Altered Responses to Cortisol in Precancerous Liver

Andersen, R.A.; Raina, Priyanka; Milholland, Richard J.

doi:10.1159/000224374

Cited by 6 publications

(4 citation statements)

References 14 publications

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“…Failure to observe hepatocarcinogens altering glucocorticoid receptors has also been reported elsewhere [15,39]. The fact that in the liver of the same animals the carcinogens inhibit glucocorticoid‐dependent induction in some enzymes (TAT, tryptophan oxygenase, alanine aminotransferase) [11–16] and have no effect in others (aspartate aminotransferase, phosphoenolpyruvate carboxykinase, to mention a few) [40,41] lends further support to the hypothesis that these hepatocarcinogens may not affect glucocorticoid receptors.…”

Section: Discussionsupporting

confidence: 56%

“…The ability of 3′‐MeDAB to inhibit glucocorticoid induction of TAT activity was observed initially in rats following treatment with the carcinogen [13]. Our previous experiments were the first to demonstrate that OAT inhibits induction of TAT in mice in the same way as 3′‐MeDAB does in rats.…”

Section: Discussionmentioning

confidence: 99%

“…A prominent epigenetic effect of DAB and 3′‐MeDAB is the inhibition of glucocorticoid‐mediated induction of some adaptive enzymes, including tryptophan oxygenase [11], alanine aminotransferase [12], and tyrosine aminotransferase (TAT; l ‐tyrosine:2‐oxoglutarate aminotransferase, EC 2.6.1.5.) [12–14] in rat liver. A number of other rat hepatocarcinogens (diethylnitrosamine [15], thioacetamid [15], aflatoxin B1 [16]) specifically block glucocorticoid induction of tyrosine aminotransferase (TAT) in rat liver, whereas the non‐carcinogens 4‐aminoazobenzene and 4′‐MeDAB do not [6,12,13].…”

Section: Introductionmentioning

confidence: 99%

“…[12–14] in rat liver. A number of other rat hepatocarcinogens (diethylnitrosamine [15], thioacetamid [15], aflatoxin B1 [16]) specifically block glucocorticoid induction of tyrosine aminotransferase (TAT) in rat liver, whereas the non‐carcinogens 4‐aminoazobenzene and 4′‐MeDAB do not [6,12,13]. We have previously demonstrated that OAT is able to reduce glucocorticoid induction of TAT in mouse liver [17].…”

Section: Introductionmentioning

confidence: 99%

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Species-specific effects of the hepatocarcinogens 3′-methyl-4-dimethyl-aminoazobenzene and ortho-aminoazotoluene in mouse and rat liver

et al. 2005

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The effects of rat-specific hepatocarcinogen 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB), mouse-specific hepatocarcinogen ortho-aminoazotoluene (OAT), non-species-specific hepatocarcinogen diethylnitrosamine (DENA), and non-carcinogenic 4'-methyl-4-dimethylaminoazobenzene (4'-MeDAB) on glucocorticoid induction of tyrosine aminotransferase (TAT) and DNA-binding activity of hepatocyte nuclear factor 3 (HNF3) family of transcription factors were investigated with carcinogen-susceptible and -resistant animals. Species-specific hepatocarcinogens 3'-MeDAB and OAT strongly inhibited glucocorticoid induction of TAT in the liver of susceptible but not resistant animals. DENA, which is highly carcinogenic for the liver of both rats and mice inhibited glucocorticoid induction of TAT in both species, while non-carcinogenic 4'-MeDAB was absolutely ineffective both in rats and mice. The inhibition of TAT activity by the carcinogens was due to reduced levels of TAT mRNA, which is most likely to be a result of the reduced rate of transcription initiation of the TAT gene. In all cases, the TAT inhibition was accompanied by significant reduction of DNA-binding activity of the HNF3 transcription factor, which is known to be critical to glucocorticoid regulation of TAT gene. We also demonstrated that the described species-specific effects of OAT and of 3'-MeDAB on HNF3 DNA-binding activity may be initiated not only by administration in vivo, but also by their direct administration to homogenate, intact nuclei or nuclear lysate, but not to nuclear extract fraction, obtained by precipitation with 0.32 g/mL of ammonium sulfate (Fraction I). We showed, that a factor responsible for this effect might be precipitated in 0.32-0.47 g/mL interval of ammonium sulfate concentration. In contrast, non-specific hepatocarcinogen DENA was effective upon being added directly to Fraction I, implying a different mechanism of its action.

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Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Species-specific effects of the hepatocarcinogens 3′-methyl-4-dimethyl-aminoazobenzene and ortho-aminoazotoluene in mouse and rat liver

et al. 2005

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In vitro measurement of carcinogen‐resistant liver cells during hepatocarcinogenesis

Laishes

Farber

1978

Intl Journal of Cancer

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Following the transfer of r a t liver cells from 2-acetylaminofluorene-induced, grey-white hyperplastic nodules t o a primary, monolayer cell culture system, the proportion of the nodule cells which were resistant t o the cytotoxic effects of aflatoxin B1 was determined normal and nodule hepatocytes were great following aflatoxin B1 treatment. Aflatoxin B1 treatment inhibited the spreading of normal hepatocytes, whereas the highly resistant nodule hepatocytes continued t o spread out on the plastic substratum. Supplementation of the culture medium with dexamethasone routinely increased the proportion of resistant normal cells exposed t o some concentrations of aflatoxin B1 but did not significantly increase the size of the resistant nodule cell population.

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Induction of glutamine synthetase by cortisol

Raina¹,

Rosen²

1968

Biochimica et Biophysica Acta (BBA) - General Subjects

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Altered Responses to Cortisol in Precancerous Liver

Cited by 6 publications

References 14 publications

Species-specific effects of the hepatocarcinogens 3′-methyl-4-dimethyl-aminoazobenzene and ortho-aminoazotoluene in mouse and rat liver

Species-specific effects of the hepatocarcinogens 3′-methyl-4-dimethyl-aminoazobenzene and ortho-aminoazotoluene in mouse and rat liver

In vitro measurement of carcinogen‐resistant liver cells during hepatocarcinogenesis

Induction of glutamine synthetase by cortisol

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