Heptachlor induced mitochondria-mediated cell death via impairing electron transport chain complex III

Seokheon Hong; Joo Yeon Kim; Joohyun Hwang; Ki Soon Shin; Shin Jung Kang

doi:10.1016/j.bbrc.2013.07.018

Heptachlor induced mitochondria-mediated cell death via impairing electron transport chain complex III

Seokheon Hong, Joo Yeon Kim, Joohyun Hwang, Ki Soon Shin, Shin Jung Kang

Research output: Contribution to journal › Article › peer-review

14 Citations (Scopus)

Abstract

Environmental toxins like pesticides have been implicated in the pathogenesis of Parkinson's disease (PD). Epidemiological studies suggested that exposures to organochlorine pesticides have an association with an increased PD risk. In the present study, we examined the mechanism of toxicity induced by an organochlorine pesticide heptachlor. In a human dopaminergic neuroblastoma SH-SY5Y cells, heptachlor induced both morphological and functional damages in mitochondria. Interestingly, the compound inhibited mitochondrial electron transport chain complex III activity. Rapid generation of reactive oxygen species and the activation of Bax were then detected. Subsequently, mitochondria-mediated, caspase-dependent apoptosis followed. Our results raise a possibility that an organochlorine pesticide heptachlor can act as a neurotoxicant associated with PD.

Original language	English
Pages (from-to)	632-636
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	437
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2013.07.018
Publication status	Published - 9 Aug 2013

Bibliographical note

Funding Information:
This work was supported by Grants from the National Research Foundation of Korea ( 2012R1A1A2007688 and 2012R1A2A2A01046822 ) and from KFDA ( 08172-466 ).

Keywords

Apoptosis
Heptachlor
Mitochondria
Parkinson's disease
Pesticide
Reactive oxygen species

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbrc.2013.07.018

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title = "Heptachlor induced mitochondria-mediated cell death via impairing electron transport chain complex III",

abstract = "Environmental toxins like pesticides have been implicated in the pathogenesis of Parkinson's disease (PD). Epidemiological studies suggested that exposures to organochlorine pesticides have an association with an increased PD risk. In the present study, we examined the mechanism of toxicity induced by an organochlorine pesticide heptachlor. In a human dopaminergic neuroblastoma SH-SY5Y cells, heptachlor induced both morphological and functional damages in mitochondria. Interestingly, the compound inhibited mitochondrial electron transport chain complex III activity. Rapid generation of reactive oxygen species and the activation of Bax were then detected. Subsequently, mitochondria-mediated, caspase-dependent apoptosis followed. Our results raise a possibility that an organochlorine pesticide heptachlor can act as a neurotoxicant associated with PD.",

keywords = "Apoptosis, Heptachlor, Mitochondria, Parkinson's disease, Pesticide, Reactive oxygen species",

author = "Seokheon Hong and Kim, {Joo Yeon} and Joohyun Hwang and Shin, {Ki Soon} and Kang, {Shin Jung}",

note = "Funding Information: This work was supported by Grants from the National Research Foundation of Korea ( 2012R1A1A2007688 and 2012R1A2A2A01046822 ) and from KFDA ( 08172-466 ).",

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AU - Hong, Seokheon

AU - Kim, Joo Yeon

AU - Hwang, Joohyun

AU - Shin, Ki Soon

AU - Kang, Shin Jung

N1 - Funding Information: This work was supported by Grants from the National Research Foundation of Korea ( 2012R1A1A2007688 and 2012R1A2A2A01046822 ) and from KFDA ( 08172-466 ).

PY - 2013/8/9

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N2 - Environmental toxins like pesticides have been implicated in the pathogenesis of Parkinson's disease (PD). Epidemiological studies suggested that exposures to organochlorine pesticides have an association with an increased PD risk. In the present study, we examined the mechanism of toxicity induced by an organochlorine pesticide heptachlor. In a human dopaminergic neuroblastoma SH-SY5Y cells, heptachlor induced both morphological and functional damages in mitochondria. Interestingly, the compound inhibited mitochondrial electron transport chain complex III activity. Rapid generation of reactive oxygen species and the activation of Bax were then detected. Subsequently, mitochondria-mediated, caspase-dependent apoptosis followed. Our results raise a possibility that an organochlorine pesticide heptachlor can act as a neurotoxicant associated with PD.

AB - Environmental toxins like pesticides have been implicated in the pathogenesis of Parkinson's disease (PD). Epidemiological studies suggested that exposures to organochlorine pesticides have an association with an increased PD risk. In the present study, we examined the mechanism of toxicity induced by an organochlorine pesticide heptachlor. In a human dopaminergic neuroblastoma SH-SY5Y cells, heptachlor induced both morphological and functional damages in mitochondria. Interestingly, the compound inhibited mitochondrial electron transport chain complex III activity. Rapid generation of reactive oxygen species and the activation of Bax were then detected. Subsequently, mitochondria-mediated, caspase-dependent apoptosis followed. Our results raise a possibility that an organochlorine pesticide heptachlor can act as a neurotoxicant associated with PD.

KW - Apoptosis

KW - Heptachlor

KW - Mitochondria

KW - Parkinson's disease

KW - Pesticide

KW - Reactive oxygen species

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JF - Biochemical and Biophysical Research Communications

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ER -

Heptachlor induced mitochondria-mediated cell death via impairing electron transport chain complex III

Abstract

Bibliographical note

Keywords

UN SDGs

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