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Sida 1 från 121 resultat
Toxicity and Role of Fumonisins in Animal Diseases and Human Esophageal Cancer.
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Fumonisins are secondary metabolites of Fusarium moniliforme , Fusarium proliferatum and several other Fusaria that commonly contaminate corn. Only recently discovered in 1988, these mycotoxins appear to be the causative agents of several toxicoses in animals that result from ingestion of moldy corn
Temporal expression of fumonisin B(1)-induced tumor necrosis factor-alpha and interferon gamma in mice.
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Fumonisin B(1) (FB(1)), a toxic metabolite of Fusarium verticillioides, is a carcinogen and causative agent of various animal diseases. Our previous studies indicated the involvement of tumor necrosis factor-alpha (TNF alpha) in FB(1)-induced toxic responses. To further investigate the time-course
Inhibition of tumor necrosis factor alpha signaling by anti-tumor necrosis factor alpha antibodies and pentoxifylline is unable to prevent fumonisin hepatotoxicity in mice.
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Fumonisin B1 (FB1), a mycotoxin from Fusarium verticillioides, disrupts sphingolipid metabolism by inhibiting ceramide synthase leading to modulation of cytokines including tumor necrosis factor (TNF) alpha. Current study investigated the effect of interrupting TNFalpha signaling, known to be
Fumonisin B1 contamination of home-grown corn in high-risk areas for esophageal and liver cancer in China.
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Fumonisin B1 (FB1) is reportedly the causative agent of several animal mycotoxicoses and has etiologically been linked to human oesophageal and liver cancer in certain areas of South Africa and China. To study a possible relationship between exposure to FB1 and human cancer risk, the current status
Chemoprotective properties of rooibos (Aspalathus linearis), honeybush (Cyclopia intermedia) herbal and green and black (Camellia sinensis) teas against cancer promotion induced by fumonisin B1 in rat liver.
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The chemoprotective properties of unfermented and fermented rooibos (Aspalathus linearis) and honeybush (Cyclopia intermedia) herbal teas, and green and black teas (Camellia sinensis) were investigated against fumonisin B1 (FB1) promotion in rat liver utilizing diethylnitrosamine (DEN) as cancer
Fumonisin B1 contamination of cereals and risk of esophageal cancer in a high risk area in northeastern Iran.
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BACKGROUND
Fumonisin B1 (FB1) is a toxic and carcinogenic mycotoxin produced in cereals due to fungal infection. This study was conducted to determine FB1 contamination of rice and corn samples and its relationship with the rate of esophageal cancer (EC) in a high risk area in northeastern
Fumonisins as a possible contributory risk factor for primary liver cancer: a 3-year study of corn harvested in Haimen, China, by HPLC and ELISA.
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Employing HPLC fluorometry, gas-liquid chromatography (GLC) and a novel enzyme-linked immunosorbent assay (ELISA) based on a monoclonal antibody, 40 corn samples, each collected in 1993 from agricultural stocks for human consumption in Haimen (Jiangsu County) and Penlai (Shandong Province), high-
The effects of dietary iron overload on fumonisin B1-induced cancer promotion in the rat liver.
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The present study was performed to determine whether excess hepatic iron modulates the cancer-initiating and promoting properties of FB1. Thirty-eight male F344 rats were divided into four dietary treatment groups: (i) control diet (AIN, n = 8); (ii) FB1 250 mg/kg diet (FB1, n = 10); (iii) 1-2%
Modulation of pre-neoplastic biomarkers induced by sequential aflatoxin B1 and fumonisin B1 exposure in F344 rats treated with UPSN clay.
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Populations consuming aflatoxin (AF) and fumonisin (FN)-contaminated foods may be at increased risk for hepatocellular carcinoma (HCC) and developmental disorders; consequently, development of intervention strategies to reduce AF/FN-induced liver disease and adverse health effects in humans could be
Implications of apoptosis for toxicity, carcinogenicity, and risk assessment: fumonisin B(1) as an example.
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The rates of cell proliferation and cell loss in conjunction with the differentiation status of a tissue are among the many factors contributing to carcinogenesis. Nongenotoxic (non-DNA reactive) chemicals may affect this balance by increasing proliferation through direct mitogenesis or through a
Elevation of sphingoid base 1-phosphate as a potential contributor to hepatotoxicity in fumonisin B1-exposed mice.
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Fumonisins are causative agents of diseases in mice and rats, including liver and renal toxicities, as well as cancer, and are specific inhibitors of ceramide synthase in the metabolism of sphingolipid. The purpose of this study was to determine whether an elevated level of sphingoid base
Selective inhibition of carbonic anhydrase IX decreases cell proliferation and induces ceramide-mediated apoptosis in human cancer cells.
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Recently, carbonic anhydrase (CA) inhibitors have been proposed as a potential new class of antitumor agents. The aim of this study was to evaluate the antitumor activity of three CA inhibitors, namely acetazolamide (AZ) and two newly synthesized aromatic sulfonamides with high affinity for CA IX,
Visualisation and quantification of fumonisins bound by lactic acid bacteria isolates from traditional African maize-based fermented cereals, ogi and mahewu.
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Consumption of fumonisin-contaminated foods has a negative influence on the health of humans (carcinogen; oesophageal cancer in Eastern Cape in South Africa). Lactic acid bacteria (LAB) have emerged as a promising natural detoxification agent against mycotoxins. The aim of this study was to
Cytotoxic and genotoxic effects of fumonisin B1 on rabbit kidney RK13 cell line.
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Fumonisins, mycotoxins produced by certain strains of Fusarium moniliforme, could induce various diseases in animals and are suspected human carcinogens. Fumonisin B1 (FB1), the most commonly found fumonisin, has been characterised as a tumour initiator and a tumour promoter, a mitogen and an
Elevation of de novo ceramide synthesis in tumor masses and the role of microsomal dihydroceramide synthase.
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Ceramide is formed through sphingomyelin hydrolysis or de novo synthesis and may play a key role in cell growth, differentiation and apoptosis. To clarify which pathway tumor cells use to form ceramide and how its formation is regulated, we determined the levels of dihydroceramide and ceramide in
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