Mechanisms of anti-carcinogenesis: the distribution and metabolism of aflatoxin B<sub>1</sub> in rainbow trout fed Aroclor 1254

Shelton, Dennis W.; Goeger, Douglas E.; Hendricks, Jerry D.; Bailey, George S.

doi:10.1093/carcin/7.7.1065

Cited by 37 publications

(17 citation statements)

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“…The opposite occurs in rainbow trout where the higher efficiency of AFBO production was associated with the high genotoxicity observed in all tissues tested. The highest peak of damage at 4 h in blood correlated well with the higher plasma levels of AFB 1 found in trout at 5 h, as indicated in kinetic studies by Shelton et al (1986). The damage to kidney cells might be due to the excretion of AFB 1 -glucuronide (Loveland et al 1984).…”

Section: Genotoxicitysupporting

confidence: 68%

Aflatoxins in aquatic species: metabolism, toxicity and perspectives

Santacroce

Conversano

Casalino

et al. 2007

Rev Fish Biol Fisheries

157

119

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Among all known mycotoxins, aflatoxins represent the most investigated, widespread and worrisome source of contamination of foods and feed worldwide. In the early 1960s, soon after the finding of aflatoxin B 1 (AFB 1 ) in the feedstuffs of aquacultured rainbow trout that had died in an epizootic of hepatomas, great scientific discoveries were made in several areas by a number of researchers under the direction of scientists like J. Halver, R. 0. Sinnhuber, G. S. Bailey, J. D. Hendricks and colleagues. Since that time, several studies have focused on the identification of new isoenzymes involved in AFB 1 metabolism and on the discovery of new modulators in AFB 1 -induced cancer initiation and progression. However, metabolic and toxicological studies on aflatoxins in marine aquacultured species are fragmented and restricted to a limited number of fish species. Aflatoxins exert a substantial impact on the fish farming production, causing disease with high mortality and a gradual decline of reared fish stock quality, thus representing a significant problem in aquaculture systems. Based on these considerations, the goals of this review article are: (1) to gather the currently available scientific information, summarising existing data on aflatoxin contamination on feeds and fishmeals, and toxicological effects induced in reared aquatic species; (2) to make a comparative analysis of AFB 1 metabolism in the most representative species studied; (3) to gain new insights on the risk of DNA damage caused by aflatoxins on fish genomes and their role in cancer development.

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Section: Genotoxicitysupporting

confidence: 68%

Aflatoxins in aquatic species: metabolism, toxicity and perspectives

Santacroce

Conversano

Casalino

et al. 2007

Rev Fish Biol Fisheries

157

119

View full text Add to dashboard Cite

show abstract

“…The induction of CYPIA by compounds such as 0-naphthoflavone (BNF), indole-3-carbinol (W3C), and polychlorinated biphenyls (PCBs) was thought to be the mechanism by which these modulators acted as chemopreventors of AFBI-initiated hepatocarcinogenesis in trout (109,110).…”

Section: Cytochromes P450mentioning

confidence: 99%

Fish models for environmental carcinogenesis: the rainbow trout.

Bailey

Williams

Hendricks

1996

Environ Health Perspect

171

114

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Progress over the past 30 years has revealed many strengths of the rainbow trout as an alternative model for environmental carcinogenesis research. These include low rearing costs, an early life-stage ultrasensitive bioassay, sensitivity to many classes of carcinogen, a well-described tumor pathology, responsiveness to tumor promoters and inhibitors, and a mechanistically informative nonmammalian comparative status. Low-cost husbandry, for example, has permitted statistically challenging tumor study designs with up to 10,000 trout to investigate the quantitative interrelationships among carcinogen dose, anticarcinogen dose, DNA adduct formation, and final tumor outcome. The basic elements of the trout carcinogen bioassay include multiple exposure routes, carcinogen response, husbandry requirements, and pathology. The principal known neoplasms occur in liver (mixed hepatocellular/cholangiocellular adenoma and carcinoma, hepatocellular carcinoma), kidney (nephroblastoma), swim bladder (adenopapilloma), and stomach (adenopapilloma). Trout possess a complex but incompletely characterized array of cytochromes P450, transferases, and other enzymic systems for phase and phase 11 procarcinogen metabolism. In general, trout exhibit only limited capacity for DNA repair, especially for removal of bulky DNA adducts. This factor, together with a high capacity for P450 bioactivation and negligible glutathione transferase-mediated detoxication of the epoxide, accounts for the exceptional sensitivity of trout to aflatoxin B1 carcinogenesis. At the gene level, all trout tumors except nephroblastoma exhibit variable and often high incidences of oncogenic Ki-ras gene mutations. Mutations in the trout p53 tumor suppressor gene have yet to be described. There are many aspects of the trout model, especially the lack of complete organ homology, that limit its application as a surrogate for human cancer research. Within these limitations, however, it is apparent that trout and other fish models can serve as highly useful adjuncts to conventional rodent models in the study of environmental carcinogenesis and its modulation. For some problems, fish models can provide wholly unique approaches.Environ Health Perspect 104(Suppl 1): 5-21 (1996)

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“…After input of PCBs into Swedish waters was forbidden, the frequency of the disease decreased drastically. However, it has since been demonstrated that PCBs are not primary carcinogens for fishes, although it has been shown that these substances do function as promoters of neoplastic lesions (Shelton et al 1986). …”

Section: Z Wmentioning

confidence: 99%

Liver anomalies in dab Limanda limanda from the southern North Sea with special consideration given to neoplastic lesions

Kranz¹,

Dethlefsen²

1990

Dis. Aquat. Org.

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Mechanisms of anti-carcinogenesis: the distribution and metabolism of aflatoxin B₁ in rainbow trout fed Aroclor 1254

Cited by 37 publications

References 0 publications

Aflatoxins in aquatic species: metabolism, toxicity and perspectives

Aflatoxins in aquatic species: metabolism, toxicity and perspectives

Fish models for environmental carcinogenesis: the rainbow trout.

Liver anomalies in dab Limanda limanda from the southern North Sea with special consideration given to neoplastic lesions

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Mechanisms of anti-carcinogenesis: the distribution and metabolism of aflatoxin B1 in rainbow trout fed Aroclor 1254

Cited by 37 publications

References 0 publications

Aflatoxins in aquatic species: metabolism, toxicity and perspectives

Aflatoxins in aquatic species: metabolism, toxicity and perspectives

Fish models for environmental carcinogenesis: the rainbow trout.

Liver anomalies in dab Limanda limanda from the southern North Sea with special consideration given to neoplastic lesions

Contact Info

Product

Resources

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Mechanisms of anti-carcinogenesis: the distribution and metabolism of aflatoxin B₁ in rainbow trout fed Aroclor 1254