Role of lycopene in preventing lipid peroxidation products, in commercial infant milk formula

2015 ◽  
pp. 1-5
Author(s):  
Oshra Saphier ◽  
Tali Silberstein ◽  
Guy Yardeni ◽  
Jeanine Blumenfeld ◽  
Israel Zilbermann ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Milk Formula ◽  
Lipid Peroxidation Products ◽  
Infant Milk Formula

Role of Radicals in the Lipid Peroxidation Products of Commercial Infant Milk Formula

2010 ◽  
Vol 58 (4) ◽  
pp. 2347-2350 ◽  
Author(s):  
Ariela Burg ◽  
Tali Silberstein ◽  
Guy Yardeni ◽  
Dorith Tavor ◽  
Jeanine Blumenfeld ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Milk Formula ◽  
Lipid Peroxidation Products ◽  
Infant Milk Formula

Lipid peroxidation and antielastase activity in the lung under oxidant stress: role of antioxidant defenses

1991 ◽  
Vol 70 (4) ◽  
pp. 1456-1462 ◽  
Author(s):  
V. Mohsenin
Keyword(s):  
Lipid Peroxidation ◽  
Oxidant Stress ◽  
Lavage Fluid ◽  
Conjugated Dienes ◽  
Antioxidant Defenses ◽  
Vitamin Supplementation ◽  
Control Group ◽  
Early Event ◽  
Lipid Peroxidation Products

The role of lipid peroxidation in the inactivation of alpha 1-protease inhibitor (alpha 1-PI) in the alveolar lining fluid of human subjects has been examined under oxidant stress. Exposure to nitrogen dioxide (NO2) at 4 ppm for 3 h resulted in a significant increase in the amount of lipid peroxidation products in the alveolar lining fluid, with conjugated dienes the predominant species. Four-week supplementation with vitamins C and E before NO2 exposure markedly decreased the levels of conjugated dienes (control 804 +/- 103 pmol/micrograms total phospholipids vs. vitamin-supplemented 369 +/- 58, P = 0.003). Malondialdehydes, although detectable in the lavage fluid, contributed little to the total amount of lipid peroxidation products, and the levels were comparable in both groups. NO2 exposure in the absence of vitamin supplementation caused a significant decrease in the elastase inhibitory capacity (EIC) of the alveolar lining fluid in the control group but not in the vitamin-supplemented group [control 3.67 +/- 0.32 micrograms alpha 1-PI/micrograms porcine pancreatic elastase (PPE) vs. vitamin-supplemented 2.75 +/- 0.17, P less than 0.03]. The vitamin-supplemented group had a lower level of conjugated dienes and a higher EIC. Conversely, the control group had higher levels of conjugated dienes and a lower EIC in their lavage fluid. These studies demonstrate that lipid peroxidation occurs as an early event during oxidant exposure in the lungs of normal subjects. The appearance of lipid peroxidation products in the lavage fluid is associated with a decrease in the EIC of the alveolar lining fluid. Vitamins C and E diminish lipid peroxidation and preserve the EIC of the lower respiratory tract fluid during oxidant stress.

scholarly journals The Role of Adrenomedullin in the Renal NADPH Oxidase and (Pro)renin in Diabetic Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Michio Hayashi ◽  
Akihiro Tojo ◽  
Tatsuo Shimosawa ◽  
Toshiro Fujita
Keyword(s):  
Lipid Peroxidation ◽  
Nadph Oxidase ◽  
Gene Knockout ◽  
Granular Cell ◽  
Diabetic Mice ◽  
Wild Mice ◽  
Positive Correlation ◽  
Lipid Peroxidation Products ◽  
Matrix Expansion

