Ratliver cells in culture: Effect of storage, long-term culture, and transformation on some enzyme levels

Idoine, Jane B.; Elliott, Jerry M.; Wilson, Marvin C.; Weisburger, Elizabeth K.

doi:10.1007/bf02797437

Cited by 63 publications

(16 citation statements)

References 25 publications

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“…The cell line used (TRL 1215) was originally derived from the liver of 10-day old Fischer F344 rats (15). The cells are diploid and normally nontumorigenic.…”

Section: Methodsmentioning

confidence: 99%

Association of arsenic-induced malignant transformation with DNA hypomethylation and aberrant gene expression

Zhao

Young

Diwan

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

514

295

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Inorganic arsenic, a human carcinogen, is enzymatically methylated for detoxication, consuming Sadenosyl-methionine (SAM) in the process. The fact that DNA methyltransferases (MeTases) require this same methyl donor suggests a role for methylation in arsenic carcinogenesis. Here we test the hypothesis that arsenic-induced initiation results from DNA hypomethylation caused by continuous methyl depletion. The hypothesis was tested by first inducing transformation in a rat liver epithelial cell line by chronic exposure to low levels of arsenic, as confirmed by the development of highly aggressive, malignant tumors after inoculation of cells into Nude mice. Global DNA hypomethylation occurred concurrently with malignant transformation and in the presence of depressed levels of S-adenosyl-methionine. Arsenic-induced DNA hypomethylation was a function of dose and exposure duration, and remained constant even after withdrawal of arsenic. Hyperexpressibility of the MT gene, a gene for which expression is clearly controlled by DNA methylation, was also detected in transformed cells. Acute arsenic or arsenic at nontransforming levels did not induce global hypomethylation of DNA. Whereas transcription of DNA MeTase was elevated, the MeTase enzymatic activity was reduced with arsenic transformation. Taken together, these results indicate arsenic can act as a carcinogen by inducing DNA hypomethylation, which in turn facilitates aberrant gene expression, and they constitute a tenable theory of mechanism in arsenic carcinogenesis.

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“…The cell line used (TRL 1215) was originally derived from the liver of 10-day old Fischer F344 rats (15). The cells are diploid and normally nontumorigenic.…”

Section: Methodsmentioning

confidence: 99%

Association of arsenic-induced malignant transformation with DNA hypomethylation and aberrant gene expression

Zhao

Young

Diwan

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

514

295

View full text Add to dashboard Cite

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“…The TRL 1215 rat liver epithelial cell line was originally derived from the liver of 10-day old Fischer F344 rats 22 and cells were cultured as described previously. 23 The cells are diploid and normally nontumorigenic.…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Cadmium‐induced malignant transformation in rat liver cells: Role of aberrant oncogene expression and minimal role of oxidative stress

Diwan

Reece

et al. 2004

Intl Journal of Cancer

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“…The ability to metabolize exogenous chemicals varies markedly between lines, and mixed function oxidation is practically limited to those reactions involving cytochrome P-448 (67)(68)(69). In a few lines, aryl hydrocarbon hydroxylase is present at levels that approach those in intact liver (69); however, this is unusual and typically the constitutive level of this enzyme is much lower (67)(68)(69).…”

Section: Cultures Of Dispersed Cellsmentioning

confidence: 98%

“…In a few lines, aryl hydrocarbon hydroxylase is present at levels that approach those in intact liver (69); however, this is unusual and typically the constitutive level of this enzyme is much lower (67)(68)(69). With repeated subculture the conistitutive level of aryl hydrocarbon hydroxylase may fall (69). Metabolic activity toward benzo(a)pyrene may be induced greatly by prior exposure to methylcholanthrene, but not to phenobarbital, (68,69).…”

Section: Cultures Of Dispersed Cellsmentioning

confidence: 99%

In vitro assay of cytotoxicity with cultured liver: accomplishments and possibilities.

Grisham¹,

Charlton²,

Kaufman³

1978

Environ Health Perspect

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Tissue cultures offer potential advantages for assaying the toxicity of chemicals and for evaluating tissue susceptibility to toxic agents. Several properties of cultured cells hinder the immediate, widespread use of tissue cultures to assay toxicity routinely. These points are illustrated by briefly reviewing attempts to utilize different types of hepatic cultures to evaluate the actions of carcinogenic chemicals in vitro. Hepatocytes in vivo apparently can metabolize all known procarcinogenic chemicals, but the process of tissue isolation and the environmental conditions in vitro may modify drastically the responses of hepatocytes and other cultured hepatic cells to toxic chemicals. Before cell cultures can be used routinely as the basis of screening systems to detect chemical toxins, specificity and sensitivity of response to chemicals representing all chemical classes must be validated by laboratory studies.

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Ratliver cells in culture: Effect of storage, long-term culture, and transformation on some enzyme levels

Cited by 63 publications

References 25 publications

Association of arsenic-induced malignant transformation with DNA hypomethylation and aberrant gene expression

Association of arsenic-induced malignant transformation with DNA hypomethylation and aberrant gene expression

Cadmium‐induced malignant transformation in rat liver cells: Role of aberrant oncogene expression and minimal role of oxidative stress

In vitro assay of cytotoxicity with cultured liver: accomplishments and possibilities.

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