TOP

Research Article

Split Viewer

Mol. Cells 2005; 20(2): 189-195

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

Ethanol Induces Cell Death by Activating Caspase-3 in the Rat Cerebral Cortex

Jae Yoon Han, Yeon Joo, Yoon Sook Kim, Young Ki Lee, Hyun Joon Kim, Gyeong Jae Cho, Wan Sung Choi, Sang Soo Kang

Abstract

Ethanol has long been implicated in triggering apoptotic neurodegeneration. We examined the effects of ethanol on the rat brain during synaptogenesis when a spurt in brain growth occurs. This period corresponds to the first 2 postnatal weeks in rats and is very sensitive to ethanol exposure. Ethanol was administered subcutaneously to 7-day- postnatal rat pups by a dosing regimen of 3 g/kg at 0 h and again at 2 h. Blood ethanol levels peaked (677 ± 16.4 mg/dl) at 4 h after the first ethanol administration. The cerebral cortexes of the ethanol-treated group showed several typical symptoms of apoptosis such as chromosome condensation and disintegration of cell bodies. Activated caspase-3 positive cells were found in the cortex within 2 h of the first injection, and reached a peak at 12 h. In addition, TUNEL staining revealed DNA fragmentation in the same regions. These results demonstrate that acute ethanol administration causes neuronal cell death via a caspase-3-dependent pathway within 24 h, suggesting that activation of caspase-3 is a marker of the developmental neurotoxicity of ethanol.

Keywords Caspase-3; Cell Death; Ethanol; Rat; Synaptogenesis; TUNEL

Article

Research Article

Mol. Cells 2005; 20(2): 189-195

Published online October 31, 2005

Copyright © The Korean Society for Molecular and Cellular Biology.

Ethanol Induces Cell Death by Activating Caspase-3 in the Rat Cerebral Cortex

Jae Yoon Han, Yeon Joo, Yoon Sook Kim, Young Ki Lee, Hyun Joon Kim, Gyeong Jae Cho, Wan Sung Choi, Sang Soo Kang

Abstract

Ethanol has long been implicated in triggering apoptotic neurodegeneration. We examined the effects of ethanol on the rat brain during synaptogenesis when a spurt in brain growth occurs. This period corresponds to the first 2 postnatal weeks in rats and is very sensitive to ethanol exposure. Ethanol was administered subcutaneously to 7-day- postnatal rat pups by a dosing regimen of 3 g/kg at 0 h and again at 2 h. Blood ethanol levels peaked (677 ± 16.4 mg/dl) at 4 h after the first ethanol administration. The cerebral cortexes of the ethanol-treated group showed several typical symptoms of apoptosis such as chromosome condensation and disintegration of cell bodies. Activated caspase-3 positive cells were found in the cortex within 2 h of the first injection, and reached a peak at 12 h. In addition, TUNEL staining revealed DNA fragmentation in the same regions. These results demonstrate that acute ethanol administration causes neuronal cell death via a caspase-3-dependent pathway within 24 h, suggesting that activation of caspase-3 is a marker of the developmental neurotoxicity of ethanol.

Keywords: Caspase-3, Cell Death, Ethanol, Rat, Synaptogenesis, TUNEL

Mol. Cells
Jun 30, 2023 Vol.46 No.6, pp. 329~398
COVER PICTURE
The cellular proteostasis network is adaptively modulated upon cellular stress, thereby protecting cells from proteostasis collapse. Heat shock induces the translocation of misfolded proteins and the chaperone protein HSP70 into nucleolus, where nuclear protein quality control primarily occurs. Nuclear RNA export factor 1 (green), nucleolar protein fibrillarin (red), and nuclei (blue) were visualized in NIH3T3 cells under basal (left) and heat shock (right) conditions (Park et al., pp. 374-386).

Share this article on

  • line
  • mail

Molecules and Cells

eISSN 0219-1032
qr-code Download