AROMATIC INFLUENCES ON THE YIELDS OF MAMMARY CANCERS FOLLOWING ADMINISTRATION OF 7,12-DIMETHYLBENZ(
            <i>a</i>
            )ANTHRACENE

Huggins, Charles; Grand, Lorraine C.; Fukunishi, Ryo

doi:10.1073/pnas.51.5.737

Cited by 92 publications

(18 citation statements)

References 8 publications

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“…In contrast, a protective effect against this carcino gen by increased liver microsomal enzyme activity has also been reported [19,21,25,28,29,32]. It appears therefore, that conclusive evidence is still lack ing either to support or to rule out the possibility that the metabolic transfor mation of DMBA is a necessary step in its carcinogenic activity.…”

Section: Introductionmentioning

confidence: 79%

Link between Carcinogenicity and Hepatic Metabolism of 7,12-Dimethylbenz(α)anthracene

Feuer¹,

Kellen²

1974

Oncology

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Inhibition of hepatic drug metabolism in the Sprague-Dawley rat by coumarin pretreatment or pregnancy reduced significantly the incidence of mammary tumors induced by 7,12-dimethylbenz(α)anthracene (DMBA) alone in untreated or nonpregnant animals. When DMBA injections were followed by coumarin treatment the rats remained unprotected against the carcinogen. These observations strongly support the conclusion that tumorigenesis by DMBA is probably due to its minor metabolites.

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Section: Introductionmentioning

confidence: 79%

Link between Carcinogenicity and Hepatic Metabolism of 7,12-Dimethylbenz(α)anthracene

Feuer¹,

Kellen²

1974

Oncology

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“…The repeated dose paradigm (fragmenting one large dose of DMBA to smaller, nonlethal fractions) is considered the optimal application model to induce malignant tumors (Gao et al 2007;Huggins et al 1966;Löscher et al 1993;Mevissen et al 1996). Depending on the particular report, term from administration of PAH to sacrifice ranges from 24 hours to 270 days.…”

Section: Discussionmentioning

confidence: 99%

Decreases in Binding Capacity of the Mitochondrial 18 kDa Translocator Protein Accompany Oxidative Stress and Pathological Signs in Rat Liver After DMBA Exposure

et al. 2010

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7,anthracene (DMBA) presents a pollutant implicated in various toxicological effects. The aim of this experiment was to study the effects of DMBA administration on oxidative stress, histopathological signs, and 18 kDa translocator protein (TSPO) binding characteristics in rat liver. We also studied the effects of dose stoichiometry, dose frequency, and duration of protocol of DMBA administration. In this study, rats surviving eighteen weeks after DMBA exposure showed mild to moderate histopathological changes in the liver, mainly characterized by glossy appearance of hepatocytes, heterochromatic nuclei, and glycogen overload in the midzonal region of the hepatic lobe. These changes were accompanied by significant rises in oxidant levels, along with declines in nonenzymic antioxidants, indicating that DMBA induced oxidative stress in the liver. This finding correlated well with decreases in TSPO binding capacity in the liver of the rats in our study. Other studies have shown that TSPO can be affected by oxidative stress, as well as contribute to oxidative stress at mitochondrial levels. Further studies are needed to assay whether the decreases in TSPO density in the liver are part of the damaging effects caused by DMBA or a compensatory response to the oxidative stress induced by DMBA.

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“…injections of DM BA (2 mg each) in a lipid emulsion on days 50, 53 and 56 [12]. A few rats received 6 mg of DM BA in a single injection.…”

Section: Methodsmentioning

confidence: 99%

DMBA, Hypertension and Impaired Adrenal Mitochondrial Differentiation

Anderson¹,

Kellen²

1973

Oncology

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Mitochondria containing reduced numbers of vesicles and electron-lucent matrices were observed more frequently in adrenal cortices from hypertensive rats previously exposed to dimethylbenz(α)anthracene. The triad of exposure to DMBA, development of hypertension, and the occurrence of structurally immature adrenal cortical mitochondria may provide the basis for a form of adrenal regeneration hypertension. However, persistence of structurally abnormal mitochondria long after exposure to the carcinogen, is remarkable. A carcinogen-induced defect in cellular response to ACTH, and/or an abnormality in the cytoplasmic synthesis of proteins required for normal mitochondrial development are among two of a number of possible explanations.

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AROMATIC INFLUENCES ON THE YIELDS OF MAMMARY CANCERS FOLLOWING ADMINISTRATION OF 7,12-DIMETHYLBENZ( a )ANTHRACENE

Cited by 92 publications

References 8 publications

Link between Carcinogenicity and Hepatic Metabolism of 7,12-Dimethylbenz(α)anthracene

Link between Carcinogenicity and Hepatic Metabolism of 7,12-Dimethylbenz(α)anthracene

Decreases in Binding Capacity of the Mitochondrial 18 kDa Translocator Protein Accompany Oxidative Stress and Pathological Signs in Rat Liver After DMBA Exposure

DMBA, Hypertension and Impaired Adrenal Mitochondrial Differentiation

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