Open Access

ARTICLE

CAS role in the brain apoptosis of Bufo arenarum induced by cypermethrin

M. F. IZAGUIRRE, M. N. VERGARA, V. H. CASCO.

Laboratorio de Microscopía, FI-Bioingeniería, UNER, Ruta 11, CC 47, suc. 3, (3100), Paraná, Entre Ríos, Argentina.
Address correspondence to: Dr. Victor Hugo Casco. Laboratorio de Microscopía. FI-Bioingeniería, UNER. C.C. 47 Suc. 3. (3100) Paraná, Entre Ríos, ARGENTINA. Fax: (+54-343) 475077. E-mail: vcasco@bioingenieria.edu.ar

BIOCELL 2006, 30(2), 309-320. https://doi.org/10.32604/biocell.2006.30.309

Abstract

CAS might have a key role in the apoptosis induced by toxins, acting as anti-apoptotic factor, stimulating the cellular proliferation and the cell contact stabilization. To start to elucidate their role in the brain apoptosis of Bufo arenarum induced by cypermethrin (CY), the expression patterns of CAS and several cell adhesion molecules (CAMs) were established.
Bufo arenarum tadpoles of the control and acute bioassay survival at different doses (39, 156, 625 and 2,500 μg CY/L) and times (24, 48, 72 and 96 h) of CY treatment were fixed in Carnoy, embedded in paraffin and sectioned. CAS and CAMs expression was determined by immunofluorescence and immunohistochemistry, respectively.
When the bioassay starts, CAS increases suggesting a proliferative or regenerative effect, but decreases when the doses and/or the biocide exposure time increases, suggesting compromise of the cellular cycle control and trigger of an apoptotic wave. However, these neurotoxic mechanisms should not involve degradation of N-cadherin and α-catenin, in contrast of β-catenin and axonal N-CAM180, at least in the initial apoptotic phase. Additionally, an adhesion compensatory mechanism by N-CAM180 is observed in the neuron cell body.
These results suggest a dual role of CAS in the cellular cycle control during the CY-induced apoptosis: induction of cell proliferation and stabilization of the cell-cell junctions by modulating CAMs expression.

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