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 Peroxynitrite-Mediated Protein Nitration and Lipid Peroxidation in a Mouse Model of Traumatic Brain Injury

2004 ◽  
Vol 21 (1) ◽  
pp. 9-20 ◽  
Author(s):  
Edward D. Hall ◽  
Megan R. Detloff ◽  
Kjell Johnson ◽  
Nancy C. Kupina
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Brain Injury ◽  
Mouse Model ◽  
Protein Nitration

scholarly journals Lipid peroxidation dominates the chemistry of DNA adduct formation in a mouse model of inflammation

2007 ◽  
Vol 28 (8) ◽  
pp. 1807-1813 ◽  
Author(s):  
Bo Pang ◽  
Xinfeng Zhou ◽  
Hongbin Yu ◽  
Min Dong ◽  
Koli Taghizadeh ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Mouse Model ◽  
Adduct Formation ◽  
Dna Adduct

Mechanisms of vascular instability in a transgenic mouse model of sickle cell disease

2000 ◽  
Vol 279 (6) ◽  
pp. R1949-R1955 ◽  
Author(s):  
K. A. Nath ◽  
V. Shah ◽  
J. J. Haggard ◽  
A. J. Croatt ◽  
L. A. Smith ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Lipid Peroxidation ◽  
Sickle Cell Disease ◽  
Mouse Model ◽  
Systolic Blood Pressure ◽  
Transgenic Mouse ◽  
Sickle Cell ◽  
Transgenic Mouse Model ◽  
Cell Disease

We investigated a transgenic mouse model of sickle cell disease, homozygous for deletion of mouse β-globin and containing transgenes for human βSand βS-antillesglobins linked to the transgene for human α-globin. In these mice, basal cGMP production in aortic rings is increased, whereas relaxation to an endothelium-dependent vasodilator, A-23187, is impaired. In contrast, aortic expression of endothelial nitric oxide synthase (NOS) is unaltered in sickle mice, whereas expression of inducible NOS is not detected in either group; plasma nitrate/nitrite concentrations and NOS activity are similar in both groups. Increased cGMP may reflect the stimulatory effect of peroxides (an activator of guanylate cyclase), because lipid peroxidation is increased in aortae and in plasma in sickle mice. Despite increased vascular cGMP levels in sickle mice, conscious systolic blood pressure is comparable to that of aged-matched controls; sickle mice, however, evince a greater rise in systolic blood pressure in response to nitro-l-arginine methyl ester, an inhibitor of NOS. Systemic concentrations of the vasoconstrictive oxidative product 8-isoprostane are increased in sickle mice. We conclude that vascular responses are altered in this transgenic sickle mouse and are accompanied by increased lipid peroxidation and production of cGMP; we suggest that oxidant-inducible vasoconstrictor systems such as isoprostanes may oppose nitric oxide-dependent and nitric oxide-independent mechanisms of vasodilatation in this transgenic sickle mouse. Destabilization of the vasoactive balance in the sickle vasculature by clinically relevant states may predispose to vasoocclusive disease.

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.

scholarly journals Comparison of the effects of deferasirox, deferoxamine, and combination of deferasirox and deferoxamine on an aplastic anemia mouse model complicated with iron overload

2018 ◽  
Vol Volume 12 ◽  
pp. 1081-1091 ◽  
Author(s):  
Dijiong Wu ◽  
Xiaowen Wen ◽  
Wenbin Liu ◽  
Huijin Hu ◽  
Baodong Ye ◽  
...  
Keyword(s):  
Mouse Model ◽  
Iron Overload ◽  
Aplastic Anemia

scholarly journals Effect of Systemic Iron Overload and a Chelation Therapy in a Mouse Model of the Neurodegenerative Disease Hereditary Ferritinopathy

PLoS ONE ◽  
2016 ◽  
Vol 11 (8) ◽  
pp. e0161341 ◽  
Author(s):  
Holly J. Garringer ◽  
Jose M. Irimia ◽  
Wei Li ◽  
Charles B. Goodwin ◽  
Briana Richine ◽  
...  
Keyword(s):  
Mouse Model ◽  
Iron Overload ◽  
Neurodegenerative Disease ◽  
Chelation Therapy

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
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