Phosphine-induced oxidative damage in rats: Role of glutathione

Ching Hung Hsu, Bei Ching Chi, Ming Yie Liu, Jih Heng Li, Chiou Jong Chen, Ruey Yu Chen

研究成果: 雜誌貢獻文章

75 引文 (Scopus)

摘要

Phosphine (PH3), generated from aluminium, magnesium and zinc phosphide, is a widely used pesticide. PH3 induces oxidative stress in insects, mammalian cells, animals, and humans. The involvement of glutathione (GSH) in PH3-induced oxidative toxicity is controversial. GSH levels in various tested tissues were reduced in aluminium phosphide-poisoned rats and humans, while the levels remained unchanged in insects and mammalian cells. This study examines the effectiveness of endogenous GSH as a protective agent against PH3-induced oxidative damage in rats. The association of PH3-induced nephrotoxicity and cardiotoxicity with free radical production was also tested. Male Wistar rats, administered intraperitoneally (I.P.) with PH3 at 4 mg/kg, were evaluated 30 min after treatment for PH3 toxicity to organs. PH3 significantly decreased GSH, GSH peroxidase and catalase, while significantly increased lipid peroxidation (as malondialdehyde and 4-hydroxyalkenals), DNA oxidation (as 8-hydroxydeoxyguaonsoine) and superoxide dismutase (SOD) levels in kidney and heart. These changes were significantly alleviated by melatonin (10 mg/kg I.P., 30 min before PH3), with the exception of SOD activity in heart tissue. The study also found that buthionine sulfoximine (1 g/kg I.P., 24 h before PH3) significantly enhanced the effect of PH3 on GSH loss and lipid peroxidation elevation in lung. These findings indicate that (1) endogenous GSH plays a crucial role as a protective factor in modulating PH3-induced oxidative damage, and (2) PH3 could injure kidney and heart (as noted earlier with brain, liver and lung) via oxidative stress and the antioxidant melatonin effectively prevents the damage.

原文英語
頁(從 - 到)1-8
頁數8
期刊Toxicology
179
發行號1-2
DOIs
出版狀態已發佈 - 九月 30 2002

指紋

phosphine
Glutathione
Rats
Oxidative stress
Melatonin
Lipid Peroxidation
Superoxide Dismutase
Toxicity
Insects
Oxidative Stress
Cells
Tissue
Buthionine Sulfoximine
Kidney
Lipids
Protective Agents
Lung
Malondialdehyde
Aluminum
Pesticides

ASJC Scopus subject areas

  • Toxicology

引用此文

Phosphine-induced oxidative damage in rats : Role of glutathione. / Hsu, Ching Hung; Chi, Bei Ching; Liu, Ming Yie; Li, Jih Heng; Chen, Chiou Jong; Chen, Ruey Yu.

於: Toxicology, 卷 179, 編號 1-2, 30.09.2002, p. 1-8.

研究成果: 雜誌貢獻文章

Hsu, CH, Chi, BC, Liu, MY, Li, JH, Chen, CJ & Chen, RY 2002, 'Phosphine-induced oxidative damage in rats: Role of glutathione', Toxicology, 卷 179, 編號 1-2, 頁 1-8. https://doi.org/10.1016/S0300-483X(02)00246-9
Hsu, Ching Hung ; Chi, Bei Ching ; Liu, Ming Yie ; Li, Jih Heng ; Chen, Chiou Jong ; Chen, Ruey Yu. / Phosphine-induced oxidative damage in rats : Role of glutathione. 於: Toxicology. 2002 ; 卷 179, 編號 1-2. 頁 1-8.
@article{0e032f8e55624c3b9e35222597c36366,
title = "Phosphine-induced oxidative damage in rats: Role of glutathione",
abstract = "Phosphine (PH3), generated from aluminium, magnesium and zinc phosphide, is a widely used pesticide. PH3 induces oxidative stress in insects, mammalian cells, animals, and humans. The involvement of glutathione (GSH) in PH3-induced oxidative toxicity is controversial. GSH levels in various tested tissues were reduced in aluminium phosphide-poisoned rats and humans, while the levels remained unchanged in insects and mammalian cells. This study examines the effectiveness of endogenous GSH as a protective agent against PH3-induced oxidative damage in rats. The association of PH3-induced nephrotoxicity and cardiotoxicity with free radical production was also tested. Male Wistar rats, administered intraperitoneally (I.P.) with PH3 at 4 mg/kg, were evaluated 30 min after treatment for PH3 toxicity to organs. PH3 significantly decreased GSH, GSH peroxidase and catalase, while significantly increased lipid peroxidation (as malondialdehyde and 4-hydroxyalkenals), DNA oxidation (as 8-hydroxydeoxyguaonsoine) and superoxide dismutase (SOD) levels in kidney and heart. These changes were significantly alleviated by melatonin (10 mg/kg I.P., 30 min before PH3), with the exception of SOD activity in heart tissue. The study also found that buthionine sulfoximine (1 g/kg I.P., 24 h before PH3) significantly enhanced the effect of PH3 on GSH loss and lipid peroxidation elevation in lung. These findings indicate that (1) endogenous GSH plays a crucial role as a protective factor in modulating PH3-induced oxidative damage, and (2) PH3 could injure kidney and heart (as noted earlier with brain, liver and lung) via oxidative stress and the antioxidant melatonin effectively prevents the damage.",
keywords = "Glutathione, Oxidative damage, Phosphine, Rats",
author = "Hsu, {Ching Hung} and Chi, {Bei Ching} and Liu, {Ming Yie} and Li, {Jih Heng} and Chen, {Chiou Jong} and Chen, {Ruey Yu}",
year = "2002",
month = "9",
day = "30",
doi = "10.1016/S0300-483X(02)00246-9",
language = "English",
volume = "179",
pages = "1--8",
journal = "Toxicology",
issn = "0300-483X",
publisher = "Elsevier Ireland Ltd",
number = "1-2",

