Glutathione deficit impairs myelin
maturation: relevance for white matter integrity in schizophrenia patients
Source (資訊來源):
Info cited on 2019-09-26-WD4 (資訊引用於 中華民國108年9月26日) by 湯偉晉
(WeiJin Tang)
#
2019年9月26日 星期四
integrity, glutathione
integrity, glutathione
Source (資訊來源):
Info cited on 2019-09-26-WD4 (資訊引用於 中華民國108年9月26日) by 湯偉晉
(WeiJin Tang)
#
Hippocampal neurons require a large pool of glutathione to sustain dendrite integrity and cognitive function; PY2018; Spain (西班牙);_WJD_2019-0926_V001R01_IR94_RvD20190926_
Hippocampal neurons require a large pool of glutathione to
sustain dendrite integrity and cognitive function; PY2018; Spain (西班牙);_WJD_2019-0926_V001R01_IR94_RvD20190926_
Source (資訊來源):
Info cited on 2019-09-26-WD4 (資訊引用於 中華民國108年9月26日) by 湯偉晉
(WeiJin Tang)
#
Chronic oxidative stress compromises telomere integrity and accelerates the onset of senescence in human endothelial cells [2004](IR92) 01.png
Chronic oxidative stress compromises telomere integrity and
accelerates the onset of senescence in human endothelial cells PY2004 IR94
Source (資訊來源):
Info cited on 2019-09-26-WD4 (資訊引用於 中華民國108年9月26日) by 湯偉晉
(WeiJin Tang)
Chronic oxidative stress compromises telomere integrity and accelerates the onset of senescence in human endothelial cells [2004](IR92) 02.png
Superoxide Dismutase in Redox Biology - The roles of superoxide and hydrogen peroxide [2011](IR93) - Ascorbate is the terminal, water-soluble, small-molecule antioxidant.png
Superoxide Dismutase in Redox Biology - The roles of superoxide and hydrogen peroxide [2011](IR93).png
2019年9月3日 星期二
Signal transduction by reactive oxygen species; PY2011;National Institutes of Health, USA (美國);_WJD_2019-0903_V001R01_IR94_RvD20190903_IR95_
Signal transduction by
reactive oxygen species; PY2011;National Institutes of Health, USA (美國);_WJD_2019-0903_V001R01_IR94_RvD20190903_IR95_
Signal transduction by reactive oxygen species;
PY2011;National Institutes of Health, USA (美國);_WJD_2019-0903_V001R01_IR94_RvD20190903_IR95_
Source (資訊來源):
Info cited on 2019-09-03-WD2 (資訊引用於 中華民國108年9月3日) by 湯偉晉
(WeiJin Tang)
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2019年9月2日 星期一
Toxic consequence of the abrupt depletion of glutathione (穀胱甘肽) in cultured rat hepatocytes.; PY1988;Thomas Jefferson University, USA (美國);_WJD_2019-0902_V001R01_IR94_
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Toxic consequence of the abrupt depletion of glutathione (穀胱甘肽) in cultured rat hepatocytes.; PY1988;Thomas
Jefferson University, USA (美國);_WJD_2019-0902_V001R01_IR94_RvD20190902_
Source (資訊來源):
Info cited on 2019-09-02-WD1 (資訊引用於 中華民國108年9月2日) by 湯偉晉
(WeiJin Tang)
#
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Arch Biochem Biophys. 1988 Sep;265(2):311-20.
Toxic consequence of the abrupt depletion of glutathione (穀胱甘肽) in cultured rat hepatocytes.
Toxic
consequence of the abrupt depletion of glutathione (穀胱甘肽) in cultured rat
hepatocytes.
Toxic consequence of the abrupt depletion of glutathione (穀胱甘肽) in cultured rat hepatocytes.
Miccadei S1, Kyle ME, Gilfor D, Farber JL.
Author information
1
Department of Pathology, Thomas Jefferson University,
Philadelphia, Pennsylvania 19107.
Thomas Jefferson University, USA (美國)
Abstract
Cultured hepatocytes were exposed to two chemicals,
dinitrofluorobenzene (DNFB) and diethyl maleate (DEM), that abruptly deplete cellular stores of glutathione (穀胱甘肽). Upon the loss of GSH, lipid peroxidation was evidenced by an accumulation
of malondialdehyde in the cultures followed by the death of the hepatocytes.
