Figures & data
Figure 1. Experimental design. Bovine and camelid neonatal PMN (isolated before vs. after colostrum consumption) were exposed to AFB1 (10 ng/ml) for 24 h. Comparative (para)clinical and hematological evaluations. Eosin/Giemsa staining of isolated PMN and whole blood smears. Magnification 1000×.
Figure 2. ATP levels in neonatal PMN. Exposure to AFB1 (10 ng/ml) for 24 h induced changes in ATP quantity in bovine (a, b) and camelid (c, d) neonatal PMN that were isolated before (a, c) vs. after (b, d) colostrum consumption. Differing superscripts indicate significant difference (p < 0.05). Values shown are mean ± SEM of 12 per species.
Figure 3. Caspases-3, -7, and -9 activities in neonatal PMN. AFB1 (10 ng/ml for 24 h)-induced changes in caspase 3/7 (a–d) and 9 (e–h) activities in bovine (a, b, e, f) and camelid (c, d, g, h) neonatal PMN isolated before (a, c, e, g) vs. after (b, d, f, h) colostrum consumption. Differing superscripts indicate significant difference (p < 0.05). Values shown are mean ± SEM of 12 per species. Doxorubicin ((Dox) (insets)) was only used as positive control for apoptosis/caspases activity; these data were not compared to any of the other groups.
Figure 4. AFB1 can induce apoptosis via caspases 3/7 and 9 activation, and ATP depletion in bovine/camelid neonatal PMN, potentially through death-receptor-mediated, free radical, and mitochondrial pathways of cell apoptosis. In the intrinsic pathways, various apoptotic stimuli (e.g. ROS, other microenvironmental stresses) mediate permeabilization of the mitochondrial outer membrane and trigger signaling pathways. Within cytosol, cytochrome c together with Apaf-1 and dATP form apoptosome complexed to which the initiator of procaspase-9 is recruited and activated. Caspase-9-catalyzed activation of caspase-3 executes final steps of apoptosis. This schematic highlights what was detected in this study.
