scholarly journals Iron Overload and Lipid Peroxidation in Biological Systems

10.5772/46181 ◽  
2012 ◽  
Author(s):  
Paula M. ◽  
Natacha E. ◽  
Susana Puntarulo
Keyword(s):  
Lipid Peroxidation ◽  
Iron Overload ◽  
Biological Systems

Specifics of Changes in the Rate of Lipid Peroxidation in Different Biological Systems of the Organism in Corazolum-Induced Epileptoid Seizures

2005 ◽  
Vol 404 (1-6) ◽  
pp. 339-341
Author(s):  
K. G. Karagezyan ◽  
L. A. Simonyan ◽  
L. M. Ovsepyan ◽  
S. S. Ovakimyan ◽  
A. A. Simonyan ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Biological Systems

TGF-beta and collagen-alpha 1 (I) gene expression are increased in hepatic acinar zone 1 of rats with iron overload

1994 ◽  
Vol 267 (5) ◽  
pp. G908-G913 ◽  
Author(s):  
K. Houglum ◽  
P. Bedossa ◽  
M. Chojkier
Keyword(s):  
Gene Expression ◽  
Lipid Peroxidation ◽  
Iron Overload ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cultured Cells ◽  
Collagen Gene ◽  
Tgf Beta ◽  
Collagen Gene Expression ◽  
I Gene

We have shown that lipid peroxidation stimulates collagen-alpha 1 (I) gene transcription in cultured cells. Because iron is a transitional metal known to induce lipid peroxidation, we investigated whether hepatic lipid peroxidation modulates collagen gene expression in iron-overloaded rats. In this animal model of hemochromatosis, we show colocalization with iron in the hepatic acinar zone 1 of both lipid peroxidation and increased collagen-alpha 1 (I) transcripts, using immunohistochemistry for malondialdehyde-protein adducts and in situ hybridization, respectively. Iron overload stimulated the expression of the cytokine transforming growth factor-beta (TGF-beta) in acinar zone 1, in spite of the minor degree of hepatocellular necrosis and inflammation. The formation of reactive aldehydes and TGF-beta, both inducers of collagen gene expression, may play a role in the stimulation of hepatic collagen production in iron overload. These mechanisms could be a link between iron overload and fibrosis in genetic hemochromatosis.

Vitamin E decreases hepatic levels of aldehyde-derived peroxidation products in rats with iron overload

1996 ◽  
Vol 270 (2) ◽  
pp. G376-G384 ◽  
Author(s):  
S. Parkkila ◽  
O. Niemela ◽  
R. S. Britton ◽  
K. E. Brown ◽  
S. Yla-Herttuala ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Iron Overload ◽  
Kupffer Cells ◽  
Laser Scanning ◽  
Laser Scanning Microscopy ◽  
Alpha Tocopherol ◽  
Confocal Laser ◽  
Hepatocellular Injury ◽  
Vitamin E Supplementation

Hepatic iron overload can cause lipid peroxidation with the formation of aldehydic products, hepatocellular injury, and fibrosis. Vitamin E (alpha-tocopherol) may prevent peroxidation-induced hepatic damage. We used confocal laser scanning microscopy, digital image analysis, and immunohistochemical methods to quantitate aldehyde-derived peroxidation products in the liver of rats with experimental iron overload with or without supplemental vitamin E. A strong autofluorescent reaction colocalizing with iron deposits was present in the livers of iron-loaded rats. Fluorescent granules were unevenly distributed in the cytosol of both hepatocytes and Kupffer cells in the periportal regions. Immunohistochemical studies revealed the presence of malon-dialdehyde adducts in the periportal regions of the ironloaded rats. Vitamin E supplementation markedly reduced the fluorescence intensity and the amount of aldehyde-derived peroxidation products and changed the distribution of stainable iron and iron-associated peroxidation products such that their levels were much decreased in Kupffer cells. These results indicate that aldehyde-derived covalent chemical addition products are formed in the liver in iron overload. Vitamin E supplementation markedly reduces the amount of these compounds and changes their cellular distribution. These findings should be implicated in the role of antioxidant therapy in conditions causing iron overload and lipid peroxidation.

