The effects of butylated hydroxytoluene on the cell cycle and chromosome morphology of phytohaemagglutinin-stimulated leucocyte cultures

Sciorra, Leonard J.; Kaufmann, B.N.; Maier, Roberta

doi:10.1016/0015-6264(74)90320-4

Cited by 20 publications

(5 citation statements)

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“…However, it was positive in a sperm abnormality assay (Brace and Heddle 1979). BHT caused chromosomal abnormalities in metaphase cells of phytohemagglutinin-stimulated leukocyte culture (Sciorra et al 1974) and 8-azaguanine resistant mutants in Chinese hamster V79 cells in the presence of S-9 fraction from mouse liver (Paschin and Bahitova 1984). It induced a weak but statistically significant increase in the rat dominant lethal test (Sheu et al 1986).…”

Section: Introductionmentioning

confidence: 97%

DNA cleavage by metabolites of butylated hydroxytoluene

1993

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The effect of butylated hydroxytoluene (BHT) and its metabolites on DNA cleavage in vitro was studied with supercoiled plasmid DNA, pUC18, by agarose gel electrophoresis. Among several BHT metabolites, 2,6-di-t-butyl-p-benzoquinone (BHT-quinone) caused cleavage of supercoiled DNA (form I) at a concentration as low as 1 x 10(-6) M. The relative amount of linear form (form III) was increased with increasing concentration of BHT-quinone. 2,6-Di-t-butyl-4-hydroperoxy-4-methyl-2,5-cyclohexadienone (BHT-peroxyquinol) and 3,5-di-t-butyl-4-hydroxybenzaldehyde (BHT-CHO) also cleaved DNA, but to a lesser extent than BHT-quinone. No DNA cleavage was detected by BHT, 2,6-di-t-butyl-4-hydroxymethyl phenol (BHT-OH), 3,5-di-t-butyl-4-hydroxybenzoic acid (BHT-COOH), 2,6-di-t-butyl-4-hydroxy-4-methyl-2,5-cyclohexadienone (BHT-quinol) or 2,6-di-t-butyl-4-methylene-2,5-cyclohexadienone (BHT-quinone methide). The DNA cleavage by BHT-quinone was inhibited by oxygen radical scavengers including superoxide dismutase (SOD), catalase, polyethylene glycol, t-butyl alcohol, dimethyl sulfoxide, sodium azide, sodium benzoate, bovine serum albumin and methionine, while it was enhanced by the addition of FeCl2. The production of superoxide radical in a solution of BHT-quinone was confirmed by cytochrome c reduction assay. Superoxide was not produced by BHT or other BHT metabolites except for BHT-quinone. These results suggest that BHT-quinone, one of the principal metabolites of BHT, cleaves DNA strands via its generation of oxygen radicals.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Introductionmentioning

confidence: 97%

DNA cleavage by metabolites of butylated hydroxytoluene

1993

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“…Neivele (1969) on the other hand, has shown increases in the rate of amino acid incroporation into proteins of microsomal fractions of liver and increased rough endoplasmic reticulum activity indicating increased protein synthesis. Differences in the timing of the cell cycle and increased cellular mortality has also been demonstrated by Sciorra et al (1974) using BHT on PHA stimulated small lymphocyte cultures.…”

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confidence: 86%

An Analysis of the Uncoiling Effect of a BHT-Tween 80/Absolute Ethanol Mixture on Velban<sup>R</sup> Arrested Human Metaphase Cells

Sciorra

Maier²,

Thompson

et al. 1976

CYTOLOGIA

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“…At the moment this is not a likely possibility. In phytohemagglutinin-stimulated lymphocytes a mixture of BHT and Tween-80 produces a marked uncoiling of chromosomes as well as extensive cell membrane damage (20,21). Vitamin E and ethoxyquin are also without any effect (Fig.…”

Section: Or Are Treated With Low Doses Of Bht (50 Mg/kg) Neverthelesmentioning

confidence: 99%

Promotion of Lung Tumors in Mice

Witschi¹

1983

Environmental Health Perspectives

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Several elements of two-stage carcinogenesis apply to the development of lung tumors in Strain A or Swiss-Webster mice. At least three agents which have been identified as promoters in skin, uri-nary bladder and liver will also enhance tumor formation in lung: phorbol, saccharin and butylated hydroxytoluene (BHT). The antioxidant BHT acts in many respects like a typical promoting agent: it is effective if animals are treated after exposure to an initiating agent, but not if they are treated beforehand. Administration of BHT can be delayed up to 5 months after urethan treatment and still enhance tumor formation. BHT enhances lung tumor formation regardless of its route of administration (IP injection, gavage, or ingestion In the diet). The lowest dose of BHT required to produce an effect has not yet been determined. In' at least one mouse strain, BHT also enhances tumor formation in animals initiated with 3-methylcholanthrene or dimethylnitrosamine. On the other hand, no evidence is available yet to show that BHT would enhance tumor development in animals treated with subcarcinogenic doses of an initiating compound. Nor has it been possible to produce more tumors with BHT in mouse strains which have a low spontaneous tumor incidence and respond poorly to urethan. The question has not been resolved whether BHT accelerates growth of preformed tumors only or whether it induces the formation of more tumors. Nevertheless, the data collected on the effects of BHT on mouse lung tumor development have broadened the concept of two-stage carcinogenesis and complement the evidence for initiation-promotion available for other epithelial tissues such as liver, colon, stomach, trachea, urinary bladder and mammary gland.

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The effects of butylated hydroxytoluene on the cell cycle and chromosome morphology of phytohaemagglutinin-stimulated leucocyte cultures

Cited by 20 publications

References 8 publications

DNA cleavage by metabolites of butylated hydroxytoluene

DNA cleavage by metabolites of butylated hydroxytoluene

An Analysis of the Uncoiling Effect of a BHT-Tween 80/Absolute Ethanol Mixture on Velban<sup>R</sup> Arrested Human Metaphase Cells

Promotion of Lung Tumors in Mice

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