Hepatic Carcinogenesis of Aflatoxin M1 in Rainbow Trout (Salmo gairdneri) and Its Enchancement by Cyclopropene Fatty Acids23

Sinnhuber, R. O.; Lee, D.J; Wales, J. H.; Landers, M. K.; Keyl, Alexander C.

doi:10.1093/jnci/53.5.1285

Cited by 88 publications

(24 citation statements)

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“…The difference between AFB 1 and AFM 1 in hepatoma incidence in the trout was found to be of a factor of 4 [9], the difference in the Salmonella/ microsome mutagenicity testwas about 30: 1 in one report [24] and about 3 : 1 in another [25]. The rate data on carcinogenicity in the rat cannot be used for a quantitative comparison of the two compounds [11,12].…”

Section: Resultsmentioning

confidence: 90%

“…Low Ievels of AFM 1 are therefore regularly detected in milk when groundnut cake has been fed, and it would be important to know more about its carcinogenicity. AF}tl 1 has been studied in the rainbow trout and was found to be strongly hepatocarcinogenic [9,10]. Due to Iack of material, only preliminary studies have been performed with mammals [11,12] and no definite conclusions on its potency could be drawn.…”

Section: IImentioning

confidence: 99%

See 1 more Smart Citation

In vivo covalent binding of aflatoxin B1 and aflatoxin M1 to liver DNA of rat, mouse and pig

Lutz

Jaggi

Lüthy

et al. 1980

Chemico-Biological Interactions

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Section: Resultsmentioning

confidence: 90%

Section: IImentioning

confidence: 99%

In vivo covalent binding of aflatoxin B1 and aflatoxin M1 to liver DNA of rat, mouse and pig

Lutz

Jaggi

Lüthy

et al. 1980

Chemico-Biological Interactions

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“…Finfish accumulate chemical contaminants from multiple sources, including sediments (Zdanowicz et al, 1986). However, even though sediments in many estuaries contain high levels of polycyclic aromatic hydrocarbons (PAHs), chlorinated pesticides, polychlorinated biphenyls (PCBs), and trace metals, and despite indications that environmental contamination is playing a major role in the development of hepatic lesions in fish (Ashley and Halver, 1961;Sinnhuber et al, 1974;Hendricks, 1982;Furness and Rainbow, 1990), cause-effect relationships between chemical contaminants and liver lesions in demersal finfish have only been inferred (Malins et al, 1984(Malins et al, , 1987Myers et al, 1990Myers et al, , 1991Johnson et al, 1993;Myers et al, 1994;Moore and Stegeman, 1994), not conclusively established. In addition, although experimental studies have been aimed at understanding the connection between specific classes of chemicals and liver lesions in fish (e.g.…”

Section: Introductionmentioning

confidence: 99%

Associations between liver lesions in winter flounder (Pleuronectes americanus) and sediment chemical contaminants from north-east United States estuaries

Chang

1998

ICES Journal of Marine Science

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Neoplastic diseases, particularly of bottom-dwelling fishes, are more prevalent in coastal areas than in areas that are relatively pristine. Although sediments in many urbanized estuaries contain high concentrations of contaminants, there is little evidence linking a specific organic or inorganic chemical to a particular liver lesion in winter flounder (Pleuronectes americanus), despite increasing study in recent years. Between 1984 and 1986, sediments and winter flounder were collected from 10 sites in the north-east United States ranging from grossly polluted to relatively unimpacted. Sediments were analysed for polycyclic aromatic hydrocarbons (PAHs), chlorinated pesticides, polychlorinated biphenyls (PCBs), and metals. Gross and microscopic pathological examinations were conducted on winter flounder liver sections. Factor and canonical correlation analyses were used to explore associations between biological and chemical measurements. Hepatitis, cholangitis, phlebitis, and macrophage aggregate hyperplasia showed positive associations with low molecular weight, petroleum-derived PAHs (naphthalene, anthracene, 1-methylnaphthalene, 2-methylnaphthalene, 2,6-dimethylnaphthalene, acenaphthene, phenanthrene, biphenyl, fluorene, and 1-methylphenanthrene), the pesticides lindane, hexachlorobenzene, heptachlor epoxide, and o,p -DDD, tri-to hexachlorobiphenyls, and chromium, cadmium, lead, thallium, and selenium, but were negatively associated with the pesticides o,p -DDT, p,p -DDT, p,p -DDE, and mirex. Cytoplasmic hepatocellular vacuolation, cytoplasmic bile duct vacuolation, neoplasms, and pre-neoplasms showed positive associations with most PAHs measured, whether petroleum-derived or combustion-derived (benzo[a]pyrene, benzo[e]pyrene, benzo [a]anthracene, dibenzo [a,h]anthracene, perylene, chrysene, and fluoranthene), the pesticides dieldrin, trans-nonachlor and alpha-chlordane, and silver, copper, antimony, and tin, but no associations with PCBs were found. Coagulative necrosis, single cell necrosis and haemorrhagic necrosis showed positive associations with hepta-to nonachlorobiphenyls and arsenic, zinc, nickel, and mercury, and negative associations with high molecular weight, combustion-derived PAHs and DDT compounds and metabolites.

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“…Metabolism of AFM 1 have been studied in vitro using liver microsomes [9]. Cyclopropenoid fatty acids (CPFA), which promote the carcinogenicity of aflatoxin B 1 , behave similarly with AFM 1 [10]. However, newborn animals that consume aflatoxins can be poisoned by the AFM 1 metabolite excreted in milk.…”

Section: Introductionmentioning

confidence: 99%

Comparative Study of Aflatoxin M1 in Livestock Livers from Minna, Nigeria

Makun¹,

Mwanza²,

Iheanacho³

et al. 2017

J Liver

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Liver as an organ of metabolism is disposed to toxins deposition and Livestock liver contributes to food security as major source of protein. Aflatoxin M1 (AFM1) is a carcinogenous metabolite aflatoxin B1 resulting from hydroxylation. To elucidate aflatoxin M1 incidence and levels in livestock livers from Minna-Nigeria, 24 hours fresh liver samples (n=122; 72 cow livers and 50 goat livers) were collected from five abattoirs and subjected to standard aflatoxin extractions via column chromatography and quantification by high performance liquid chromatography. Data showed the presence of AFM1 in some livestock livers. However, detected toxin levels in mean percentages and correlation of variation amongst the individual livestock livers was evident, with a 83.3% (60/72) incidence and a mean detection level of 1.464 µg/kg in cattle livers, as compared to 58.0% (29/50) incidence and a mean of 0.425 µg/kg in goats livers. Contamination in some samples; 52% (26/50) of goat liver and 62.5% (45/72) cow liver exceeded the EU, US and FDA limit of 0.05 µg/kg, indicating human exposure to animal liver with high level aflatoxin contamination. Therefore, there is a need to limit the exposure to aflatoxin by enforcing regulatory limits on animal feed.

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Hepatic Carcinogenesis of Aflatoxin M1 in Rainbow Trout (Salmo gairdneri) and Its Enchancement by Cyclopropene Fatty Acids23

Cited by 88 publications

References 0 publications

In vivo covalent binding of aflatoxin B1 and aflatoxin M1 to liver DNA of rat, mouse and pig

In vivo covalent binding of aflatoxin B1 and aflatoxin M1 to liver DNA of rat, mouse and pig

Associations between liver lesions in winter flounder (Pleuronectes americanus) and sediment chemical contaminants from north-east United States estuaries

Comparative Study of Aflatoxin M1 in Livestock Livers from Minna, Nigeria

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