PMID- 18837652
OWN - NLM
STAT- MEDLINE
DCOM- 20081216
LR  - 20181113
IS  - 1557-7716 (Electronic)
IS  - 1523-0864 (Print)
IS  - 1523-0864 (Linking)
VI  - 11
IP  - 1
DP  - 2009 Jan
TI  - H2S protects against methionine-induced oxidative stress in brain endothelial 
      cells.
PG  - 25-33
LID - 10.1089/ars.2008.2073 [doi]
AB  - Homocysteine (Hcy) causes cerebrovascular dysfunction by inducing oxidative 
      stress. However, to date, there are no strategies to prevent Hcy-induced 
      oxidative damage. Hcy is an H2S precursor formed from methionine (Met) 
      metabolism. We aimed to investigate whether H2S ameliorated Met-induced oxidative 
      stress in mouse brain endothelial cells (bEnd3). The bEnd3 cells were exposed to 
      Met treatment in the presence or absence of NaHS (donor of H2S). Met-induced cell 
      toxicity increased the levels of free radicals in a concentration-dependent 
      manner. Met increased NADPH-oxidase-4 (NOX-4) expression and mitigated 
      thioredxion-1(Trx-1) expression. Pretreatment of bEnd3 with NaHS (0.05 mM) 
      attenuated the production of free radicals in the presence of Met and protected 
      the cells from oxidative damage. Furthermore, NaHS enhanced inhibitory effects of 
      apocynin, N-acetyl-l-cysteine (NAC), reduced glutathione (GSH), catalase (CAT), 
      superoxide dismutase (SOD), Nomega-nitro-l-arginine methyl ester (L-NAME) on ROS 
      production and redox enzymes levels induced by Met. In conclusion, the 
      administration of H2S protected the cells from oxidative stress induced by 
      hyperhomocysteinemia (HHcy), which suggested that NaHS/H2S may have therapeutic 
      potential against Met-induced oxidative stress.
FAU - Tyagi, Neetu
AU  - Tyagi N
AD  - Department of Physiology and Biophysics, School of Medicine, University of 
      Louisville, Louisville, Kentucky 40202, USA. suresh.tyagi@louisville.edu
FAU - Moshal, Karni S
AU  - Moshal KS
FAU - Sen, Utpal
AU  - Sen U
FAU - Vacek, Thomas P
AU  - Vacek TP
FAU - Kumar, Munish
AU  - Kumar M
FAU - Hughes, William M Jr
AU  - Hughes WM Jr
FAU - Kundu, Soumi
AU  - Kundu S
FAU - Tyagi, Suresh C
AU  - Tyagi SC
LA  - eng
GR  - R01 HL088012-03/HL/NHLBI NIH HHS/United States
GR  - R01 NS051568/NS/NINDS NIH HHS/United States
GR  - R01 HL088012/HL/NHLBI NIH HHS/United States
GR  - NS-51568/NS/NINDS NIH HHS/United States
GR  - HL-75185/HL/NHLBI NIH HHS/United States
GR  - R01 NS051568-02/NS/NINDS NIH HHS/United States
GR  - HL-71010/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Antioxid Redox Signal
JT  - Antioxidants & redox signaling
JID - 100888899
RN  - 0 (Acetophenones)
RN  - 0 (Formazans)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tetrazolium Salts)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 23305-68-2 (MTT formazan)
RN  - AE28F7PNPL (Methionine)
RN  - B6J7B9UDTR (acetovanillone)
RN  - EC 1.11.1.6 (Catalase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - GAN16C9B8O (Glutathione)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
RN  - WYQ7N0BPYC (Acetylcysteine)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Acetophenones/metabolism
MH  - Acetylcysteine/metabolism
MH  - Animals
MH  - Brain/*cytology
MH  - Catalase/metabolism
MH  - Cell Line, Transformed
MH  - Cell Survival/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Endothelial Cells/drug effects/*metabolism
MH  - Formazans/metabolism
MH  - Glutathione/metabolism
MH  - Homocysteine/biosynthesis
MH  - Hydrogen Sulfide/metabolism/pharmacology/*therapeutic use
MH  - Methionine/*toxicity
MH  - Mice
MH  - Models, Biological
MH  - NG-Nitroarginine Methyl Ester/metabolism
MH  - Oxidative Stress/*drug effects
MH  - Reactive Oxygen Species/metabolism
MH  - Superoxide Dismutase/metabolism
MH  - Tetrazolium Salts/metabolism
MH  - Time Factors
PMC - PMC2742910
EDAT- 2008/10/08 09:00
MHDA- 2008/12/17 09:00
PMCR- 2010/01/01
CRDT- 2008/10/08 09:00
PHST- 2008/10/08 09:00 [pubmed]
PHST- 2008/12/17 09:00 [medline]
PHST- 2008/10/08 09:00 [entrez]
PHST- 2010/01/01 00:00 [pmc-release]
AID - 10.1089/ars.2008.2073 [pii]
AID - 10.1089/ars.2008.2073 [doi]
PST - ppublish
SO  - Antioxid Redox Signal. 2009 Jan;11(1):25-33. doi: 10.1089/ars.2008.2073.