Pretreatment of the
hepatocytes with a ferric iron
chelator, deferoxamine,
or the addition of an antioxidant, N,N'-diphenyl-p-phenylenediamine (DPPD), to
the culture medium prevented both the lipid peroxidation and the cell death
produced by either DNFB or DEM. However, neither deferoxamine nor DPPD
prevented the depletion of GSH caused by either agent. Inhibition of glutathione (穀胱甘肽) reductase by 1,3-bis(2-chloroethyl)-1-nitrosourea
(BCNU) or inhibition of catalase by aminotriazole sensitized the hepatocytes to
the cytotoxicity of DNFB. In a similar manner, pretreatment with BCNU
potentiated the cell killing by DEM. DPPD and deferoxamine protected
hepatocytes pretreated with BCNU and then exposed to DNFB or DEM. These data indicate that an abrupt depletion of GSH leads
to lipid peroxidation and cell death in cultured hepatocytes. It is proposed
that GSH depletion sensitizes the hepatocyte to its constitutive flux of
partially reduced oxygen species. Such an oxidative stress is normally
detoxified by GSH-dependent mechanisms. However, with GSH depletion these
activated oxygen species are toxic as a result of the iron-dependent formation
of a potent oxidizing species.
Begin_電腦自動翻譯的內容_Y2019m09d02h15m08Rn0660_
(請注意：電腦自動翻譯的內容，可能會夾雜一些錯誤！)
抽象
將培養的肝細胞暴露於兩種化學物質，即二硝基氟苯（DNFB）和馬來酸二乙酯（DEM），其突然耗盡穀胱甘肽的細胞儲存。在GSH喪失後，脂質過氧化通過培養物中丙二醛的積累隨後肝細胞的死亡得到證實。用鐵螯合劑，去鐵胺或添加抗氧化劑N，N'-二苯基
- 對苯二胺（DPPD）預處理肝細胞，防止DNFB產生的脂質過氧化和細胞死亡或DEM。然而，去鐵胺和DPPD均未阻止任何一種藥物引起的GSH耗竭。
1,3-雙（2-氯乙基）-1-亞硝基脲（BCNU）對穀胱甘肽還原酶的抑製或氨基三唑對過氧化氫酶的抑制使肝細胞對DNFB的細胞毒性敏感。以類似的方式，用BCNU預處理增強了DEM對細胞的殺傷作用。
DPPD和去鐵胺保護用BCNU預處理的肝細胞，然後暴露於DNFB或DEM。這些數據表明GSH的突然耗盡導致培養的肝細胞中的脂質過氧化和細胞死亡。提出GSH耗竭使肝細胞對其部分還原的氧物種的組成型通量敏感。這種氧化應激通常通過GSH依賴性機制解毒。然而，隨著GSH耗盡，這些活化的氧物質由於鐵依賴性形成有效的氧化物質而具有毒性。
End_電腦自動翻譯的內容_Y2019m09d02h15m08Rn0660_
PMID: 3421709 DOI: 10.1016/0003-9861(88)90133-6
[Indexed for MEDLINE]
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- --- ---Mitochondrial oxidative stress and dysfunction in arsenic neurotoxicity: A review.; PY2016;Maharshi Dayanand University, India (印度);_WJD_2019-0902_
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Mitochondrial oxidative stress and dysfunction in arsenic
neurotoxicity: A review.; PY2016;Maharshi Dayanand University, India (印度);_WJD_2019-0902_V001R01_IR92_RvD20190902_
Source (資訊來源):
Info cited on 2019-09-02-WD1 (資訊引用於 中華民國108年9月2日) by 湯偉晉
(WeiJin Tang)
#
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J Appl Toxicol. 2016 Feb;36(2):179-88. doi:
10.1002/jat.3256. Epub 2015 Oct 29.
Mitochondrial oxidative stress and dysfunction in arsenic
neurotoxicity: A review.
Mitochondrial
oxidative stress and dysfunction in arsenic neurotoxicity: A review.
Mitochondrial oxidative stress and dysfunction in arsenic
neurotoxicity: A review.
Mitochondrial
oxidative stress and dysfunction in arsenic neurotoxicity: A review.
Mitochondrial oxidative stress and dysfunction in arsenic
neurotoxicity: A review.
Prakash C1, Soni M1, Kumar V1.
