Effects of 4-week treatment with gastric carcinogens and enhancing agents on proliferation of gastric mucosa cells in rats

Ohgaki, Hideaki; Szentirmay, Zoltán; Take, Machiko; Sügimura, Takashi

doi:10.1016/0304-3835(89)90018-9

Cited by 27 publications

(18 citation statements)

References 12 publications

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“…In another study, Ohgaki et al (1989) investigated the effects of Pyrocatechol on the proliferation of pyloric mucosa cells. Five male F344 rats were given feed containing 0.8% Pyrocatechol for 4 weeks.…”

Section: Carcinogenicitymentioning

confidence: 99%

Amended Final Report On the Safety Assessment of Pyrocatechol

Andersen¹

1997

Int J Toxicol

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Pyrocatechol is a phenol used primarily in hair dyes but has one reported use in skin care preparations. When this ingredient was first reviewed it was concluded that Pyrocatechol was safe for use in formulations designed for discontinuous, brief use followed by rinsing from the skin and hair at concentrations of up to 1.0%. This amendment to that report was prepared in order to incorporate the results from several studies, including those reporting immunologic, carcinogenic, and cocarcinogenic effects of Pyrocatechol. In vitro, Pyrocatechol has been shown to affect several immunologic and other properties of murine bone marrow cells, both alone and when combined with hydroquinone. Pyrocatechol, when produced as an hepatic metabolite of benzene, has been reported to concentrate in the bone marrow and to adversely affect hematopoietic precursor cells. These effects are somewhat species specific. In vivo, dermal exposure of mice to Pyrocatechol affects the number and distribution of Langerhans cells at the site of exposure but is not associated with a change in contact sensitivity. Oral exposure of pregnant rats to Pyrocatechol did result in an increase in teratogenic effects. The results of a micromass teratogen test in vitro were also positive. Pyrocatechol was tested in a number of bacterial and mammalian mutagenesis systems. Both negative and positive results were observed. Carcinogenicity studies were conducted in rats and mice. Pyrocatechol was provided in the feed. While adenomatous hyperplasia was noted in both species, adenocarcinomas were seen in male and female rats only. In cocarcinogenesis studies there is a similar pattern of hyperplasia and adenomas of the glandular stomach in the groups exposed to Pyrocatechol alone. When administered with several other carcinogens, Pyrocatechol had a cocarcinogenic effects. Pyrocatechol was not a tumor promoter in dermal studies. Based on these data and the significant potential for skin absorption of Pyrocatechol in leave-on preparations, it was concluded that Pyrocatechol is unsafe for use in leave-on cosmetic formulations. Pyrocatechol used in a rinseoff application such as hair dyes may not present a similar concern if Pyrocatechol is completely and rapidly oxidized. Because no data were available, it was concluded that there are insufficient data to support the safety of this ingredient. The data needed to complete the safety assessment include the extent and rate of oxidation when used in hair dyeing. If not rapidly and completely oxidized, then further chemical characterization of cosmetic grade Pyrocatechol is needed, along with cutaneous absorption data in aqueous and at RYERSON UNIV on June 15, 2015 ijt.sagepub.com Downloaded from

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Section: Carcinogenicitymentioning

confidence: 99%

Amended Final Report On the Safety Assessment of Pyrocatechol

Andersen¹

1997

Int J Toxicol

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“…In experiments with rats dosed with MNNG, NaCl was shown to have a promotional effect of induction of gastric adenocarcinoma when salt is given intragastrically weekly or in the diet during 12–20 weeks exposure to MNNG in drinking water (Newberne et al ., 1987, Takahashi et al ., 1983, Tatematsu et al ., 1975). It is also known that salt causes damage to rat gastric surface epithelium followed by proliferation of gastric epithelium (Charnley and Tannenbaum, 1985, Furihata et al ., 1984, Ohgaki et al ., 1989, Sorbye et al ., 1988). In one study, 80% of rats given salt in the diet and MNNG in drinking water developed adenocarcinomas in the antrum, but not in the corpus (Takahashi et al ., 1983).…”

