Liver Cirrhosis Food List
Fumonisins have been shown to have diverse biological and toxicological effects. The mechanism of fumonisin toxicity is not well understood. Studies have shown that fumonisins inhibit ceramide synthase. Fumonisins have been shown to be hepatotoxic and carcinogenic in rats resulting in liver cirrhosis and hepatic nodules, adenofibrosis, hepato-cellular carcinoma, ductular carcinoma, and cholangio-carcinoma (Gelderblom et al. 1988 1991 1992b 1993 1994 Marasas 1996). Studies on rats by Riley et al. (1996) suggested that fumonisin B1 (FB1) might act primarily as a tumor promoter. The tumor promoting activity of fumonisins has also been proposed by Huang et al. (1995), Wattenberg et al. (1996) to have been resulted from the stimulation or
We know a great deal about the chemical nature of microbial toxins and their physiological affects on humans and animal models. Microbial foodborne toxins range in size from relatively large-molecular-weight toxic proteins produced by toxigenic bacteria to small-molecular-weight toxic organic compounds produced by toxigenic molds, algae and (rarely) certain bacterial species. These toxins induce a range of toxin-specific adverse effects that include vomiting and diarrhea (e.g., staphylococcal enterotoxins), paralysis and death (e.g., botulinal neurotoxins), and acute hepatic necrosis and cirrhosis and ultimately hepatocarcinoma (e.g., aflatoxin produced by toxigenic species of the mold genus Aspergillus). Notably, all of these foodborne toxins induce acute toxic effects that are evident within a few hours to a few days after exposure. In some cases chronic toxicity may also occur (e.g., long-term paralysis from exposure to a botulinal neurotoxin or liver cancer from aflatoxin...
Cohort studies in farmers or agricultural workers have mostly been targeted at cancer outcomes those focused on other health issues are scarce. The overall findings suggest that farmers and farm residents experience less cancer and more favorable mortality patterns, except from accidents, than their respective control groups. Liver cirrhosis as a cause of death was significantly
Aflatoxins are produced by species of Aspergillus flavus and Aspergillus parasiticus in various commodities including maize, rice, barley, wheat, sorghum, peanuts and copra. Asper-gillus flavus produces only aflatoxins B1 and B2 whereas A. parasiticus produces aflatoxins Bi, B2, Gi and G2. The toxicological effects of aflatoxins are dose-dependent. At high doses they are lethal if consumed, causing liver, myocardial and kidney tissue damage. At sub-lethal doses aflatoxins cause chronic toxicity, e.g. liver cirrhosis, and at low-level exposure, they are potent human hepatocellular carcinogens (Wild and Turner, 2002). Aflatoxins also are mutagenic and teratogenic and can depress cell-mediated immunity (Williams et al., 2004). Recently these toxins have been implicated in the stunting of children in Benin and Togo, where growth was reduced in children eating foods highly contaminated with aflatoxins introduced at weaning (Gong et al., 2002). Aflatoxin B1 acts synergistically with...
Peripheral nervous system much earlier than in any other organ system. This explains why, except in cases of deliberate poisoning, as in suicide, manifest liver or kidney damage due to insecticide use hardly ever occurs in persons who handle them professionally. One exception to this statement may be lead arsenate, which was used as an insecticide in vineyards in the past and allegedly caused liver cirrhosis and liver cancer in wine growers. Such cases have been acknowledged as an occupational disease in Germany however, some doubted the relevance of arsenic as the major culprit. Elevated liver enzyme activities in professional pesticide sprayers have occasionally been reported, whereas others did not confirm these findings (19-25).
F. verticillioides or pure FmB1 to rats resulted in cirrhosis and hepatic nodules, adenofibrosis, hepatocellular carcinoma-ductular carcinoma, and cholangiocarcinoma (Gelderblom et al. 2001 Haschek et al. 2001). Kidney is also a target organ, and tubular nephrosis was found both in rats and in horses of field cases associated with equine leukoencephalomalacia (ELEM). In addition to FmB1, which was originally found to be a potent cancer-causing agent, FmB2 and FmB3 have also been found to be carcinogens and have cancer initiation and promoting activities in rats. The effective dose of FmB1 for cancer initiation in rat liver depends both on the levels and on the duration of exposure. In cell culture systems, FmB1 has been demonstrated to be mitogenic and cytotoxic, without genotoxic effects (Gelderblom et al. 2001). Kidney cells have also been shown to be targeted by these toxins.
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