File
name:
Loss of the mitochondrial lipid cardiolipin leads to decreased glutathione synthesis; PY2020; Wayne State
University;_WJD_2024-0810_IR95_IR96_V001R01_
##
Loss of the mitochondrial
lipid cardiolipin leads to decreased glutathione synthesis; PY2020; Wayne State
University;_WJD_2024-0810_IR95_IR96_V001R01_
##
Maturation of cytosolic Iron-sulfur proteins requires glutathione
細胞質液 裡面的 鐵硫蛋白 的成熟需要 穀胱甘肽
Maturation of cytosolic Iron-sulfur proteins requires glutathione (細胞質液 裡面的 鐵硫蛋白 的成熟需要 穀胱甘肽)
細胞質液 裡面的 鐵硫蛋白 的成熟需要 穀胱甘肽 (Maturation of
cytosolic Iron-sulfur proteins
requires glutathione)
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2024-08-10
Loss of the mitochondrial lipid cardiolipin leads to decreased glutathione synthesis
Source or References (資訊來源或是參考的資訊):
https://pubmed.ncbi.nlm.nih.gov/31672571/
Info cited on 2024-08-10-WD6 (資訊引用於 中華民國113年西元2024年8月10日) by 湯偉晉 (WeiJin Tang)
#
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Biochim Biophys Acta Mol Cell Biol Lipids
. 2020 Feb;1865(2):158542. doi: 10.1016/j.bbalip.2019.158542. Epub 2019 Oct 28.
Loss of the mitochondrial lipid cardiolipin leads to decreased glutathione synthesis
Loss of the
mitochondrial lipid cardiolipin leads to decreased glutathione synthesis
Loss of the mitochondrial lipid cardiolipin leads to decreased glutathione synthesis
Vinay A Patil 1, Yiran Li 1, Jiajia Ji 1, Miriam L Greenberg 2
Affiliations collapse
Affiliations
1Department of Biological Sciences, Wayne State University, Detroit, MI, USA.
2Department of Biological Sciences, Wayne State University, Detroit, MI, USA.
Electronic address: mgreenberg@wayne.edu.
PMID: 31672571 PMCID: PMC6980711 DOI: 10.1016/j.bbalip.2019.158542
Abstract
Previous studies demonstrated that loss of CL in the yeast mutant crd1Δ leads
to perturbation of mitochondrial iron‑sulfur (FeS) cluster biogenesis,
resulting in decreased activity of mitochondrial and cytosolic Fe-S-requiring
enzymes, including aconitase and sulfite reductase. In the current study, we
show that crd1Δ cells exhibit decreased levels of glutamate and cysteine and are
deficient in the essential antioxidant, glutathione, a tripeptide of glutamate, cysteine, and glycine. Glutathione is the most
abundant non-protein thiol essential for maintaining intracellular redox
potential in almost all eukaryotes, including yeast. Consistent with glutathione deficiency, the
growth defect of crd1Δ cells at elevated temperature was rescued by
supplementation of glutathione
or glutamate and cysteine.
Sensitivity to the oxidants iron (FeSO4) and hydrogen peroxide (H2O2), was
rescued by supplementation of glutathione.
The decreased intracellular glutathione
concentration in crd1Δ was restored by supplementation of glutamate and cysteine, but not by
overexpressing YAP1, an activator of expression of glutathione biosynthetic enzymes. These
findings show for the first time that CL plays a critical role in regulating
intracellular glutathione
metabolism.
Keywords: Barth syndrome; Cardiolipin;
Fe-S cluster; Glutathione;
Mitochondria; Reactive oxygen species (ROS).
Copyright © 2019 Elsevier B.V. All rights reserved.
PubMed Disclaimer
Conflict of interest statement
Declaration of competing interest
This article was prepared while Vinay A. Patil was employed at Wayne State
University. The opinions expressed in this article are the author’s own and do
not reflect the view of the Food and Drug Administration, the Department of
Health and Human Services, or the United States Government.
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