}

TY - JOUR

T1 - Phosphine-induced oxidative damage in rats

T2 - Role of glutathione

AU - Hsu, Ching Hung

AU - Chi, Bei Ching

AU - Liu, Ming Yie

AU - Li, Jih Heng

AU - Chen, Chiou Jong

AU - Chen, Ruey Yu

PY - 2002/9/30

Y1 - 2002/9/30

N2 - Phosphine (PH3), generated from aluminium, magnesium and zinc phosphide, is a widely used pesticide. PH3 induces oxidative stress in insects, mammalian cells, animals, and humans. The involvement of glutathione (GSH) in PH3-induced oxidative toxicity is controversial. GSH levels in various tested tissues were reduced in aluminium phosphide-poisoned rats and humans, while the levels remained unchanged in insects and mammalian cells. This study examines the effectiveness of endogenous GSH as a protective agent against PH3-induced oxidative damage in rats. The association of PH3-induced nephrotoxicity and cardiotoxicity with free radical production was also tested. Male Wistar rats, administered intraperitoneally (I.P.) with PH3 at 4 mg/kg, were evaluated 30 min after treatment for PH3 toxicity to organs. PH3 significantly decreased GSH, GSH peroxidase and catalase, while significantly increased lipid peroxidation (as malondialdehyde and 4-hydroxyalkenals), DNA oxidation (as 8-hydroxydeoxyguaonsoine) and superoxide dismutase (SOD) levels in kidney and heart. These changes were significantly alleviated by melatonin (10 mg/kg I.P., 30 min before PH3), with the exception of SOD activity in heart tissue. The study also found that buthionine sulfoximine (1 g/kg I.P., 24 h before PH3) significantly enhanced the effect of PH3 on GSH loss and lipid peroxidation elevation in lung. These findings indicate that (1) endogenous GSH plays a crucial role as a protective factor in modulating PH3-induced oxidative damage, and (2) PH3 could injure kidney and heart (as noted earlier with brain, liver and lung) via oxidative stress and the antioxidant melatonin effectively prevents the damage.

AB - Phosphine (PH3), generated from aluminium, magnesium and zinc phosphide, is a widely used pesticide. PH3 induces oxidative stress in insects, mammalian cells, animals, and humans. The involvement of glutathione (GSH) in PH3-induced oxidative toxicity is controversial. GSH levels in various tested tissues were reduced in aluminium phosphide-poisoned rats and humans, while the levels remained unchanged in insects and mammalian cells. This study examines the effectiveness of endogenous GSH as a protective agent against PH3-induced oxidative damage in rats. The association of PH3-induced nephrotoxicity and cardiotoxicity with free radical production was also tested. Male Wistar rats, administered intraperitoneally (I.P.) with PH3 at 4 mg/kg, were evaluated 30 min after treatment for PH3 toxicity to organs. PH3 significantly decreased GSH, GSH peroxidase and catalase, while significantly increased lipid peroxidation (as malondialdehyde and 4-hydroxyalkenals), DNA oxidation (as 8-hydroxydeoxyguaonsoine) and superoxide dismutase (SOD) levels in kidney and heart. These changes were significantly alleviated by melatonin (10 mg/kg I.P., 30 min before PH3), with the exception of SOD activity in heart tissue. The study also found that buthionine sulfoximine (1 g/kg I.P., 24 h before PH3) significantly enhanced the effect of PH3 on GSH loss and lipid peroxidation elevation in lung. These findings indicate that (1) endogenous GSH plays a crucial role as a protective factor in modulating PH3-induced oxidative damage, and (2) PH3 could injure kidney and heart (as noted earlier with brain, liver and lung) via oxidative stress and the antioxidant melatonin effectively prevents the damage.

KW - Glutathione

KW - Oxidative damage

KW - Phosphine

KW - Rats

UR - http://www.scopus.com/inward/record.url?scp=0037200817&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037200817&partnerID=8YFLogxK

U2 - 10.1016/S0300-483X(02)00246-9

DO - 10.1016/S0300-483X(02)00246-9

M3 - Article

C2 - 12204537

AN - SCOPUS:0037200817

VL - 179

SP - 1

EP - 8

JO - Toxicology

JF - Toxicology

SN - 0300-483X

IS - 1-2

ER -