Effects of catechol, sodium chloride and ethanol either alone or in combination on gastric carcinogenesis in rats pretreated with N-methyl-N′-nitro-N-nitrosoguanidine

Wada, Shigetsugu; Hirose, Masao; Shichino, Yutaka; Ozaki, Keisuke; Hoshiya, Toru; Kato, Koji; Shirai, Tomoyuki

doi:10.1016/s0304-3835(97)00407-2

Cited by 16 publications

(8 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…HQ exposure has also been shown to cause monosomy of chromosome 5, 7, or 8 in the human lymphoblastoid cell lines GMO9948 (Stillman et al 1997), renal adenoma in male rats (Whysner et al 1985), and micronucleus formation in mouse bone marrow cells (Marrazini et al 1994). Increase in the carcinogenicity of methylnitrosamine and N-methyl-N-nitronitrosoguanidine in the presence of HQ substantiates its co-carcinogenic potential (Wada et al 1998). Genotoxic potential of HQ in relation to GSTs (GSTM1, GSTT1, and GSTP1) has been demonstrated in the Caucasian population using SCE and CBMN assays, suggesting that GSTM1 is one isoform modulating its genotoxicity (Silva et al 2004).…”

Section: Introductionmentioning

confidence: 79%

GSTM1, GSTT1, and GSTP1 Polymorphism in North Indian Population and its Influence on the Hydroquinone-Induced In Vitro Genotoxicity

Kumar

Chauhan

Paul

et al. 2008

Toxicology Mechanisms and Methods

View full text Add to dashboard Cite

Glutathione S transferase (GST) gene polymorphism examined among north Indians and correlated with hydroquinone (HQ) genotoxicity to help in clinical prediction of susceptibility of HQ toxicity. Lymphocytes of individuals with/without GSTM1, GSTT1, and GSTP1 (ile/ile or val/val) were exposed to HQ (20, 40, or 80 microM) and examined chromosomal aberrations (CA) or cytokinesis-block micronucleus assays. Among north Indians the frequencies of GSTM1 (null), GSTT1 (null), and both null were found to be 41.1, 21.9, and 12.7%, whereas frequencies of GSTP1 with (ile/ile) or (ile/val), or (val/val) were 52, 42.1, or 5.9%, respectively. Individuals with null GSTM1, GSTT1, and GSTP1 (val/val) showed inhibition of mitotic index (MI) and significant (p < 0.01) induction of CA as compared to individuals with GSTM1, GSTT1, and GSTP1 (ile/ile). Micronucleus formation was found to be significant (p < 0.05 or 0.01) in both the genotypes. Results indicate that GSTM1, GSTT1 (null), and GSTP1 (val/val) are sensitive to HQ genotoxicity.

show abstract

Section: Introductionmentioning

confidence: 79%

GSTM1, GSTT1, and GSTP1 Polymorphism in North Indian Population and its Influence on the Hydroquinone-Induced In Vitro Genotoxicity

Kumar

Chauhan

Paul

et al. 2008

Toxicology Mechanisms and Methods

View full text Add to dashboard Cite

show abstract

“…Exposure to 400 ppm MNNG in drinking water for 50 weeks resulted in gastric adenocarcinomas in 63.6% of gerbils [40]. Using MNNG-induced gastric cancer model, it has been reported that administration of high-salt diet [41,42], calcium-deficient diet [43], catechol [44], or IL-1β [45] promotes gastric cancer development.…”

