However, ERK 1/2 phosphorylation was shown to be involved in apoptotic morphological changes induced by heat stress at jejunal level ( Yu

et al., 2010). Similarly, a recent paper has indicated a correlation between decreased intestinal barrier function, decreased expression of tight junction proteins and the intestinal activation of MAPK ( Hu et al., 2012). So, the present results taken together with previous works allow to hypothesize that intestinal morphological alterations, such apical lyses of enterocytes and villi atrophy, were associated with changes in the tight junctions of the epithelium and the apoptosis induced by MAPK activation after exposure to DON. In conclusion, we demonstrated that, Selleckchem Alpelisib in in vivo and ex vivo models, the histological changes induced by DON are similar as well as the response observed for the expression of MAPK in both models. This strongly suggests that intestinal toxicity of DON involve MAPK activation. In addition, using histological and protein expression analysis, we confirmed that the explant model is a good alternative for the studies focused on gastrointestinal toxicity following exposure to low doses of toxins. This work was financially supported by the CAPES/COFECUB (593/08) international cooperation program, CNPq grant (474583/2010-4) and the French ANR Project DON & Co. “
“The Phoneutria nigriventer spider, popularly known as the wandering armed spider or banana spider accounts

for most notified cases of accidents in Brazil. The Selleck Gemcitabine majority of accidents only cause local edema and pain; less than 1% is considered severe ( Bucaretchi et al., 2000). Patients severely envenomed Fossariinae show tachycardia, hypertension, priapism, agitation, blurred vision, convulsion, and in some cases pulmonary edema and death. P. nigriventer venom (PNV) contains a notable amount of biologically active peptides, most of which are Na+, K+ and Ca2+ channel-acting neuropeptides which affect neurotransmitter release ( Fontana and Vital Brazil, 1985; Love and Cruz-Höfling, 1986; Gomez et al., 2002). In rats, the

venom induces excitatory effects such as intense salivation, lachrymation, piloerection, priapism, tonic convulsion and spastic and flaccid paralysis of the hindlimbs ( Diniz, 1963; Schenberg and Pereira Lima, 1971; Le Sueur et al., 2003; Rapôso et al., 2007; Mendonça et al., 2012). Transmission electron microscopy has shown that the venom can cause BBBb, evidenced by extravasation of extracellular tracer from brain microvessels and the presence of perivascular edema and edematous electron lucent endfeet of the perivascular astrocyte population ( Le Sueur et al., 2003, 2004; Rapôso et al., 2007). Swelling of astrocytic endfeet that follows BBB impairment may result from osmotic imbalance and accumulation of fluid into the brain provoking edema. The regulation of water permeability across the BBB is fundamental to maintain brain homeostasis.