Fine-structural alterations in cell particles during chemical carcinogenesis

Arcos, Joseph C.; Arcos, Martha

doi:10.1016/0006-3002(58)90421-9

Cited by 38 publications

(6 citation statements)

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“…The carcinogenic activation of DAB was suggested to proceed via oxidative mono-demethylation accompanied by N-oxidation, yielding the 4-hydroxy derivative of DAB , leading to the formation of a nitrenium ion which eventually attacks the position-8 of guanosine on DNA molecules [6]. Structural abnormalities of liver microsomes from rats fed 3'methyl-4-dimethylaminoazobenzene (3'Me-DAB), have been demonstrated by Arcos and Arcos[7]. Porter and Bruni[8] implicated that administration of (3'Me-DAB) could destroy organization of the rough endoplasmic reticulum and aggregation of the smooth form Porter and Bruni[8].…”

Section: Introductionmentioning

confidence: 99%

Aminoazo dye-protein-adduct enhances inhibitory effect on digestibility and damages to Gastro-Duodenal-Hepatic axis

Peng

Chen

et al. 2017

PLoS ONE

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4-Dimethylaminoazobenzene (DAB, methyl yellow, or butter yellow), a human carcinogen, has been banned for use in foods since 1988. In 2014, DAB adulteration in Tofu occurred in Taiwan. We hypothesize that DAB can form [DAB•SBP]adduct adduct with soybean protein (SBP) which could damage Gastro-Duodenal-Hepatic axis. Sprague-Dawley rats gavage fed [DAB•SBP]adduct adduct revealed severely reduced body weight and damaged duodenum, liver, hepatic mitochondria, and spleen. Hepatic levels of glutathione and ATP were severely reduced. Serum GOT and GPT were substantially elevated. Analysis by the adsorption isotherm clearly revealed DAB formed very stable [DAB•SBP]adduct adduct at 1:1 molar ration (Phase A). The equilibrium constant of this colloidal adduct [DAB•SBP]adduct was KeqA = ∝, behaving as the most stable and toxic species. At higher protein concentration (Phase C) it formed conjugate [DAB×SBPgross]conjugate, with KeqC = 3.23×10−2 mg/mL, implicating a moderately strong adsorption. The in vitro pepsin digestibility test showed apparently reduced digestibility by 27% (by Ninhydrin assay) or 8% (by Bradford assay). Conclusively, this is the first report indicating that [DAB•SBP]adduct potentially is capable to damage the Gastro-Duodenal-Hepatic axis.

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Section: Introductionmentioning

confidence: 99%

Aminoazo dye-protein-adduct enhances inhibitory effect on digestibility and damages to Gastro-Duodenal-Hepatic axis

Peng

Chen

et al. 2017

PLoS ONE

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“…A'eldstra, 1956). Because of steric hindrance between the 2-methyl group and the a-azo nitrogen in 2-Me-DAB (Arcos and Arcos, 1958), it may be expected that the spatial configuration of this compound and of 3'-Me-DAB may not be so closely similar as suggested by the simple observation of the structural formulae. Steric hindrance in 2-Me-DAB is also suggested by the high basicity of the amino nitrogen (Cilento, 1960), because of interference with the resonance involving the azo double boiid and consequent increase of the electron density at the amino nitrogen.…”

Section: Pha8e Diagram8mentioning

confidence: 99%

“…3'-w_e--__DAB and 2-Me-DAB were prepared in our laboratory following the standardized procedure of Miller, Sapp and Miller (1949 (Price et al, 1949(Price et al, , 1950Hultin, 1956) ; (b) the close similarity of the spatial configurations of the two dyes (see " Phase Diagrams "), and (c) the fact that both 2-Me and 3'-Me-DAB are linked in the soluble cytoplasm to the same electrophoretic protein fraction (Sorof et al, 1951 ; Wirtz and Arcos, 1958 suggestive of a limited inhibition of 3'-Me-DAB tumorigenesis by 2-Me-DAB. The statistical significance of this apparent difference is, however, low (P -0-30).…”

