Aflatoxin B1 and fumonisin B1 affect the oxidative status of bovine peripheral blood mononuclear cells.
Mycotoxins are secondary metabolites having a high cytotoxic potential. They are produced by molds and released in food and feed. To date, the mechanisms underlying the mycotoxin-induced cytotoxicity have not been fully clarified. The induction of oxidative stress, as a possible mechanism, has been postulated. This in vitro study was focused on the effect of two widely occurring mycotoxins, aflatoxin B(1) (AFB(1)) and fumonisin B(1) (FB(1)), on the oxidative status of bovine peripheral blood mononuclear cells (PBMC) incubated for 2 and 7 days at different levels of AFB(1) (0, 5 and 20 μg/ml) and FB(1) (0, 35 and 70 μg/ml). Reactive oxygen metabolites (ROM), intracellular thiols (SH), malondialdehyde (MDA) and gene expression of cytoplasmic superoxide dismutase (SOD) and glutathione peroxidase (GSHPX-1) were measured on PBMC after incubation. The highest concentration of AFB(1) and all concentrations of FB(1) caused an increase (p<0.05) of intracellular ROM without any time dependent effect. Intracellular SH decreased with 20 μg AFB(1)/ml (p<0.05) and the effect was particularly marked after 7 days of exposure. Intracellular SH were not affected by FB(1) even though a lower (p<0.05) SH level after 2 days exposure than after 7 days was observed. MDA increased (p<0.05) in AFB(1) or FB(1) treated PBMC. The exposure to FB(1) for 7 days increased MDA (p<0.05) only in cells treated with 70 μg/ml. Exposure of PBMC to AFB(1) reduced SOD mRNA while FB(1) decreased both SOD and GSHPX-1 mRNA abundance. These results demonstrate that, even though by different mechanisms, AFB(1) and FB(1) may induce cytotoxicity through an impairment of the oxidative status of PBMC.
Department of Animal Science, University of Tuscia, Via S.C. De Lellis, 01100 Viterbo, Italy. bernab@unitus.it
Umberto
U
Bernabucci
Luciana
L
Colavecchia
Pier Paolo
PP
Danieli
Loredana
L
Basiricò
Nicola
N
Lacetera
Alessandro
A
Nardone
Bruno
B
Ronchi
D016604:Aflatoxin B1 / Q000633:toxicity*; D000818:Animals; D002417:Cattle; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D005260:Female; D037341:Fumonisins / Q000633:toxicity*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000235:genetics / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D009183:Mycotoxins / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000032:analysis; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D000094765:Glutathione Peroxidase GPX1
D037341:Fumonisins; D009183:Mycotoxins; D017382:Reactive Oxygen Species; D013438:Sulfhydryl Compounds; C056933:fumonisin B1; D008315:Malondialdehyde; D016604:Aflatoxin B1; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D000094765:Glutathione Peroxidase GPX1