA was similar to the appearance of control cells. However, when BHT and BHA concentrations were increased to 1000 ppm (4.5 and 5.5 mM, respectively), marked cell lysis was seen after a 1 h exposure period. The results of this study suggest that both BHT and BHA, in relatively large concentrations, produce injury to myocardial cells in culture.

Animals↗
PubMed1989

Inhibition of binding of 2-acetylaminofluorene to DNA by butylated hydroxytoluene and butylated hydroxyanisole in vitro.

Numerous studies have shown that the food antioxidants butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA), under specific exposure conditions, can inhibit hepatocarcinogenesis induced by various carcinogens. The purpose of the present work was to study the biochemical mechanisms responsible for the anticarcinogenic activity of BHA and BHT using in vitro systems. The effects of BHA and BHT on the binding of 2-acetylaminofluorene (2-AAF) to DNA was determined in a microsomal system and in primary cultures of rat hepatocytes. It was found that both antioxidants reduce the binding of 2-AAF and that of N-OH-2-acetylaminofluorene (N-OH-2-AAF) to calf thymus DNA in the presence of liver microsomes. The inhibition was however more pronounced with the parent compound. Lower levels of DNA binding were also detected in hepatocytes incubated with 2-AAF along with BHA or BHT. These results suggest that phenolic antioxidants can exert anticarcinogenic activity through modulation of carcinogen interaction with DNA which may reflect on alteration in carcinogen metabolic activation.

2-Acetylaminofluorene↗
PubMed1986

Modulation of benzo[a]pyrene-induced morphological transformation of Syrian hamster embryo cells by butylated hydroxytoluene and butylated hydroxyanisole.

The Syrian hamster embryo cell transformation assay has been used to investigate the effect of two synthetic antioxidants on morphological transformation induced by the initiator benzo[a]pyrene (BP). A two-stage protocol was employed with an initiation phase of 2 days and a subsequent promotion phase of 5 days. When 10 microM butylated hydroxytoluene (BHT) were present in the promotion phase instead of the solvent the transformation frequency at 0.1 micrograms BP/ml increased from 0.27% to 0.55%; at 100 microM of BHT the transformation frequency was 0.77%. Butylated hydroxyanisole (BHA) also enhanced the percentage of transformed colonies from 0.40% (10 microM) to 0.49% (100 microM), respectively. No significant initiating activity was detected for both antioxidants when tested in the initiation phase instead of BP; when the antioxidants were applied simultaneously with BP (1 microgram/ml) during the initiation phase the transformation frequency was decreased from 0.64% to 0.15% (100 microM BHT) and to 0.17% (100 microM BHA), respectively. These results show that the dual action of phenolic antioxidants on chemical carcinogenesis, which depends on the administration schedule, can be imitated in an in vitro test system. In addition to their anti-initiation effect, BHT and BHA, while devoid of intrinsic initiator potency, exert a moderate promotional activity on hamster embryo cell cultures. Their ability to enhance tumorigenesis by various carcinogens in vivo is likely to be at least partially related to such promotion-like effects on cell growth and morphology.

Animals↗
PubMed1983

Effect of butylated hydroxytoluene and butylated hydroxyanisole on the mutagenicity of 3,2'-dimethyl-4-aminobiphenyl.

This study was undertaken to investigate the possible antimutagenic effects of butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) on 3,2'-dimethyl-4-aminobiphenyl (DMAB)-induced mutagenicity, using the Ames Salmonella/mammalian microsome system. The addition of 100-250 micrograms of BHT or 25-500 micrograms of BHA/plate was found to inhibit DMAB-induced mutagenicity in Salmonella strains TA 98 and TA 100. In TA 100, the mutagenicity was further inhibited with the addition of S9 prepared from the livers of rats fed a 0.6% BHT diet as compared to S9 from the animals fed a diet containing no BHT.

Aminobiphenyl Compounds↗
PubMed1976

Inactivation of the enveloped bacteriophage phi6 by butylated hydroxytoluene and butylated hydroxyanisole.

Butylated hydroxytoluene (BHT) is a potent inactivator of the enveloped bacterial virus ø6 at concentrations as low as 3 x 10(-5) M. The viral envelope is not removed by BHT treatment, in contrast to the effects of exposure to the detergent Triton X-100. BHT-treated viruses are morphologically indistinguishable from controls but are defective in their ability to attach to the host cell. Temperature at the time of exposure was found to be a crucial factor in the effectiveness of BHT against ø6. A precipitous drop in the degree of inactivation by 3 x 10(-5) M BHT occurred when the temperature was lowered from 20 to 15 C. Calcium ions were found to potentiate the effect of BHT, particularly at lower temperatures where BHT alone was relatively ineffective. Barium and strontium, but not magnesium, were also effective in enhancing the activity of BHT. A structurally related molecule, butylated hydroxyanisole (BHA), was also found to inactivate ø6 virus, but higher concentrations were required than with BHT. Both BHT and BHA are commonly used as food additives, have apparent low toxicity to humans and other animals, and are potentially useful as antiviral agents.

Anisoles↗
PubMed1984

Comparative effect of the induction of the subunits of rat liver glutathione S-transferases by butylated hydroxytoluene.

When butylated hydroxytoluene (BHT) was administered to rats, the smallest subunit Ya (Mr 22,000) of rat liver GSH S-transferases was found to undergo maximum induction. It is suggested that the differential induction of GSH S-transferase activities by BHT towards different substrates may be due to the differences in the induction of the constituent subunits of GSH S-transferases.

Animals↗