Section: Chemical Carcinogenesis Models Of Gastric Cancermentioning

confidence: 99%

Mouse Models of Gastric Cancer

Hayakawa

Fox

Gonda

et al. 2013

Cancers

View full text Add to dashboard Cite

Animal models have greatly enriched our understanding of the molecular mechanisms of numerous types of cancers. Gastric cancer is one of the most common cancers worldwide, with a poor prognosis and high incidence of drug-resistance. However, most inbred strains of mice have proven resistant to gastric carcinogenesis. To establish useful models which mimic human gastric cancer phenotypes, investigators have utilized animals infected with Helicobacter species and treated with carcinogens. In addition, by exploiting genetic engineering, a variety of transgenic and knockout mouse models of gastric cancer have emerged, such as INS-GAS mice and TFF1 knockout mice. Investigators have used the combination of carcinogens and gene alteration to accelerate gastric cancer development, but rarely do mouse models show an aggressive and metastatic gastric cancer phenotype that could be relevant to preclinical studies, which may require more specific targeting of gastric progenitor cells. Here, we review current gastric carcinogenesis mouse models and provide our future perspectives on this field.

show abstract

“…One week later, animals were either fed the basal diet (MNNG-alone) or a diet containing catechol at 8,000 ppm (MNNG + Catechol) for 12 weeks. The selected dose of catechol has shown to promote induction of both forestomach and glandular stomach carcinomas after 51-week administration in a two-stage model (Wada et al, 1998). After cessation of tumor-promotion, all animals were killed by exsanguination from the abdominal aorta under deep anesthesia and target organs were removed.…”

Section: Animal Experimentsmentioning

confidence: 99%

Fluctuations in cell proliferation, apoptosis, and cell cycle regulation at the early stage of tumor promotion in rat two-stage carcinogenesis models

et al. 2012

View full text Add to dashboard Cite

-We previously demonstrated that 28-day administration of carcinogens that evoked cell proliferation as determined by immunoreactivity for Ki-67 or minichromosome maintenance 3 (Mcm3), in many target organs, increased the numbers of topoisomerase (Topo) IIα + , ubiquitin D (Ubd) + , and TUNEL + apoptotic cells. We also found increased co-expression of Topo IIα and Ubd, suggestive of increased spindle checkpoint disruption at the M phase. To investigate the roles of these markers in the early stages of carcinogenesis, we examined distribution changes in several carcinogenic target organs using rat initiation-promotion models. Promoting agents targeting the liver (piperonyl butoxide, methapyrilene hydrochloride), thyroid (sulfadimethoxine), urinary bladder (phenylethyl isothiocyanate), and forestomach and glandular stomach (catechol) were administered to rats after initiation treatment for each target organ. Numbers of Ki-67 + , Mcm3 + , Topo IIα + and TUNEL + cells increased within preneoplastic lesions as determined by glutathione S-transferase placental form in the liver or phospho-p44/42 mitogen-activated protein kinase in the thyroid, and hyperplastic lesions having no known preneoplastic markers in the urinary bladder, forestomach and glandular stomach. On the other hand, Ubd + cells did not increase within these preneoplastic lesions, but increased within hyperplastic lesions. These results suggest that both cell proliferation and apoptosis may be involved in the formation of preneoplastic lesions in the liver and thyroid examined here; however, spindle checkpoint disruption may not be involved in this process. Changes in hyperplastic lesions of the urinary bladder, forestomach and glandular stomach are similar to the 28-day carcinogen-treated cases, suggestive of the hyperplastic cellular character before the preneoplastic state.

show abstract

Effects of catechol, sodium chloride and ethanol either alone or in combination on gastric carcinogenesis in rats pretreated with N-methyl-N′-nitro-N-nitrosoguanidine

Cited by 16 publications

References 33 publications

GSTM1, GSTT1, and GSTP1 Polymorphism in North Indian Population and its Influence on the Hydroquinone-Induced In Vitro Genotoxicity

GSTM1, GSTT1, and GSTP1 Polymorphism in North Indian Population and its Influence on the Hydroquinone-Induced In Vitro Genotoxicity

Mouse Models of Gastric Cancer

Fluctuations in cell proliferation, apoptosis, and cell cycle regulation at the early stage of tumor promotion in rat two-stage carcinogenesis models

Contact Info

Product

Resources

About