In a previous work we have reported that synthetic copper (I)-nicotinate complex efficiently prevented induced nephrotoxicity by Aflatoxin B1 (AFB1) specifically by promoting phase II detoxificating glutathioneS-transferase activity. This work has been conducted to evaluate the antitoxic effect of the complex on the metabolism of AFB1. Forty five healthy male Wister albino rats were intoxicated (20 µg/kg B.W.) day after day for five weeks. The individually collected urine was assayed for AFB1, AFM1 and AFQ1 contents by HPLC technique. One third of them were co-treated by butylated hdroxytoluene (BHT) (0.05 g/kg B.W.), the second was co-treated by the copper complex (400 µg/kg B.W.) while the last was only intoxicated untreated group. Significant increase in the less toxic AFM1 and AFQ1 metabolites was recorded by any of the co-treating agents. The output of the least toxic AFQ1 fraction was significantly increased by the copper complex as regard to the BHT, (P <0.05). Conclusively, AFM1 and AFQ1 fractions in the urine that were promoted by the two tested agents may be related to their potentiating activity upon the phase I detoxificating CYP 1A2 and 3A4 enzyme families respectively. The significantly increased detoxified AFQ1 metabolite may be preferentially promoted by the copper (I)-nicotinate complex. This beneficial detoxificating effect of the copper complex has been obviously confirmed by observed great reduction in the immunohistochemical detection of vascular endothelial growth factor that was highly initiated by aflatoxicosis. Hence, such a complex could be saftly accepted as a highly potent antitoxic agent against aflatoxicosis