Developing Central Nervous System and Vulnerability to Platinum Compounds
Figure 1
Cell death and damage of proliferating and differentiating cells at PD11. TUNEL reaction, Bax and Bcl2 immunoreactions. Treatment with dose of 5 μg/g b.w. At PD11, in comparison with control rats (a)–(c), TUNEL positive dying cells increase in the EGL after cisPt (d) as well as Bax immunopositivity (e), especially in nests of cells (e, insert: arrow), while Bcl2 labelling decreases (f); in the Purkinje cell bodies, the immunopositivity for Bax is high (e), while Bcl2 is lowered (f). After PtAcacDMS, there are no changes of TUNEL reactivity (g); Bax-labelled (h) microglial-like cells (h, insert: arrows) are more distinguishable in the EGL, and Bax immunopositivity increases in the Purkinje cells (h); the labelling for Bcl2 (i) is present in some proliferating cells of the EGL (I, insert: arrow). Treatment with dose of 10 μg/g b.w. There is a further increase of dying cells after cisPt (j) in the EGL, where nests of Bax immunopositive cells (k) and Bcl2 immunonegative cells (l inserts: arrows) are evident; weak Bcl2 immunopositivity is shown in the EGL and in the Purkinje cells (l, insert: arrow). In comparison with control rats (a), no changes are observed after PtAcacDMS regards TUNEL reaction (m), but several Bax immunopositive microglial-like cells (n) are detectable in the EGL (insert: arrows) as well as some Bcl2 cells (o, insert: arrows); there is an increased Bcl2 immunoreactivity in the Purkinje cell bodies (o). Magnification: 40x; insert: 100x.
