sinigrin and indole-3-carbinol

The aim of the study was to investigate the effect of storage on the contents of glucosinolates (GLS) and their degradation products in a boiled white cabbage. A 24h storage at 4 °C resulted in a decrease in GLS content (20-40%, depending on the cooking time applied) in the edible parts. The most significant losses were observed for sinigrin (20-45%), and the least for glucobrassicin (12-32%). Storage had a diversified effect on GLS breakdown products (indole-3-acetonitrile, indole-3-carbinol, ascorbigen and 3,3'-diindolylmethane released from glucobrassicin and 4-methylsulfinylbutanenitrile released from glucoiberin) in the boiled cabbage. The increase in the content of indole-3-acetonitrile, especially considerable within the first 24h of storage (and a simultaneous decrease in glucobrassicin) clearly indicates that degradation of GLS may occur during storage or cooling to 4 °C.

Topics: Ascorbic Acid; Brassica; Drug Stability; Fermentation; Food Handling; Food Preservation; Glucosinolates; Hot Temperature; Indoles

The modifying effects of indole-3-carbinol (I3C) and sinigrin (SIN) on the initiation and post-initiation phases of tongue carcinogenesis induced by 4-nitroquinoline 1-oxide (4-NQO) were investigated in male ACI/N rats. Rats were divided into eight groups: group 1 was given 4-NQO (10 ppm) in the drinking water for 12 weeks, starting at 7 weeks of age; groups 2 and 3 were given 4-NQO and fed the diets containing I3C (1,000 ppm) and SIN (1,200 ppm) for 14 weeks, respectively, starting at 6 weeks of age; groups 4 and 5 were given 4-NQO and then they were fed I3C and SIN containing diets for 23 weeks, respectively, starting one week after 4-NQO exposure; groups 6 and 7 were given I3C and SIN alone, respectively, during the experiment; group 8 served as an untreated control. At the termination of the experiment (week 37), the incidence of tongue neoplasms (squamous cell papilloma and carcinoma) in group 2 (1/15, 7%), group 3 (1/15, 7%), group 4 (3/15, 20%) or group 5 (2/15, 13%) was significantly smaller than that in group 1 (12/17, 71%) (P = 0.0003, P = 0.005 or P = 0.002). No tongue carcinomas developed in rats of groups 2, 3, and 5. Similarly, the incidence of preneoplastic lesions (hyperplasia and dysplasia) of the tongue in group 2 (11/15, 73%), group 3 (10/15, 67%), group 4 (11/15, 73%) or group 5 (10/15, 67%) was significantly lower than that in group 1 (17/17, 100%) (P = 0.04 or P = 0.02). There were no tongue neoplasms in rats of groups 6, 7, and 8. Administration of I3C and SIN also caused significant decreases in the number and area of silver-stained nucleolar organizer regions protein (AgNORs), a new cell proliferation index, of tongue squamous epithelium. Thus, I3C and SIN inhibited rat tongue carcinogenesis in both the initiation and post-initiation phases, when administered in these respective phases together with, or following treatment with, 4-NQO.

Topics: 4-Nitroquinoline-1-oxide; Animals; Anticarcinogenic Agents; Antioxidants; Body Weight; Carcinoma, Squamous Cell; Glucosinolates; Hyperplasia; Indoles; Liver; Male; Organ Size; Papilloma; Precancerous Conditions; Rats; Rats, Inbred ACI; Tongue; Tongue Neoplasms

The modifying effects of sinigrin (Sin) and indole-3-carbinol (I3C) on the hepatocarcinogenesis induced by diethylnitrosamine (DEN) were investigated in male ACI/N rats. Rats were divided into six groups: group 1 was given DEN (40 p.p.m.) in the drinking water for 5 weeks, starting at 7 weeks of age; group 2 was treated with DEN and diet containing 1200 p.p.m. Sin; group 3 received DEN and diet containing 1000 p.p.m. I3C; group 4 was given Sin diet alone; group 5 was given I3C diet alone; and group 6 served as controls. The diet containing Sin or I3C was fed to the rats starting at 6 weeks of age until 1 week after the carcinogen exposure. At termination of the experiment (week 29), the incidences of iron-excluding altered foci (11.22 +/- 3.22/cm2) and liver cell tumors (6/12, 50%) and the tumor multiplicity (0.9/rat) in rats of group 2 were significantly smaller than those of group 1 (foci incidence, 48.33 +/- 6.34/cm2, tumor incidence, 10/10, 100%; multiplicity, 9.5/rat) (P less than 0.02). Similarly, the incidence of iron-excluding hepatocellular foci (17.65 +/- 4.67/cm2) and tumor multiplicity (2.4/rat) with a slight reduction of tumor incidence (9/12, 75%) in rats of group 3 were significantly lower than those of group 1 (P less than 0.001). There were no liver cell neoplasms in rats of groups 4, 5 and 6. Thus, Sin and I3C inhibited the hepatocarcinogenesis induced by DEN when they were administered concurrently with the carcinogen.

Topics: Animals; Diethylnitrosamine; DNA; Glucosinolates; Indoles; Liver Neoplasms, Experimental; Male; Precancerous Conditions; Rats; Rats, Inbred ACI; Thioglycosides

The effects of dietary sinigrin and indole-3-carbinol (I3C) on DNA methylation and O6-methylguanine--DNA-transmethylase activity, factors which may be of importance in the induction of tumorigenicity by the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), were investigated. Additionally, the effects of dietary sinigrin on NNK tumorigenicity were assessed in a two-year bioassay in F344 rats. DNA methylation in target tissues of NNK tumorigenesis was examined in F344 rats administered [3H-CH3]NNK (0.6 mg/kg, four doses) s.c. and fed control or experimental diets for two weeks. Dietary sinigrin at a concentration of 3 mumol/g diet decreased 7-methylguanine formation in hepatic DNA, but had no effect on 7-methylguanine levels of lung or nasal mucosa DNA. Dietary I3C at a concentration of 30 mumol/g diet increased 7-methylguanine levels in hepatic DNA, but decreased DNA methylation in lung and nasal mucosa. No effects on O6-methylguanine--DNA-transmethylase activity were observed in tissue extracts derived from the livers, lungs and nasal mucosae of rats fed diets containing sinigrin or I3C. These results suggested that dietary sinigrin might reduce the incidence of NNK-induced hepatic tumors with no effect on NNK tumorigenesis of the lung and nasal cavity, whereas I3C might increase hepatic tumor incidence and reduce NNK tumorigenesis of the lung and nasal cavity. The bioassay results showed that dietary sinigrin had no effect on NNK tumorigenesis in these target tissues. However, dietary sinigrin plus NNK resulted in a significant incidence of pancreatic tumors, a rare occurrence in F344 rats. While the results from DNA methylation studies are in agreement with the bioassay data for lung and nasal cavity, the absence of any inhibitory effect of dietary sinigrin on NNK hepatic tumorigenesis indicates that factors other than DNA methylation and O6-methylguanine repair should be considered in assessing the effects of dietary compounds on NNK hepatic tumorigenesis. The contrary effects on NNK-induced hepatic DNA methylation by sinigrin and I3C, two major components of cruciferous vegetables, demonstrate the complexities of dietary modulation of carcinogenesis.

Topics: Animals; Carcinogens; Diet; DNA; Glucosinolates; Indoles; Liver Neoplasms; Lung Neoplasms; Male; Methylation; Methyltransferases; Neoplasms, Experimental; Nitrosamines; Nose Neoplasms; O(6)-Methylguanine-DNA Methyltransferase; Pancreatic Neoplasms; Rats; Rats, Inbred F344; Thioglycosides