Abstract: Aflatoxin-contaminated food poses a serious risk to both human
and animal health. Copper (1)-nicotinate (Cu+-nicotinate) complex
potentiated the prophylactic effect against chronic aflatoxicosis in the
experimental animals through the synthesis of less toxic metabolites M1
and Q1 which are easily excreted in urine. To investigate the action of the
safety Cu+-nicotinate complex on gene expression of Cytochrome 450
(CYP450) system, the liver tissue samples of orally administered rats for 3
weeks with aflatoxin B1 (AFB1; 30 μg/kg body weight), with and without
association of the copper complex (400 μg/kg body weight) were assayed
for their gene expression of CYP450 families including 1A2, 3A2 and
2C11 as well as histopathological examination of the hepatic tissue samples
was performed. The obtained data denoted that the Cu+-nicotinate complex
significantly reduced gene expression of CYP2C11 and CYP3A2 that
enhancing the most toxic epoxide metabolite. On the contrary, this complex
enhanced the expression of CYP1A2 that synthesize the less toxic
metabolite M1 and Q1. The histopathological examination mostly
confirmed such observation as the signs of aflatoxicosis were absent in
Cu+-nicotinate-treated group. Consequently, it could be predicted that the
Cu+-nicotinate complex may be medically used as an inhibitory food
additive agent against exposure of aflatoxicosis in the intact animals since
the complex contains the copper and nicotinic acid, the two daily required
biochemical elements for sustaining live in healthy conditions.