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.
| Original language | English |
|---|---|
| Pages (from-to) | 1-8 |
| Number of pages | 8 |
| Journal | Toxicology |
| Volume | 179 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - Sep 30 2002 |
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Keywords
- Glutathione
- Oxidative damage
- Phosphine
- Rats
ASJC Scopus subject areas
- Toxicology
Cite this
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.
In: Toxicology, Vol. 179, No. 1-2, 30.09.2002, p. 1-8.Research output: Contribution to journal › Article
}
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 -