Endogenous Labile Iron Pool-Mediated Free Radical Generation for Cancer Chemodynamic Therapy

2020 ◽  
Vol 142 (36) ◽  
pp. 15320-15330 ◽  
Author(s):  
Lisen Lin ◽  
Sheng Wang ◽  
Hongzhang Deng ◽  
Weijing Yang ◽  
Lang Rao ◽  
...  
Keyword(s):  
Free Radical ◽  
Free Radical Generation ◽  
Labile Iron Pool ◽  
Radical Generation ◽  
Labile Iron ◽  
Iron Pool

scholarly journals Implication of Dietary Iron-Chelating Bioactive Compounds in Molecular Mechanisms of Oxidative Stress-Induced Cell Ageing

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 491
Author(s):  
Alexandra Barbouti ◽  
Nefeli Lagopati ◽  
Dimitris Veroutis ◽  
Vlasios Goulas ◽  
Konstantinos Evangelou ◽  
...  
Keyword(s):  
Free Radical ◽  
Molecular Mechanisms ◽  
Cellular Systems ◽  
Free Radical Theory ◽  
Radical Theory ◽  
Cellular Protection ◽  
Lipofuscin Accumulation ◽  
Labile Iron Pool ◽  
Labile Iron ◽  
Iron Pool

One of the prevailing perceptions regarding the ageing of cells and organisms is the intracellular gradual accumulation of oxidatively damaged macromolecules, leading to the decline of cell and organ function (free radical theory of ageing). This chemically undefined material known as “lipofuscin,” “ceroid,” or “age pigment” is mainly formed through unregulated and nonspecific oxidative modifications of cellular macromolecules that are induced by highly reactive free radicals. A necessary precondition for reactive free radical generation and lipofuscin formation is the intracellular availability of ferrous iron (Fe2+) (“labile iron”), catalyzing the conversion of weak oxidants such as peroxides, to extremely reactive ones like hydroxyl (HO•) or alcoxyl (RO•) radicals. If the oxidized materials remain unrepaired for extended periods of time, they can be further oxidized to generate ultimate over-oxidized products that are unable to be repaired, degraded, or exocytosed by the relevant cellular systems. Additionally, over-oxidized materials might inactivate cellular protection and repair mechanisms, thus allowing for futile cycles of increasingly rapid lipofuscin accumulation. In this review paper, we present evidence that the modulation of the labile iron pool distribution by nutritional or pharmacological means represents a hitherto unappreciated target for hampering lipofuscin accumulation and cellular ageing.

scholarly journals Analysis of yggX and gshA Mutants Provides Insights into the Labile Iron Pool in Salmonella enterica

2008 ◽  
Vol 190 (23) ◽  
pp. 7608-7613 ◽  
Author(s):  
Michael P. Thorgersen ◽  
Diana M. Downs
Keyword(s):  
Salmonella Enterica ◽  
Iron Chelator ◽  
Fenton Chemistry ◽  
Labile Iron Pool ◽  
Growth Defects ◽  
Labile Iron ◽  
Iron Pool ◽  
Mutant Phenotypes ◽  
Permeable Iron ◽  
Iron Chelator Deferoxamine

ABSTRACT Strains of Salmonella enterica lacking YggX and the cellular reductant glutathione exhibit defects similar to those resulting from iron deficiency and oxidative stress. Mutant strains are sensitive to hydrogen peroxide and superoxide, deregulate the expression of the Fur-regulated gene entB, and fail to grow on succinate medium. Suppression of some yggX gshA mutant phenotypes by the cell-permeable iron chelator deferoxamine allowed the conclusion that increased levels of cellular Fenton chemistry played a role in the growth defects. The data presented are consistent with a scenario in which glutathione acts as a physiological chelator of the labile iron pool and in which YggX acts upstream of the labile iron pool by preventing superoxide toxicity.

Myocardial haem proteins, oxidant stress & free radical generation

1990 ◽  
Vol 9 ◽  
pp. 182
Author(s):  
Catherine Rice-Evans ◽  
Jeremy J.O. Turner ◽  
Emma Newman ◽  
Michael J. Davies
Keyword(s):  
Free Radical ◽  
Oxidant Stress ◽  
Free Radical Generation ◽  
Radical Generation ◽  
Haem Proteins
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