scholarly journals Labile iron pool as a parameter to monitor iron overload and oxidative stress status in β-thalassemic erythrocytes

2018 ◽  
Vol 94 (4) ◽  
pp. 631-636 ◽  
Author(s):  
Boonyanuch Chutvanichkul ◽  
Phantip Vattanaviboon ◽  
Sumana Mas-oodi ◽  
Yaowalak U-pratya ◽  
Wanchai Wanachiwanawin
2013 ◽  
Vol 33 (5) ◽  
pp. 534-541 ◽  
Author(s):  
Y Li ◽  
Y Deng ◽  
Y Tang ◽  
H Yu ◽  
C Gao ◽  
...  

Accumulating evidence has shown that ethanol-induced iron overload plays a crucial role in the development and progression of alcoholic liver disease. We designed the present study to investigate the potential protective effect of quercetin, a naturally occurring iron-chelating antioxidant on alcoholic iron overload and oxidative stress. Ethanol-incubated (100 mmol/L) rat primary hepatocytes were co-treated by quercetin (100 µmol/L) and different dose of ferric nitrilotriacetate (Fe-NTA) for 24 h. When the hepatic enzyme releases in the culture medium, redox status of hepatocytes and the intercellular labile iron pool (LIP) level were assayed. Our data showed that Fe-NTA dose dependently induced cellular leakage of aspartate transaminase and lactate dehydrogenase, glutathione depletion, superoxide dismutase inactivation, and overproduction of malondialdehyde) and reactive oxygen species (ROS) of intact and especially ethanol-incubated hepatocytes. The oxidative damage resulted from ethanol, Fe-NTA, and especially their combined treatment was substantially alleviated by quercetin, accompanying the corresponding normalization of intercellular LIP level. Iron in excess, thus, may aggravate ethanol hepatotoxicity through Fenton-active LIP, and quercetin attenuated ethanol-induced iron and oxidative stress. To maintain intercellular LIP contributes to the hepatoprotective effect of quercetin besides its direct ROS-quenching activity.


Microbiology ◽  
2009 ◽  
Vol 155 (1) ◽  
pp. 295-304 ◽  
Author(s):  
Michael P. Thorgersen ◽  
Diana M. Downs

The response of a cell to integrated stresses was investigated using environmental and/or genetic perturbations that disrupted labile iron homeostasis and increased oxidative stress. The effects of the perturbations were monitored as nutritional requirements, and were traced to specific enzymic targets. A yggX gshA cyaY mutant strain required exogenous thiamine and methionine for growth. The thiamine requirement, which had previously been linked to the Fe–S cluster proteins ThiH and ThiC, was responsive to oxidative stress and was not directly affected by manipulation of the iron pool. The methionine requirement was associated with the activity of sulfite reductase, an enzyme that appeared responsive to disruption of labile iron homeostasis. The results are incorporated in a model to suggest how the activity of iron-containing enzymes not directly sensitive to oxygen can be decreased by oxidation of the labile iron pool.


2002 ◽  
Vol 36 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Giuliana Zanninelli ◽  
Olivier Loréal ◽  
Pierre Brissot ◽  
Abraham M Konijn ◽  
Itzchak N Slotki ◽  
...  

2012 ◽  
Vol 03 (08) ◽  
pp. 1140-1150 ◽  
Author(s):  
Somdet Srichairatanakool ◽  
Kanokwan Kulprachakarn ◽  
Kanjana Pangjit ◽  
Kovit Pattanapanyasat ◽  
Suthat Fuchaeron

2009 ◽  
Vol 46 (1) ◽  
pp. 59-66 ◽  
Author(s):  
Shigemiki Omiya ◽  
Shungo Hikoso ◽  
Yukiko Imanishi ◽  
Atsuhiro Saito ◽  
Osamu Yamaguchi ◽  
...  

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