The Effects of Curcumin on Aflatoxin B1- Induced Toxicity in Rats

• Published in: Biocontrol Science Vol. 20; no. 3; pp. 171 - 177
• Main Authors: POAPOLATHEP, SARANYA, IMSILP, KANJANA, MACHII, KENJI, KUMAGAI, SUSUMU, POAPOLATHEP, AMNART
• Format: Journal Article
• Language: English
• Published: Japan The Society for Antibacterial and Antifungal Agents, Japan 2015; Japan Science and Technology Agency
• Subjects: Administration, Oral; Aflatoxin B1; Aflatoxin B1 - toxicity; Animals; Carcinogens - toxicity; Curcumin; Curcumin - administration & dosage; Disease Models, Animal; DNA Adducts - analysis; Enzyme Inhibitors - administration & dosage; Glutathione Transferase - analysis; Hepatocarcinogenicity; Liver - enzymology; Male; Mutagens - toxicity; Poisoning - drug therapy; Rats; Rats, Inbred F344; Toxicity
• ISSN: 1342-4815; 1884-0205
• DOI: 10.4265/bio.20.171

To evaluate the potential of curcumin on toxic and carcinogenic effects of Aflatoxin B1 (AFB1) in relation to AFB1 metabolism, we studied the effects of curcumin on hepatic AFB1-DNA adduct formation and glutathione S-transferase (GST) activity, and the toxic effects of AFB1 in male Fischer 344 rats. Oral administration of curcumin to 5-week-old male rats at a dose of 8 or 80 mg/kg for five consecutive days for three weeks resulted in reduction of AFB1-DNA adduct formation mediated by both liver microsomal and postmitochondrial fractions. The activity of liver GST toward a universal substrate, CDNB, was increased in curcuminadministered rats. As for the acute toxicity of AFB1, curcumin was orally administered to rats for 3 weeks and then AFB1 was given by intragastric intubation. The result showed a decrease of plasma AST and ALT activities in curcumin-treated rats compared with those which received AFB1 alone. Moreover, we have observed that curcumin also reduced glutathione S-transferase placental form positive single cells and foci caused by AFB1 treatment. These results demonstrate the potential of curcumin to reduce the toxic and carcinogenic effects of AFB1 by modulating hepatic drug metabolizing enzymes responsible for AFB1 metabolism.