Author information
1
Department of Biochemistry, Maharshi Dayanand University,
Rohtak, 124001, Haryana, India.
Abstract
Arsenic is a toxic metalloid
present ubiquitously on earth. Since the last decade, it has gained considerable attention due
to its severe neurotoxic effects. Arsenic can cross the blood-brain barrier and accumulate in different regions of the brain
suggesting its role in neurological diseases. Arsenic
exposure has been associated with reactive oxygen species generation, which is supposed to be one of the mechanisms of arsenic-induced oxidative stress. Mitochondria, being the major source of reactive oxygen species
generation may present an important target of arsenic toxicity. It is
speculated that the proper functioning of the brain depends largely on
efficient mitochondrial functions. Multiple
studies have reported evidence of brain mitochondrial impairment after arsenic
exposure. In
this review, we have evaluated the proposed mechanisms of arsenic-induced
mitochondrial oxidative stress and dysfunction. The understanding of molecular
mechanism of mitochondrial dysfunction may be helpful to develop therapeutic
strategies against arsenic-induced neurotoxicity. The ameliorative measures
undertaken in arsenic-induced mitochondrial dysfunction have also been
highlighted.
Copyright © 2015 John Wiley & Sons, Ltd.
KEYWORDS:
arsenic; membrane potential; mitochondrial dysfunction;
neurotoxicity; oxidative stress
PMID: 26510484 DOI: 10.1002/jat.3256
[Indexed for MEDLINE]
KEYWORDS added by WeiJin Tang:
Glutathione,
cysteine
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- --- ---Changes in certain hematological and physiological variables following single gallium arsenide exposure in rats.; PY1997;Defense Research & Development Establishment, Gwalior, India (印度);_WJD_2019-0902_
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Changes in certain hematological and physiological variables
following single gallium arsenide exposure in rats.; PY1997;Defense Research
& Development Establishment, Gwalior, India (印度);_WJD_2019-0902_V001R01_IR92_RvD20190902_
Source (資訊來源):
Info cited on 2019-09-02-WD1 (資訊引用於 中華民國108年9月2日) by 湯偉晉
(WeiJin Tang)
#
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Biol Trace Elem Res. 1997 Sep;58(3):197-208.
Changes in certain hematological and physiological variables
following single gallium arsenide exposure in rats.
Changes
in certain hematological and physiological variables following single gallium
arsenide exposure in rats.
Changes in certain hematological and physiological variables
following single gallium arsenide exposure in rats.
Flora SJ1, Dube SN, Vijayaraghavan R, Pant SC.
Author information
1
Division of Pharmacology and Toxicology, Defense Research
& Development Establishment, Gwalior, India.
Abstract
Gallium
arsenide (GaAs), a group III-VA intermetallic semiconductor, possesses
superior electronic and optical properties and has a wide application in
electronic industry. Exposure
to GaAs in the semiconductor industries could be a possible occupational risk. The
aim of the present study was to determine the dose-dependent effect of single oral exposure to
GaAs (500, 1000, or 2000 mg/kg) on some biochemical variables in heme synthesis pathway and
few selected physiological
variables at d 1, 7, and 15 following administration. The results
indicate that GaAs produced a significant effect on the activity of
delta-aminolevulinic acid dehydratase (ALAD) in blood and heart (particularly
at d 7) following exposure to 2000 mg/kg, whereas
urinary delta-aminolevulinic acid (ALA) excretion was elevated only at d 7.
No marked influence of GaAs on blood hemoglobin, zinc
protoporphyrin, and packed cell volume was noticed. Blood glutathione (GSH) was significantly
reduced at d 7, but remained unchanged at two
other time intervals. On the other hand, heart GSH contents remained uninfluenced on GaAs
exposure. Most of the physiological variables, viz. blood pressure, heart and
respiration rate, and twitch response, remained unchanged, except for some
minor alterations observed at d 7 and 15 following exposure to GaAs at a dose
of 2000 mg/kg. Blood gallium concentration was not detectable in normal animals
and rats exposed to 500 mg/kg GaAs. Blood arsenic concentration was, however,
detectable even at the a lower dose level and increased in a dose-dependent
manner. All these changes
showed a recovery pattern at d 21, indicating that the alterations are
reversible.
PMID: 9403132
[Indexed for MEDLINE]
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