Protective Effects of Selenium on Aflatoxin B1-induced Mitochondrial Permeability Transition, DNA Damage, and Histological Alterations in Duckling Liver

Aflatoxin B-1 (AFB(1)) is a mycotoxin that causes cytotoxicity through oxidative damage to its target organs. The liver is the first target of AFB(1) damage. The aim of this study was to evaluate the protective effect of selenium on AFB(1)-induced hepatic mitochondrial damage in ducklings using molecular biological and histopathological techniques. Aflatoxin was administered via intragastric intubation (0.1 mg/kg body weight), daily for 21 days. The experimental group also received intragastric sodium selenite (1 mg/kg body weight), while the control group was given the same volume of dimethyl sulfoxide (DMSO). Sequence analysis of the mitochondrial DNA D-loop region showed that AFB(1) induced damage. All AFB(1)-administrated ducklings were identified as having D-loop mitochondrial DNA mutations. Mutations were detected in two ducklings that had received both AFB(1) and selenium. Mitochondrial swelling assays showed that opening of the mitochondrial permeability transition pores was increased in ducklings that had received AFB(1) for 14 and 21 days (P < 0.05). Selenium significantly attenuated these adverse effects of AFB(1). After AFB(1) exposure, histological alterations were observed, including fat necrosis, steatosis, and formation of lymphoid nodules with infiltrated lymphocytes. These histological abnormalities were also attenuated by treatment with selenium. The overall data indicated that selenium exerts a potent protective effect against AFB(1)-induced hepatic mitochondrial damage, possibly through its antioxidant activity.