Graduate Thesis Or Dissertation
 

Effect of various parameters on in vivo Aflatoxin B₁ binding to rainbow trout (Salmo gairdneri) liver DNA

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  • Aflatoxin B₁ (AFB₁,) is a potent liver carcinogen to a number of animal species including rainbow trout (Salmo gairdneri). Microsomal activation is required for the in vitro conversion of AFB, to a reactive metabolite, thought to be the AFB₁,-2,3-oxide, which will bind nucleic acids, produce toxicity, and cause mutagenesis. Nucleic acid-AFB₁ adduct formation is believed to be an indication of cancer initiation. Initial time-course and dosage experiments were conducted to establish fundamental binding data in rainbow trout. Dietary casein and fish protein concentrate (FPC) fed at 40, 50, 60, or 70% in the diet, and cyclopropenoid fatty acids (CPFA), were measured for their effect on in vivo AFB₁, binding to trout liver DNA. Both were previously reported to dramatically alter AFB₁, induced hepatocarcinogenesis. Rainbow trout and coho salmon (Oncorhynchus kisutch), two Salmonid species varying greatly in their sensitivity to AFB₁, were compared for their relative ability to produce AFB₁-DNA adducts. Correlations between trout liver mixed function oxidase (MFO) activity and AFB₁, binding to trout liver DNA were attempted by use of β-napthoflavone, a powerful enzyme inducer in rainbow trout. Binding of AFB₁, to trout liver DNA over the 48 hour(h) period studied reached a maximum value at 24 h. Increasing AFB₁, dosage produced a linear response in AFB₁-DNA adduct formation. Binding was significantly greater in the 70% casein fed fish than in the 70% FPC group. Binding in the 40, 50, and 60% casein fish was non-significantly greater than the corresponding FPC groups. AFB₁, binding to liver DNA was greatest in each source at the 60% protein level. Binding in rainbow trout was at least 20-fold greater by comparison than in coho salmon. CPFA reduced AFB₁, binding to trout liver DNA at each protein diet employed, although non-significantly. Pretreatment of fish with β-napthoflavone reduced the total level of AFB₁ in the liver and AFB₁-DNA adduct formation by 55 and 40%, respectively. Dietary protein and CPFA apparently alter tumor formation through promoter effects since binding was unaffected. The tumor resistance of coho salmon and β-napthoflavone pretreated animals is possibly due to reduced initiation of of the toxic lesion.
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Déclaration de droits
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