scholarly journals Moderate Iron Overload Enhances Lipid Peroxidation in Livers of Rats, but Does Not Affect NF-κB Activation Induced by the Peroxisome Proliferator, Wy-14,643

2002 ◽  
Vol 132 (9) ◽  
pp. 2525-2531 ◽  
Author(s):  
Joan G. Fischer ◽  
Howard P. Glauert ◽  
Taofei Yin ◽  
Mary L. Sweeney-Reeves ◽  
Nicolas Larmonier ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Iron Overload ◽  
Peroxisome Proliferator

Lipid peroxidation and protein modification in a mouse model of chronic iron overload

Metabolism ◽  
2002 ◽  
Vol 51 (5) ◽  
pp. 645-651 ◽  
Author(s):  
Mark A. Sochaski ◽  
Wally J. Bartfay ◽  
Suzanne R. Thorpe ◽  
John W. Baynes ◽  
Emma Bartfay ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Mouse Model ◽  
Iron Overload ◽  
Protein Modification

scholarly journals MiR-137 Boosts the Neuroprotective Effect of Endothelial Progenitor Cell Derived-Exosomes in Oxyhemoglobin Treated SH-SY5Y Cells Partially via COX2/PGE2 Pathway

2020 ◽  
Author(s):  
Yuchen Li ◽  
Jinju Wang ◽  
Shuzhen Chen ◽  
Pei Wu ◽  
Shancai Xu ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Ischemic Stroke ◽  
Glutathione Peroxidase ◽  
Iron Overload ◽  
Mitochondrial Dysfunction ◽  
Neuroprotective Effect ◽  
Endothelial Progenitor ◽  
Neuroprotective Effects ◽  
Protection Mechanism ◽  
Beneficial Effects

Abstract Background: We have previously verified the beneficial effects of exosomes from endothelial progenitor cells (EPC-EXs) in ischemic stroke. However, the effects of EPC-EXs in hemorrhagic stroke have not been investigated. Additionally, miR-137 is reported to regulate ferroptosis and to be involved in the neuroprotection against ischemic stroke. Hence, the present work explored the effects of miR-137-overexpressing EPC-EXs on apoptosis, mitochondrial dysfunction, and ferroptosis in oxyhemoglobin (oxyHb)-injured SH-SY5Y cells. Methods: The lentiviral miR-137 was transfected into EPCs and then the EPC-EXs were collected. RT-PCR was used to detect the miR-137 level in EPCs, EXs and neurons. The uptake mechanisms of EPC-EXs in SH-SY5Y cells were explored by the co-incubation of Dynasore, Pitstop 2, Ly294002 and Genistein. After the transfection of different types of EPC-EXs, flow cytometry and expression of cytochrome c and cleaved caspase-3 were used to detect the apoptosis of oxyHb-injured neurons. Neuronal mitochondrial function was assessed by reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP) depolarization, and cellular ATP content. Cell ferroptosis was measured by lipid peroxidation, iron overload, degradation of glutathione and glutathione peroxidase 4. Additionally, recombinational PGE2 was used to detect if activation of COX2/PGE2 pathway could reverse the protection of miR-137 overexpression.Results: The present work showed 1) EPC-EXs could be taken in by SH-SY5Y cells via caveolin-/clathrin-mediated pathways and macropinocytosis; 2) miR-137 was decreased in neurons after oxyHb treatment, and EXsmiR-137 could restore the miR-137 levels; 3) EXsmiR-137 worked better than EXs in reducing the number of apoptotic neurons and pro-apoptotic protein expression after oxyHb treatment; 4) EXsmiR-137 are more effective in improving the cellular MMP, ROS and ATP level; 5) EXsmiR-137, but not EXs, protected oxyHb-treated SH-SY5Y cells against lipid peroxidation, iron overload, degradation of glutathione and glutathione peroxidase 4; 6) EXsmiR-137 suppressed the expression of the COX2/PGE2 pathway, and activation of the pathway could partially reverse the neuroprotective effects of EXsmiR-137. Conclusion: MiR-137 overexpression boosts the neuroprotective effects of EPC-EXs against apoptosis and mitochondrial dysfunction in oxyHb-treated SH-SY5Y cells. Furthermore, EXsmiR-137 rather than EXs can restore the decrease in miR-137 levels and inhibit ferroptosis, and the protection mechanism might involve the miR-137-COX2/PGE2 signaling pathway.