Adrenomedullin has an antioxidative action and protects organs in various diseases. To clarify the role of adrenomedullin in diabetic nephropathy, we investigated the NADPH oxidase expression, renin-secreting granular cell (GC) hyperplasia, and glomerular matrix expansion in the streptozotocin (STZ)-induced diabetic adrenomedullin gene knockout (AMKO) mice compared with the STZ-diabetic wild mice at 10 weeks. The NADPH oxidase p47phox expression and lipid peroxidation products were enhanced in the glomeruli of the diabetic mice compared with that observed in the controls in both wild and AMKO mice. These changes were more obvious in the AMKO mice than in the wild mice. Glomerular mesangial matrix expansion was more severe in the diabetic AMKO mice than in the diabetic wild mice and exhibited a positive correlation with the degree of lipid peroxidation products in the glomeruli. Proteinuria was significantly higher in the diabetic AMKO mice than in the diabetic wild mice. The GC hyperplasia score and the renal prorenin expression were significantly increased in the diabetic AMKO mice than in the diabetic wild mice, and a positive correlation was observed with the NADPH oxidase expression in the macula densa. The endogenous adrenomedullin gene exhibits an antioxidant action via the inhibition of NADPH oxidase probably by suppressing the local renin-angiotensin system.

Role of Reactive Lipid Peroxidation Products in Neutrophil Oxidative Burst

2014 ◽  
Vol 76 ◽  
pp. S150
Author(s):  
Morgan L Locy ◽  
Balu K Chacko ◽  
Stephanie B Wall ◽  
Philip A Kramer ◽  
Saranya Ravi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Burst ◽  
Lipid Peroxidation Products ◽  
Neutrophil Oxidative Burst

scholarly journals Clinical Prognosis for SAH Consistent with Redox Imbalance and Lipid Peroxidation

Molecules ◽  
2020 ◽  
Vol 25 (8) ◽  
pp. 1921
Author(s):  
Iwona Jarocka-Karpowicz ◽  
Anna Syta-Krzyżanowska ◽  
Jan Kochanowicz ◽  
Zenon Dionizy Mariak
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Defense ◽  
Clinical Status ◽  
Clinical Prognosis ◽  
Lipid Peroxidation Products ◽  
Plasma Glutathione Peroxidase ◽  
Systemic Level ◽  
Angio Ct ◽  
Plasma Glutathione

Subarachnoid hemorrhage (SAH) accounts for 3% of all strokes. As more and more data indicates the role of oxidative stress in acute brain damage caused by SAH, an attempt was made to correlate the clinical status of patients with systemic level of antioxidants and lipid peroxidation products. The hemorrhage was diagnosed with brain computed tomography (CT) and aneurysm with angio-CT and angiography, while the vasospasm was monitored with transcranial Doppler. Plasma glutathione peroxidase activity (GSH-Px) and vitamin A, E, and C levels were determined spectrophotometrically and by HPLC, respectively. The levels of polyunsaturated fatty acids (PUFAs) cyclization products were determined by GC–MS, while F2-isoprostanes and neuroprostanes (NP) were determined by LC–MS. SAH was accompanied by changes in antioxidant capacity in blood plasma, including initially (day 1) an increase in GSH-Px activity, followed by its decrease and a progressive decrease in glutathione (GSH) levels and vitamins A, E, and C. On the other hand, levels of PUFAs cyclization products, F2-isoprostanes, and neuroprostanes were highest on day 1 (two and eight times higher, respectively) and decreased over time. The levels of 4-HNE (4-hydroxynonenal), 4-ONE (4-oxononenal), and MDA (malondialdehyde) changed similarly. In contrast, the 4-HHE (4-hydroxyhexenal) level reduced after SAH increased significantly after a week. It was found that the deterioration of the overall clinical and neurological condition of SAH patients due to cerebral edema, intracranial hemorrhage, or vasoconstriction corresponded to reduced antioxidant defense and, as a consequence, increased lipid peroxidation and slower observed changes in regression. It can be concluded that monitoring the level of lipid peroxidation products (neuroprostanes, 4-ONE, and MDA) can support the monitoring of the clinical status of patients, especially with regard to the assessment of vasospasm.

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