Induction of oxidative stress by endosulfan and protective effect of lipid-soluble antioxidants against endosulfan-induced oxidative damage

Ho Yong Sohn; Chong Suk Kwon; Gi Seok Kwon; Jung Bok Lee; Eungbin Kim

doi:10.1016/j.toxlet.2004.03.004

Induction of oxidative stress by endosulfan and protective effect of lipid-soluble antioxidants against endosulfan-induced oxidative damage

Ho Yong Sohn, Chong Suk Kwon, Gi Seok Kwon, Jung Bok Lee, Eungbin Kim

Department of Systems Biology

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

57 Citations (Scopus)

Abstract

The toxic mechanism of endosulfan, a widely used organochlorine pesticide, was investigated in Saccharomyces cerevisiae and human cell lines. A concentration-dependent inhibition of cell growth was observed when S. cerevisiae was exposed to endosulfan, and its cytotoxicity (IC₅₀) was found to be 49 μM and 86 μM in HepG2 and HeLa human cell lines, respectively. The treatment of S. cerevisiae with endosulfan resulted in oxidative damage, as demonstrated by thiobarbituric acid-reactive substance (TBARS) production, in a dose-dependent manner, and the growth inhibition was recovered by treatment with lipid-soluble antioxidants, such as α-tocopherol or β-carotene, suggesting that endosulfan toxicity may be closely associated with endosulfan-induced reactive oxygen species (ROS) generation. The inhibition of cellular respiration by endosulfan treatment and the recovery of respiration activity by antioxidant treatment confirmed that endosulfan induces oxidative stress and inhibits respiration via ROS generation. These results suggest that unicellular yeast might provide a useful system for elucidating the toxicity of endosulfan.

Original language	English
Pages (from-to)	357-365
Number of pages	9
Journal	Toxicology Letters
Volume	151
Issue number	2
DOIs	https://doi.org/10.1016/j.toxlet.2004.03.004
Publication status	Published - 2004 Jul 15

Bibliographical note

Funding Information:
This work was supported by a grant from BioGreen 21 Program, Rural Development Administration, Republic of Korea (1000520030096000).

All Science Journal Classification (ASJC) codes

Toxicology

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10.1016/j.toxlet.2004.03.004

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title = "Induction of oxidative stress by endosulfan and protective effect of lipid-soluble antioxidants against endosulfan-induced oxidative damage",

abstract = "The toxic mechanism of endosulfan, a widely used organochlorine pesticide, was investigated in Saccharomyces cerevisiae and human cell lines. A concentration-dependent inhibition of cell growth was observed when S. cerevisiae was exposed to endosulfan, and its cytotoxicity (IC50) was found to be 49 μM and 86 μM in HepG2 and HeLa human cell lines, respectively. The treatment of S. cerevisiae with endosulfan resulted in oxidative damage, as demonstrated by thiobarbituric acid-reactive substance (TBARS) production, in a dose-dependent manner, and the growth inhibition was recovered by treatment with lipid-soluble antioxidants, such as α-tocopherol or β-carotene, suggesting that endosulfan toxicity may be closely associated with endosulfan-induced reactive oxygen species (ROS) generation. The inhibition of cellular respiration by endosulfan treatment and the recovery of respiration activity by antioxidant treatment confirmed that endosulfan induces oxidative stress and inhibits respiration via ROS generation. These results suggest that unicellular yeast might provide a useful system for elucidating the toxicity of endosulfan.",

author = "Sohn, {Ho Yong} and Kwon, {Chong Suk} and Kwon, {Gi Seok} and Lee, {Jung Bok} and Eungbin Kim",

note = "Funding Information: This work was supported by a grant from BioGreen 21 Program, Rural Development Administration, Republic of Korea (1000520030096000).",

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AU - Lee, Jung Bok

AU - Kim, Eungbin

N1 - Funding Information: This work was supported by a grant from BioGreen 21 Program, Rural Development Administration, Republic of Korea (1000520030096000).

PY - 2004/7/15

Y1 - 2004/7/15

N2 - The toxic mechanism of endosulfan, a widely used organochlorine pesticide, was investigated in Saccharomyces cerevisiae and human cell lines. A concentration-dependent inhibition of cell growth was observed when S. cerevisiae was exposed to endosulfan, and its cytotoxicity (IC50) was found to be 49 μM and 86 μM in HepG2 and HeLa human cell lines, respectively. The treatment of S. cerevisiae with endosulfan resulted in oxidative damage, as demonstrated by thiobarbituric acid-reactive substance (TBARS) production, in a dose-dependent manner, and the growth inhibition was recovered by treatment with lipid-soluble antioxidants, such as α-tocopherol or β-carotene, suggesting that endosulfan toxicity may be closely associated with endosulfan-induced reactive oxygen species (ROS) generation. The inhibition of cellular respiration by endosulfan treatment and the recovery of respiration activity by antioxidant treatment confirmed that endosulfan induces oxidative stress and inhibits respiration via ROS generation. These results suggest that unicellular yeast might provide a useful system for elucidating the toxicity of endosulfan.

AB - The toxic mechanism of endosulfan, a widely used organochlorine pesticide, was investigated in Saccharomyces cerevisiae and human cell lines. A concentration-dependent inhibition of cell growth was observed when S. cerevisiae was exposed to endosulfan, and its cytotoxicity (IC50) was found to be 49 μM and 86 μM in HepG2 and HeLa human cell lines, respectively. The treatment of S. cerevisiae with endosulfan resulted in oxidative damage, as demonstrated by thiobarbituric acid-reactive substance (TBARS) production, in a dose-dependent manner, and the growth inhibition was recovered by treatment with lipid-soluble antioxidants, such as α-tocopherol or β-carotene, suggesting that endosulfan toxicity may be closely associated with endosulfan-induced reactive oxygen species (ROS) generation. The inhibition of cellular respiration by endosulfan treatment and the recovery of respiration activity by antioxidant treatment confirmed that endosulfan induces oxidative stress and inhibits respiration via ROS generation. These results suggest that unicellular yeast might provide a useful system for elucidating the toxicity of endosulfan.

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Induction of oxidative stress by endosulfan and protective effect of lipid-soluble antioxidants against endosulfan-induced oxidative damage

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