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PubMed1976

[Influence of fish smoking technology on nitrosamine concentration in them].

Under study was the content of total nitrosoamines in chiloed and bloated cod prepared by three ways: 1) by common bloating with fire-wood smoke; 2) by sawdust cold smoke (produced by means of a smoke generator) in thermal treatment with gas combustion products; 3) by the smoking fluid "Vakhtol" also in thermal treatment with gas combustion products. The common bloating resulted in the appearance of large amounts of total nitrosoamines in the foodstuff (from 200 to 900 mKg/Kg). Fish treatment with sawdust smoke would cause an insignificant increase in the content of these agents only in some cases. Whereas an application of the smoking fluid fails to produce any increase in nitrosoamines content. The use of wood-fire smoke for bloating Trachurus did not change its nitrosoamines content at all. The content of nitrosoamines was found to depend also on the duration of cod preservation in a frozen state.

Animals↗
PubMed1999

Increased expression of cyclooxygenase-2 in rat lung tumors induced by the tobacco-specific nitrosamine 4-(methylnitrosamino)-4-(3-pyridyl)-1-butanone: the impact of a high-fat diet.

Aberrant or excessive expression of cyclooxygenase (COX)-2 has been implicated in the pathogenesis of many disease processes, including carcinogenesis. COX-2 expression was immunohistochemically examined in archival samples (D. Hoffmann et al., Cancer Res., 53: 2758-2761, 1993) of lung neoplasms (adenomas, adenocarcinomas, and adenosquamous carcinomas) induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in male F344 rats that had been fed either a semipurified AIN-76A diet with high-fat (HF; 23.5% corn oil) or low-fat (LF; 5% corn oil) content. The intensity and extent of COX-2 positivity was graded from 0 (undetectable or negligible expression) to grades 1 (<30% expression), 2 (30-60% expression), 3 (60-90% expression), and 4 (>90% expression). The scoring criteria were similar to those used with specimens from human lung cancers (T. Hida et al., Cancer Res., 58: 3761-3764, 1998). In group 1 (NNK plus HF diet), adenomas, adenocarcinomas, and adenosquamous carcinomas were of mean grades 2, 3, and 4, respectively; in group 2 (NNK plus LF diet), the corresponding mean grades were 1, 1, and 3. Although control rats, given HF (group 3) or LF (group 4) diets but no NNK, developed spontaneous lung tumors, the expression of COX-2 was either negligible (one adenoma of grade 0 in group 3) or of a very low grade (one adenocarcinoma of grade 1 in group 4). In addition, the latency of the tumors in the peripheral lung in assays with NNK is significantly shorter in rats maintained on the HF diet than in those on LF diet. COX-2 expression was not evident in normal lung tissues. We report here for the first time that NNK induces increasingly higher levels of COX-2 expression with progressive stages of lung tumorigenesis when rats are fed the HF diet. The increase in COX-2 expression may be associated with the development of lung tumors induced by NNK. This well-defined animal model is valuable for studying modulation of COX-2 expression in lung carcinogenesis by various factors, including dietary components.

Animals↗
PubMed2000

Augmentation of UDP-GalNAc: Fucalpha1-2Gal alpha1-3 N-acetylgalactosaminyl transferase activity in nitrosamine-induced hamster pancreatic cancers.

Pancreatic cancers induced by N-nitrosobis(2-oxopropyl)amine (BOP) in hamsters produce blood group-A antigen (BG-A Ag), which is not present in the normal pancreas. To understand the neo-expression mechanism of BG-A Ag, we examined uridine diphosphate (UDP)-N-acetylgalactosamine (GalNAc): fucose (Fuc) alpha1-2 galactose (Gal) alpha1-3 GalNAc transferase (alpha1-3 GalNAc Tf) activity, the enzyme responsible for BG-A production. The specific activity of alpha1-3 GalNAc Tf in pancreatic cancers was approximately 8,000 nmole/g protein/h, whereas it was absent from the normal pancreas. Although the antrum and colon express A-Tf and BG-A Ag, the divalent cation requirements of alpha1-3 GalNAc Tf in these tissues were different from those of cancers. These results suggest that alpha1-3 GalNAc Tf is activated during BOP-induced pancreatic carcinogenesis, and that there are multiple alpha1-3 GalNAc Tf isozymes present in hamster tissues.

Animals↗