Section: Dietary Factors and Gastric Cancermentioning

confidence: 99%

Dietary Factors ModulateHelicobacter-associated Gastric Cancer in Rodent Models

Fox

Wang

2013

Toxicol Pathol

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Since its discovery in 1982, the global importance of H. pylori-induced disease, particularly in developing countries, remains high. The use of rodent models particularly mice, and the unanticipated usefulness of the gerbil to study H. pylori pathogenesis have been used extensively to study the interactions of the host, the pathogen and the environmental conditions influencing the outcome of persistent H. pylori infection. Dietary factors in humans are increasingly recognized as being important factors in modulating progression and severity of H. pylori-induced gastric cancer. Studies using rodent models to verify and help explain mechanisms whereby various dietary ingredients impact disease outcome should continue to be extremely productive.

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“…Sodium chloride has been shown to promote tumor formation initiated by genotoxic agents in various organs (reviewed in Anderson 1989;Cohen and Roe 1997). This activity was considered to be the result of a stimulation of cell division (Charnley and Tannenbaum 1985;Ohgaki et al 1989), a likely risk factor in carcinogenesis (Preston-Martin et al 1990;Cohen and Ellwein 1991). Its measurement has been proposed as a short-term test for the detection of the nongenotoxic carcinogens (Buesser and Lutz 1987;Butterworth et al 1991).…”

Section: Introductionmentioning

confidence: 99%

Stimulation of cell division in the rat by NaCl, KCl, MgCl 2 , and CaCl 2 , and inhibition of the sodium chloride effect on the glandular stomach by ascorbic acid and β-carotene

Lugli

Lutz²

1999

Journal of Cancer Research and Clinical Oncology

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Three questions associated with the stimulation of cell division by chloride salts have been investigated: (i) whether cations other than sodium show a similar effect, (ii) whether vitamins can have a preventive activity, and (iii) whether subchronic treatment with sodium chloride in the diet is also effective. Male Fischer 344 rats were given solutions of the chloride salts of sodium, potassium, magnesium, and calcium by oral gavage. Water was used for control. After 4 h, a 24-h osmotic minipump containing 5-bromo-2'-deoxyuridine was implanted subcutaneously. The forestomach and glandular stomach, as well as liver and bladder were analyzed immunohistochemically 24 h later for the proportion of cells in S phase as an indicator of the rate of replicative DNA synthesis. For both the forestomach and the glandular stomach, potassium was as potent as sodium, and the divalent cations Mg and Ca were even more potent on a molar basis. Supplementation of the diet with ascorbic acid (2 g/kg food) or beta-carotene (12.5 mg/kg food) for 1 week before gavage of the sodium chloride solution resulted in an inhibition of the stimulation of cell division. A putative tumor-chemopreventive activity of the two vitamins might therefore not only rely on their antioxidative properties but may include effects on the cell cycle. A 4-week treatment with a sodium chloride supplement in the diet (2% and 4% supplement) resulted in a significant stimulation of cell division not only in both parts of the stomach and in the bladder (with the 4% supplement) but also in the liver (even with the 2% supplement). Sodium-chloride-stimulated cell turnover therefore is a sustained effect.

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Effects of 4-week treatment with gastric carcinogens and enhancing agents on proliferation of gastric mucosa cells in rats

Cited by 27 publications

References 12 publications

Amended Final Report On the Safety Assessment of Pyrocatechol

Amended Final Report On the Safety Assessment of Pyrocatechol

Dietary Factors ModulateHelicobacter-associated Gastric Cancer in Rodent Models

Stimulation of cell division in the rat by NaCl, KCl, MgCl 2 , and CaCl 2 , and inhibition of the sodium chloride effect on the glandular stomach by ascorbic acid and β-carotene

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