Effects of glyoxal and methyiglyoxal administration on gastric carcinogenesis in Wistar rats after initiation with N-methyl-N′ -nitro-N-nitrosoguanidine

Abstract

Glyoxal and methylglyoxal were tested for tumor-promoting potential in a two-stage stomach carcinogenesis model. Male outbred Wistar rats were initially given N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in the drinking water (100 mg/l) along with a 10% sodium chloride dietary supplement for 8 weeks. Thereafter, they were returned to basal diet and maintained on drinking water containing no addition or either 0.5% glyoxal or 0.25% methylglyoxal for 32 weeks and then killed for necropsy and histological examination at week 40. Glyoxal treatment significantly increased the incidence of adenocarcinomas in the pylorus of the glandular stomach of rats pretreated with MNNG and sodium chloride. Furthermore, although methylglyoxal did not enhance the development of adenocarcinomas, the incidence of hyperplasias in the pylorus was significantly increased. The results indicate that glyoxal exerts tumor promoting activity on rat glandular stomach carcinogenesis and that methylglyoxal might also have promoting potential.

Promotion by ethanol of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats

“…Our present results are different from those of Takahashi et al (1986). They found that EtOH ingestion after MNNG treatment did not promote gastric carcinogenesis, but rather tended to decrease cancer development.…”

“…They found that EtOH ingestion after MNNG treatment did not promote gastric carcinogenesis, but rather tended to decrease cancer development. This difference may be due to the fact that we injected EtOH i.p., while Takahashi et al (1986) applied EtOH by ingestion. Ingested EtOH is known to damage the gastric mucosa (Williams, 1956), which would increase the sloughing off of the precancerous and/or cancerous foci (Palmer & Humphreys, 1944).…”

“…Alcohol-induced cancers tend to occur either at sites of direct contact with ingested alcohol, such as the mouth and oesophagus, or at known sites of alcohol toxicity (the liver). However, Takahashi et al (1986) found that ethanol (EtOH) did not affect experimental tumour development in the stomach. EtOH was found to increase the epithelial proliferation of stomach fundic mucosa, but this effect is simply an enhancement of gastric mucosal regeneration in response to the mucosal injury induced by topical EtOH (Willems et al, 1971;Seitz et al, 1983).…”

Hydrogen peroxide tooth-whitening (bleaching) products: Review of adverse effects and safety issues

“…72 These results have been disputed due to the small number of animals studied. Further studies in hampsters given up to 70mg/kg of H 2 O 2 by oral intubation for up to six months 73,74 or up to 3% H 2 O 2 in combination with DMBA applied five times daily for 16-20 weeks on the buccal epithelium 75 did not show any sign of carcinogenesis. Further studies on skin have concluded that H 2 O 2 is inactive as a tumour promoter or carcinogen.…”

Enhancement by thyroxine of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats

“…Watanabe et al (1992) found that oral administration of NaCl after MNNG pretreatment significantly increased the incidence of gastric cancers and that it also significantly increased the height of the pyloric mucosa. Many investigators (Takahashi et al, 1986;Tatsuta et al, 1988a;Kobori et al, 1984) have indicated that enhancing effects on gastric carcinogenesis may be related to stimulation of cell proliferation and elongation of the mucosa. These findings suggest that a non-genotoxic component increases tumour yield when administered subsequent to a genotoxic agent.…”