Comparative study of the toxic effects of fumonisin B1 in rat C6 glioma cells and p53-null mouse embryo fibroblasts

Fumonisin B1: A Neurotoxic Mycotoxin / Fumonizin B1: Neurotoksični Mikotoksin

“…This study suggests that lipid peroxidation is involved in FB 1 cytotoxicity. The same group confi rmed this observation in their subsequent study (32). In rat C6 glioblastoma and p53 null mouse MEF embryonic fi broblasts, FB 1 (3 μmol L -1 to 36 μmol L -1 for 24 h) induced lipid peroxidation that was prevented by pre-incubation of cells with vitamin E (25 μmol L -1 for 24 h).…”

“…Interestingly, in human SH-SY5Y neuroblastoma FB 1 did not increase ROS. In a study that followed (33), this group of scientists established higher ROS production and lipid peroxidation, and lower glutathione levels in human U-118MG glioblastoma cells after treatment with 0.1 μmol L -1 to 100 μmol L -1 FB 1 for 24 h to 144 h. They also observed DNA laddering and higher caspase-3 activity and concluded, similarly to Mobio et al (32), that oxidative stress may be involved in FB 1 -induced apoptosis. Moreover, they suggested a possible sequence of events, as follows: activation of caspase-3 (that was observed at the earliest time point) increases ROS production leading to lipid peroxidation and reduction of intracellular glutathione level, and finally to DNA fragmentation and cell death.…”

“…In the next study by the same authors (53) on C6 glioblastoma cells treated with FB 1 (3 μmol L -1 to 27 μmol L -1 for 24 h) DNA fragmentation parameters such as DNA laddering, DNA damage verifi ed by the comet assay, and evident apoptotic bodies (revealed by chromatin staining with acridine orange and ethidium bromide) pointed to the pro-apoptotic effect of FB 1 . To check the involvement of p53 gene in FB 1 -induced apoptosis and cell cycle, the same group of authors used two cell types, rat C6 glioblastoma with normal p53 status, and p53-null MEF mouse embryonic fi broblasts (32). FB 1 treatment (3 μmol L -1 to 36 μmol L -1 for 24 h, 48 h, and 72 h) induced DNA fragmentation in both cell types.…”

Assessment of the Biosafety of the Bioinsecticide Agerin on Different Biological Systems

“…Wu et al (2000) indicated that deltamethrin leads to the persistent increase of p53 and Bax expression and transient elevation of Bcl-2 expression, resulting in an increased ratio of Bax to Bcl-2, which may contribute to apoptotic cell death in rat brain following deltamethrin treatment. Mobio et al (2003) suggested a possible loss of protective mechanisms (such as p53-dependent apoptosis cycle arrest) in FB 1 -damage MEF cells and confirm that cells lacking mechanisms governed by p53 gene would susceptible to neoplastic cascade or mutation following DNA lesions induced by this mycotoxin. Wang et al (2005) reported that expression of p53 and Bax in each treatment group increased significantly compared with that in control group (p<0.05), with the exception of 0.1 microg/kg LR exposure group.…”

Fumonisins: oxidative stress-mediated toxicity and metabolism in vivo and in vitro

“…There has been considerable focus for the last several years on the potential of FB 1 to induce oxidative stress. In vitro studies conducted on several cell lines have suggested the possible role of oxidative stress on FB 1 -induced cytotoxicity and apoptosis (Bernabucci et al 2011;Domijan et al 2015;Ferrante et al 2002;Kang and Alexander 1996;Klaric et al 2007;Kouadio et al 2005;Mary et al 2012;Mobio et al 2003;Stockmann-Juvala et al 2004a, b). Similar results were also observed in mice (Abbes et al 2015), rats (Hassan et al 2014) and broiler chicks (Poersch et al 2014).…”