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Figure 1. Time-dependent depolymerization of F-actin promoted by YTX in IPLB-LdFB and NIH3T3 cell lines evidenced by FITC-phalloidin labeling and DAPI nuclear counterstaining. IPLB-LdFB: control cells (A); and IPLB-LdFB after 24 h (B), 48 h (C) and 72 h (D) incubation with 100 nM YTX; NIH3T3 control cells (E); and NIH3T3 cells after 24 h (F); 48 h (G); 72 h (H) incubation with 100 nM YTX. Bar = 10 μm. (Reprinted with permission from [30]).
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Figure 2. Lysosomal damage promoted by YTX in IPLB-LdFB cell lines evidenced by neutral red (AâD), acridine orange (EâH) and acid phosphatase activity (IâN) methods. A, E, I) IPLB-LdFB control cells; B, F, L) IPLB-LdFB cells after 8 h incubation with 100 nM YTX; C, G, M) IPLB-LdFB cells after 12 h incubation with 100 nM YTX; D, H, N) IPLB-LdFB cells after 24 h incubation with 100 nM YTX. Bar = 10 μm. (Reprinted with permission from [30]).
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Figure 3. Immunolocalization of Ca2+-binding proteins and cytoskeleton components in the cerebellum cortex from control (A, C) and 420 μg/kg YTX injected mice (B, D). In treated samples, the positivity to anti-calbindin D-28K mAb (A, B) and to anti-β-tubulin (C, D) decrease. Bar = 10 μm. (Reprinted with permission, modified from [22]).
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Figure 4. Number of apoptotic cells recorded in thymic sections from control, 420 and 10 μg/kg YTX injected mice (*, ** p < 0.05 versus control; ** p < 0.05 versus *). (Reprinted with permission from [40]).
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Figure 5. Sections of thymus from control (A) and 10 μg/kg YTX injected mice (B) immunostained with anti-cytokeratin 1/5/10/14 mAb. Note the changes in organization of the medullary epithelial compartment with modifications in cell morphology and cytokeratin immunoreactivity. Bar = 10 μm. (Reprinted with permission, modified from [40]).
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Figure 6. Longitudinal sections from E. crypticus controls (A, C) and specimens treated with 100 nM OA for 24 h (D) and 200 nM OA for 12 h (B) stained with gallocyanin-chrome alum (A), Mallory-Azan stain (B) and immunostained with anti-IL-6 polyclonal antibody (C, D). (A) The chloragogenous tissue (c) from controls formed one or two layers of round vacuolated and basophilic cells surrounding the intestine (i). (B) After OA treatment, the tissue showed a higher number of cell layers and expanded into the celomatic cavity. The toxin also induced an increase in the number of circulating celomocytes. (C, D) Immunonegative chloragocytic cells, arrows; immunopositive amoebocytes, arrowheads. Bar = 10 μm. (Reprinted with permission, modified from [68]).
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Figure 7. FETAX bioassay: time- and concentration-dependent effects of OA on embryo mortality (*p < 0.05 versus control). (Reprinted with permission from [80]).
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Figure 8. Images of control (A) and 1 nM OA treated (B) X. laevis early larval stages: note the tail folding and the reduced size at the end of toxin treatment. Bar = 1 mm. (Reprinted with permission from [80]).
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Figure 9. FETAX bioassay: time- and concentration- dependent effects of PTX on sample mortality (*p < 0.05 versus control). (Reprinted with permission from [81]).
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Figure 10. FETAX bioassay: percentage of dead samples compared to the initial embryo number (*p < 0.05 versus control). (Reprinted with permission from [81])
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Figure 11. bmp4 expression levels in X. laevis embryonic and early larval stages after toxin treatments. Bars represent standard deviation (SD) from the mean value of light intensity registered for each sample and normalized versus control value (*p < 0.05). (Reprinted with permission from [82]).
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Figure 12. myf5 expression levels in X. laevis embryonic and early larval stages after toxin treatments. Bars represent SD from the mean value of light intensity registered for each sample and normalized versus control value (*p < 0.05). (Reprinted with permission from [82]).
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