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Mol. Cells 2002; 13(2): 221-227

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

Methamphetamine-induced Apoptosis in a CNS-derived Catecholaminergic Cell Line

Hyun Jin Choi, Tae Moo Yoo, Soo Youn Chung, Ji Sun Yang, Joo-Il Kim, Eun Sook Ha, Onyou Hwang

Abstract

Methamphetamine (METH) causes neurotoxic dam-ages to the dopaminergic system in mammals, but whether it exerts toxicity to dopamine cells in culture has not been fully explored. In order to develop an in vitro model of METH-induced dopamine neurotoxicity toward more systemical examination of the mechan-ism, we investigated METH toxicity in a clonal dopa-mine producing cell line (CATH.a). We show in the present study that METH produces a time- and dose-dependent increase in cell death via a process similar to apoptosis. The METH toxicity seems to be produced by oxidative stress, as it was attenuated by the antioxi-dant glutathione, and to involve dopamine because dopamine release and synthesis inhibitors attenuated the toxicity. This catecholaminergic cell line derived from the central nervous system may become a useful in vitro model to elucidate the mechanism underlying the METH-induced dopaminergic neuronal damage.

Keywords Apoptosis, Dopamine, Oxid, Methamphetamine, CATH.a

Article

Research Article

Mol. Cells 2002; 13(2): 221-227

Published online April 30, 2002

Copyright © The Korean Society for Molecular and Cellular Biology.

Methamphetamine-induced Apoptosis in a CNS-derived Catecholaminergic Cell Line

Hyun Jin Choi, Tae Moo Yoo, Soo Youn Chung, Ji Sun Yang, Joo-Il Kim, Eun Sook Ha, Onyou Hwang

Abstract

Methamphetamine (METH) causes neurotoxic dam-ages to the dopaminergic system in mammals, but whether it exerts toxicity to dopamine cells in culture has not been fully explored. In order to develop an in vitro model of METH-induced dopamine neurotoxicity toward more systemical examination of the mechan-ism, we investigated METH toxicity in a clonal dopa-mine producing cell line (CATH.a). We show in the present study that METH produces a time- and dose-dependent increase in cell death via a process similar to apoptosis. The METH toxicity seems to be produced by oxidative stress, as it was attenuated by the antioxi-dant glutathione, and to involve dopamine because dopamine release and synthesis inhibitors attenuated the toxicity. This catecholaminergic cell line derived from the central nervous system may become a useful in vitro model to elucidate the mechanism underlying the METH-induced dopaminergic neuronal damage.

Keywords: Apoptosis, Dopamine, Oxid, Methamphetamine, CATH.a

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).

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