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confidence: 99%

“…Careinogenesis may result then from : (a) intake of 3'-Me-DAB in excess over the metabolic capacity of the enzyme systems in the microsomes, which excess will be available for alteration of this cell organelle proper (Arcos and Arcos, 1958 ; Porter and Bruni, 1959), and of other cellular components, e.g. the mitochondria (Arcos, Griffith and Cunningham, 1960), at a rate which is proportional to the amount of non-metabolized dye, such as may be the case with the 0-035 and 0-06 per cent diets, or (b) competition of 2-Me and 3'-Me-DAB at " sites of loss " (cf.…”

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confidence: 99%

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Ratio Dependent Synergism in Azo-dye Carcinogenesis

Arcos¹,

Griffith²

1961

Br J Cancer

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A SCARCrTY of information exists in the literature on the hepatocareinogenic effects of combinations of azo dyes, similar to the competition in epithelial carcinogenesis between polycyclic.hydrocarbons as described first by Lacassagne, BuuHoi and Rudali (1945). In the reports available on synergism among azo carcinogens only the synergistic effect of 4-dimethylaminoazobenzene (DAB) and 4'-methyl-DAB has been confirmed (MacDonald et al., 1952;Corre-Hurst et al., 1953). The final assessment of the synergism between DAB and 3'-methyl-DAB (3'-Me-DAB) described in the 1953 report will require further experiments, however, in view of the fact that the authors found a higher tumor incidence with DAB than with 3'-Me-DAB, which is the inverse of the generally accepted relative carcinogenicites of the two compounds. Inhibitory effect among azo carcinogens has been reported by Crabtree (1955) who described inhibition of DAB induced hepatic tumorigenesis by certain non-carcinogenic derivatives of azobenzene.These observations have now been extended by studying the carcinogenic effect of dietary mixtures of the potent hepatic carcinogen, 3'-Me-DAB, of its relatively inactive isomer, 2-Me-DAB, and of the parent compound DAB. This report describes the synergistic effect of 3'-Me-DAB and of 2-Me-DAB when these dyes are present in a. 1 : 2 proportion in the diet. However, when these two azo compounds are present in a ratio of I : 1, the synergistic effect is -abolished, and the comparison of the tumor incidences may be considered suggestive of a limited inhibitory effect of 2-Me-DAB on 3'-Me-DAB tumorigenesis. In relation to this biological effect the phase diagram of 2-Me and 3'-Me-DAB has been studied to bring evidence for their actual similarity of spatial configuration. MATERIALS AND METHODSCare and feeding of animals.-Sprague-Dawley male rats, weighing 180 to 230 g. at the beginning of the experiment and housed two to a cage, were used.

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“…Arcos and Arcos (1958) have advanced information concerning the modification of the macromolecular organization of the microsomes when inducing chemical carcinogenesis. Although they prefer to regard the alterations in the ergastoplasm (microsomal pellets) as the major participant in carcinogenesis, the observations by, Bernhard and Rouiller (1956) that mitochondria govern ergastoplasmic formation, and the finding of Clerici and Cudkowicz (1956) and Emmelot and Bos (1955) that the mitochondria are specifically altered during carcinogenesis, prevent full acceptance of their thesis that the microsomes are more directly involved in carcinogenesis than other cell particles.…”

Section: Cytochondria and Carcinogenesismentioning

confidence: 99%

Cytochondrial Aspects of Cellular Pathology

Harman¹

1958

J Clin Pathol

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Fine-structural alterations in cell particles during chemical carcinogenesis

Cited by 38 publications

References 13 publications

Aminoazo dye-protein-adduct enhances inhibitory effect on digestibility and damages to Gastro-Duodenal-Hepatic axis

Aminoazo dye-protein-adduct enhances inhibitory effect on digestibility and damages to Gastro-Duodenal-Hepatic axis

Ratio Dependent Synergism in Azo-dye Carcinogenesis

Cytochondrial Aspects of Cellular Pathology

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