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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
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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