Chemoprevention by naturally occurring and synthetic agents in oral, liver, and large bowel carcinogenesis

Mori, Hideki; Tanaka, Takuji; Sugie, Shigeyuki; Yoshimi, Naoki; Kawamori, Toshihiko; Hirose, Yoshinobu; Ohnishi, Masami

doi:10.1002/(sici)1097-4644(1997)27+<35::aid-jcb8>3.0.co;2-2

Cited by 54 publications

(22 citation statements)

References 31 publications

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“…Cy is unstable under physiological conditions and degraded to PC, even if Cy were absorbed into the circulatory system. It is known that PC has a protective potency in carcinogenesis [18]. C3G feeding is expected to improve the antioxidant capability and chemically prevent carcinogenesis in vivo.…”

Section: C3g and Its Metabolites In The Tissuementioning

confidence: 99%

Absorption and metabolism of cyanidin 3‐O‐β‐D‐glucoside in rats

1999

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We have clarified for the first time how cyanidin 3-O-L L-D-glucoside (C3G), which is a potent antioxidant anthocyanin, is absorbed and metabolized in vivo. Rats were orally administered C3G (0.9 mmol/kg body weight), and C3G rapidly appeared in the plasma. However, the aglycon of C3G (cyanidin; Cy) was not detected, although it was present in the jejunum. Protocatechuic acid (PC), which may be produced by degradation of Cy, was present in the plasma and the concentration was 8-fold higher than that of C3G. These results suggest that plasma PC and C3G may contribute to the antioxidant activity of the plasma. In the liver and kidney, C3G was metabolized to methylated C3G (methyl-C3G), suggesting that C3G and/or methyl-C3G act as antioxidants in the tissues.z 1999 Federation of European Biochemical Societies.

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Section: C3g and Its Metabolites In The Tissuementioning

confidence: 99%

Absorption and metabolism of cyanidin 3‐O‐β‐D‐glucoside in rats

1999

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“…Modulation of phase I or II enzymes, and suppression of lipid peroxidation or DNA adduct formation are one of them. 37,38) Reddy et al reported that organosulfur compounds increase glutathione S-transferase (GST) and NAD(P)H-dependent quinone reductase (NAD(P)H:QR) in the liver.…”

Section: Discussionmentioning

confidence: 99%

Chemopreventive Effects of Scordinin on Diethylnitrosamine and Phenobarbital‐induced Hepatocarcinogenesis in Male F344 Rats

Watanabe

Sugie

Okamoto

et al. 2001

Japanese Journal of Cancer Research

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Modifying effects of scordinin, a biological active component in garlic, on diethylnitrosamine (DEN)-and phenobarbital (PB)-induced hepatocarcinogenesis were examined in rats. Male F344 rats, 5 weeks old, were divided into 8 groups. After a week, groups 1-5 were given DEN (100 mg/ kg body weight, i.p.) once a week for 3 weeks, whereas groups 6-8 received vehicle treatment. Group 2 was given 600 ppm scordinin-containing diet in the initiation phase. From 4 weeks after the start of experiment, groups 3 and 5 were fed scordinin, and groups 1-3 and 7 received drinking water containing 500 ppm PB. Group 6 was given scordinin diet alone throughout the experiment (24 weeks). The incidences of hepatocellular adenoma and carcinoma were significantly smaller in group 3 than those in group 1 (P < < < <0.005 and P < < < <0.05, respectively). The average numbers of liver neoplasms in groups 2 and 3 were significantly smaller than in group 1 (P < < < <0.01 and P < < < <0.0001, respectively). Glutathione S-transferase placental form-positive foci were also significantly decreased by scordinin treatment in the initiation or promotion phase. Scordinin significantly decreased the mean number of nucleolar organizer regions' protein (AgNORs)/nucleus in hepatocellular adenoma and carcinoma. AgNORs/nucleus in the non-lesional area was also significantly decreased by scordinin treatment during the promotion phase. These results suggest that scordinin is a promising chemopreventive agent for liver neoplasia.

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“…35,36) Shin and Lin 37) have reported that curcumin inhibited TPA-induced lipid peroxidation and 8-hydroxydeoxyguanosine formation in mouse fibroblasts. Such antioxidative properties may be involved in the chemopreventive effect on esophageal carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Chemopreventive Effect of Curcumin on N‐Nitrosomethylbenzylamine‐induced Esophageal Carcinogenesis in Rats

Ushida

Sugie

Kawabata

et al. 2000

Japanese Journal of Cancer Research

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Modifying effects of curcumin (derived from the rhizome of Curcuma longa L.) during the initiation or post-initiation phase of N-nitrosomethylbenzylamine (NMBA)-induced esophageal carcinogenesis were investigated in male F344 rats. Five-week-old rats were divided into 5 groups, and groups 1, 2 and 3 were given intraperitoneal injections of NMBA (0.5 mg/kg body weight/injection 15 times) for 5 weeks from 7 weeks old to induce esophageal neoplasms. Groups 2 and 3 were fed the diet containing 500 ppm curcumin during the initiation and post-initiation phases, respectively. Group 4 was given the diet containing curcumin throughout the experiment, and group 5 was kept on the basal diet alone and served as an untreated control. Incidence and multiplicity of esophageal neoplasms of group 1 (NMBA alone) were 66.7% and 0.83 ± ± ± ±0.70, respectively. Those of groups 2 and 3 were significantly less than those of group 1 (39.3%, 0.46 ± ± ± ±0.64, P < < < <0.05; 33.3%, 0.36 ± ± ± ±0.56, P < < < <0.05, respectively). Furthermore, the incidence and multiplicity of esophageal preneoplastic lesions (moderate or severe epithelial dysplasia) of group 2 (57.1%, 0.61 ± ± ± ±0.57; 40%, 0.29 ± ± ± ±0.46) or 3 (56.7%, 0.67 ± ± ± ±0.66; 23.3%, 0.23 ± ± ± ±0.43) were less than those of group 1 (100%, 1.67 ± ± ± ±0.70; 70.8%, 0.92 ± ± ± ±0.72) (P < < < <0.05). In this experiment, feeding of curcumin significantly decreased the expression of cell proliferation biomarkers (5-bromo-2′ ′ ′ ′-deoxyuridine labeling index) in the non-lesional esophageal epithelium (P < < < <0.01). These findings indicate that curcumin inhibits NMBA-induced esophageal carcinogenesis when given during the post initiation as well as initiation phase. This inhibition may be related to suppression of the increased cell proliferation induced by NMBA in the esophageal epithelium.

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Chemoprevention by naturally occurring and synthetic agents in oral, liver, and large bowel carcinogenesis

Cited by 54 publications

References 31 publications

Absorption and metabolism of cyanidin 3‐O‐β‐D‐glucoside in rats

Absorption and metabolism of cyanidin 3‐O‐β‐D‐glucoside in rats

Chemopreventive Effects of Scordinin on Diethylnitrosamine and Phenobarbital‐induced Hepatocarcinogenesis in Male F344 Rats

Chemopreventive Effect of Curcumin on N‐Nitrosomethylbenzylamine‐induced Esophageal Carcinogenesis in Rats

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