OBJECTIVETo study the combined toxic effects of fumonisin B(1) (FB(1)) and aflatoxin B(1) (AFB(1)) on Sprague-Dawley (SD) rats.

METHODAll 60 SD male rats were divided into five groups randomly according to the body weight (12 every group). They were given FB(1) (100 microg/kg bw), AFB(1) (100 microg/kg bw), FB(1) plus AFB(1) (100 microg/kg bw respectively), FB(1) plus AFB(1) (50 microg/kg bw respectively) and distilled water respectively by gavage. The experiment persisted 30 days to observe the changes of growth and development, the food used rate, the haematological indexes, the blood biochemical indexes and the viscera histopathology.

RESULTSAt the end of the experiment, the mean body weight increased in the FB(1) plus AFB(1) (100 microg/kg bw respectively) group was (164.9 +/- 19.8) g and the mean body weight increased in the control group was (203.7 +/- 17.1) g. And the food used rate in the FB(1) plus AFB(1) (100 microg/kg bw respectively) group was (25.3 +/- 1.6)% and the food used rate in the control group was (28.1 +/- 1.2)%. There were significant differences in the mean body weight increased and the food used rate between the FB(1) plus AFB(1) (100 microg/kg bw respectively) group and the control group (P < 0.05). While there were no significant differences of body weights and food used rates between controls and AFB(1), FB(1), and low dose AFB(1) + FB(1) groups (P > 0.05). The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutaminetransferase (gamma-GT) in serum of all of the treatment groups were increased, but the increasing extent was severe in the AFB(1) + FB(1) high dose group. At the same time the liver weight and kidney weight were decreased and the liver occurred with the remarkable histopathological lesions in the AFB(1) + FB(1) high dose group. The activity of superoxide dismutase (SOD) in serum was decreased and the level of malondialdehyde (MDA) in serum was elevated in treatment groups.

CONCLUSIONSThe combined toxic effects of AFB(1) and FB(1) existed in male SD rats. Our results provided the basic data for studying the combined effects on human exposed to these two mycotoxin at the same time.

Aflatoxin B1 ; toxicity ; Animals ; Fumonisins ; toxicity ; Male ; Mycotoxins ; toxicity ; Rats ; Rats, Sprague-Dawley ; Toxicity Tests

The present study was conducted to investigate the effect of silymarin on experimental liver toxication induced by Fumonisin B1 (FB1) in BALB/c mice. The mice were divided into six groups (n = 15). Group 1 served as the control. Group 2 was the silymarin control (100 mg/kg by gavage). Groups 3 and 4 were treated with FB1 (Group 3, 1.5 mg/kg FB1, intraperitoneally; and Group 4, 4.5 mg/kg FB1). Group 5 received FB1 (1.5 mg/kg) and silymarin (100 mg/kg), and Group 6 was given a higher dose of FB1 (4.5 mg/kg FB1) with silymarin (100 mg/kg). Silymarin treatment significantly decreased (p < 0.0001) the apoptotic rate. FB1 administration significantly increased (p < 0.0001) proliferating cell nuclear antigen and Ki-67 expression. Furthermore, FB1 elevated the levels of caspase-8 and tumor necrosis factor-alpha mediators while silymarin significantly reduced (p < 0.0001) the expression of these factors. Vascular endothelial growth factor (VEGF) and fibroblast growth factor-2 (FGF-2) expressions were significantly elevated in Group 4 (p < 0.0001). Silymarin administration alleviated increased VEGF and FGF-2 expression levels (p < 0.0001). In conclusion, silymarin ameliorated toxic liver damage caused by FB1 in BALB/c mice.
Animals ; Antioxidants/*pharmacology ; Apoptosis/drug effects ; Cell Proliferation/drug effects ; Female ; Fibroblast Growth Factor 2/genetics/metabolism ; Fumonisins/*toxicity ; Gene Expression Regulation/drug effects ; Hepatocytes/*drug effects ; Ki-67 Antigen/metabolism ; Liver/drug effects ; Mice ; Mice, Inbred BALB C ; Mycotoxins/*toxicity ; Neovascularization, Physiologic/drug effects ; Proliferating Cell Nuclear Antigen/metabolism ; Silymarin/*pharmacology ; Tumor Necrosis Factor-alpha/metabolism ; Vascular Endothelial Growth Factor A/genetics/metabolism