Potential protective effect of vitamin C on carcinogenesis caused by nitrosamine in drinking water: an experimental study on Wistar rats.

In an experiment with Wistar rats the question of whether oral vitamin C application has a protective effect in liver carcinogenesis caused by N-nitrosodiethylamine in drinking water (n = 104) was studied. When comparing four groups (without carcinogen, with carcinogen and carcinogen plus vitamin C alternately and concomitantly) significant statistical differences in the linear regression were noted. Ninety per cent of the rats developed hepatocellular carcinomas when only carcinogen was administered whereas the rate with additional administration of vitamin C alternately and concomitantly was 68% and 55%, respectively. Without carcinogen no tumour developed. The results suggest that vitamin C may delay the development of liver cancer upon oral administration of N-nitrosodiethylamine. The explanation for this fact is still hypothetical.

Inhibition by selenium of intrahepatic cholangiocarcinoma induction in Syrian golden hamsters by N'-nitrosobis(2-oxopropyl)amine.

The effects of selenium supplementation on induction of cholangiocarcinomas and related precancerous lesions in female Syrian Golden hamsters by N'-nitrosobis(2-oxopropyl)amine (BOP) were investigated. Four-week-old animals were divided into two groups according to the selenium level contained in the drinking water (0.1 ppm or 4.0 ppm) and fed a purified diet containing less than 0.05 ppm of the trace element. Starting at Week 4 of the experiment, hamsters were administered 10 weekly injections of BOP (10 mg/kg body wt) and then killed 18 weeks after the last carcinogen administration. Animals receiving physiological saline alone served as controls. Cholangiocellular carcinomas tended to be reduced, and putative preneoplastic lesions of cholangiofibrosis were significantly decreased in the high-as opposed to the low-selenium groups in terms of both incidence rate and number per effective animal. The respective high and low selenium values for incidence and number were 24/38% and 0.34/0.66, respectively, for cholangiocarcinomas and 50/89% and 1.21/8.44, respectively, for cholangiofibroses. Proliferation of intrahepatic bile ducts was also significantly inhibited in the high-selenium group along with cyst formation. Biochemical investigation revealed both selenium level and glutathione peroxidase activity to be significantly greater in the high-than in the low-selenium group livers. The results thus suggest that selenium may inhibit BOP-induction of bile duct lesions, possibly via glutathione peroxidase-mediated alteration of carcinogenesis.

[Epidemiology of primary liver cancer in French Polynesia]. / Epidémiologie du cancer primitif du foie en Polynésie française.

Thirty-one cases of primary liver cancer recorded since 1980 to 1988 in French Polynesia are studied. Four risk factors are brought to the fore: male, more than 50 years old, birth in Austral archipelago and in this case AgHBs carriage. The relative risk for birth in Austral archipelago reach to 9.23. The relative risk for AgHBs carriers from this archipelago reach to 42.7. Costs of primary liver cancer and to immunization against hepatitis B virus are compared. Authors suggest to start an immunization program.

Metaplastic pancreatic cells in liver tumors induced by diethylnitrosamine.

Metaplastic pancreatic cells have been infrequently observed in fish liver tumors induced by chemical carcinogens. An investigation with nitrosamine-exposed trout was undertaken to characterize the relationships of metaplastic pancreatic cells with other cell types. Eight-week-old rainbow trout (Salmo gairdneri) were fed a control diet or diets containing 500 ppm beta-naphthoflavone (BNF), 2000 ppm indole-3-carbinol (13C), or 100 ppm Aroclor 1254 (PCB) for 6 weeks. The fish were then exposed to 250 ppm diethylnitrosamine for 24 hr in an aqueous aquarium bath and reared on control diet for 39 weeks postexposure. Livers were excised, processed to paraffin sections, and stained with hematoxylin and eosin for histological evaluation. Metaplastic pancreatic cells were found only in tumors. Of the tumors with metaplastic pancreatic cells, 100/105 (95.2%) contained neoplastic cholangiolar components. Only 5/105 (4.76%) were hepatocellular carcinomas. 13C pretreatment inhibited the incidence of cholangiolar tumors (cholangioma 3.6% vs 31.3%, cholangiocarcinoma 3.6% vs 13.0%) and metaplastic pancreatic cells (5.1% vs 19.1%), whereas BNF and PCB had no effect. A hepatocellular origin for metaplastic pancreatic cells is supported. Cholangiolar neoplasia is associated with the expression, growth, or survival of metaplastic pancreatic cells in liver tumors. Hepatocarcinogenicity should not be described entirely by hepatocellular events since cholangiolar and metaplastic pancreatic cells can respond associatively to carcinogens and dietary modulators.

Cholangiocarcinoma associated with liver fluke infection: a preventable source of morbidity in Asian immigrants.

In the Far East infection with the liver flukes Clonorchis sinensis and Opisthorchis viverrini is the most frequently documented cause of cholangiocarcinoma. Liver fluke infection in the United States remains a health problem for more than 500,000 Southeast Asian refugees who have immigrated to this country since 1975. Recent surveys have revealed that up to 26% of Asian immigrants have an active liver fluke infection. However, the common clinical manifestations of this condition, as well as the possibility of developing such long-term sequelae as cholangiocarcinoma, remain unknown to many physicians providing care for this population. This report describes a clinically unsuspected C. sinensis infection associated with cholangiocarcinoma in an elderly Chinese immigrant, and emphasizes the importance of early diagnosis and treatment of all liver fluke infections in the prevention of bile duct neoplasms in high risk populations.