scholarly journals MiR-137 Boosts the Neuroprotective Effect of Endothelial Progenitor Cell Derived-Exosomes in Oxyhemoglobin Treated SH-SY5Y Cells Partially via COX2/PGE2 Pathway

2020 ◽  
Author(s):  
Yuchen Li ◽  
Jinju Wang ◽  
Shuzhen Chen ◽  
Pei Wu ◽  
Shancai Xu ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Ischemic Stroke ◽  
Glutathione Peroxidase ◽  
Iron Overload ◽  
Mitochondrial Dysfunction ◽  
Neuroprotective Effect ◽  
Endothelial Progenitor ◽  
Neuroprotective Effects ◽  
Protection Mechanism ◽  
Beneficial Effects

Abstract Background: We have previously verified the beneficial effects of exosomes from endothelial progenitor cells (EPC-EXs) in ischemic stroke. However, the effects of EPC-EXs in hemorrhagic stroke have not been investigated. Additionally, miR-137 is reported to regulate ferroptosis and to be involved in the neuroprotection against ischemic stroke. Hence, the present work explored the effects of miR-137-overexpressing EPC-EXs on apoptosis, mitochondrial dysfunction, and ferroptosis in oxyhemoglobin (oxyHb)-injured neurons.Methods: The lentiviral miR-137 was transfected into EPCs and then the EPC-EXs were collected. RT-PCR was used to detect the miR-137 level in EPCs, EXs and neurons. The uptake mechanisms of EPC-EXs in neurons were explored by the co-incubation of Dynasore, Pitstop 2, Ly294002 and Genistein. After the transfection of different types of EPC-EXs, flow cytometry and expression of cytochrome c and cleaved caspase-3 were used to detect the apoptosis of oxyHb-injured neurons. Neuronal mitochondrial function was assessed by reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP) depolarization, and cellular ATP content. Cell ferroptosis was measured by lipid peroxidation, iron overload, degradation of glutathione and glutathione peroxidase 4. Additionally, recombinational PGE2 was used to detect if activation of COX2/PGE2 pathway could reverse the protection of miR-137 overexpression.Results: The present work showed 1) EPC-EXs could be taken in by SH-SY5Y cells via caveolin-/clathrin-mediated pathways and macropinocytosis; 2) miR-137 was decreased in neurons after oxyHb treatment, and EXs miR-137 could restore the miR-137 levels; 3) EXs miR-137 worked better than EXs in reducing the number of apoptotic neurons and pro-apoptotic protein expression after oxyHb treatment; 4) EXs miR-137 are more effective in improving the cellular MMP, ROS and ATP level; 5) EXs miR-137 , but not EXs, protected oxyHb-treated neurons against lipid peroxidation, iron overload, degradation of glutathione and glutathione peroxidase 4; 6) EXs miR-137 suppressed the expression of the COX2/PGE2 pathway, and activation of the pathway could partially reverse the neuroprotective effects of EXs miR-137 .Conclusion: MiR-137 overexpression boosts the neuroprotective effects of EPC-EXs against apoptosis and mitochondrial dysfunction in oxyHb-treated neurons. Furthermore, EXs miR-137 rather than EXs can restore the decrease in miR-137 levels and inhibit ferroptosis, and the protection mechanism might involve the miR-137-COX2/PGE2 signaling pathway.

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