End products of lipid peroxidation in alcohol-induced liver disorders

1986 ◽  
Vol 101 (1) ◽  
pp. 32-35
Author(s):  
A. S. Loginov ◽  
K. D. Dzhalalov ◽  
A. N. Erin ◽  
L. L. Prilipko
Keyword(s):  
Lipid Peroxidation ◽  
Liver Disorders ◽  
End Products

Moderate zinc restriction during fetal and postnatal growth of rats: effects on adult arterial blood pressure and kidney

2008 ◽  
Vol 295 (2) ◽  
pp. R543-R549 ◽  
Author(s):  
Analía Lorena Tomat ◽  
Felipe Inserra ◽  
Luciana Veiras ◽  
María Constanza Vallone ◽  
Ana María Balaszczuk ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Lipid Peroxidation ◽  
Systolic Blood Pressure ◽  
Zinc Deficiency ◽  
Control Diet ◽  
Adult Life ◽  
Fetal Life ◽  
Arterial Blood ◽  
End Products

Intrauterine and postnatal zinc restriction may result in an adverse environment for the development of cardiovascular and renal systems. This study evaluated the effects of moderate zinc deficiency during fetal life, lactation, and/or postweaning growth on systolic blood pressure, renal function, and morphology in adult life. Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy up to weaning. After weaning, male offspring of each group of mothers were fed low or control zinc diet. Systolic blood pressure, creatinine clearance, proteinuria, renal morphology, renal apoptosis. and renal oxidative stress state were evaluated after 60 days. Zinc deficiency during pre- and postweaning growth induced an increase in systolic blood pressure and a decrease in the glomerular filtration rate associated with a reduction in the number and size of nephrons. Activation of renal apoptosis, reduction in catalase activity, glutathione peroxidase activity, and glutathione levels and increase in lipid peroxidation end products could explain these morphometric changes. Zinc deficiency through pre- and postweaning growth induced more pronounced renal alteration than postweaning zinc deficiency. These animals showed signs of renal fibrosis, proteinuria, increased renal apoptosis, and higher lipid peroxidation end products. A control diet during postweaning growth did not totally overcome renal oxidative stress damage, apoptosis, and fibrosis induced by zinc deficiency before weaning. In conclusion, zinc deficiency during a critical period of renal development and maturation could induce functional and morphological alterations that result in elevated blood pressure and renal dysfunction in adult life.

Synthesis and incorporation of an advanced lipid peroxidation end-product building block into collagen mimetic peptides

2017 ◽  
Vol 53 (60) ◽  
pp. 8459-8462 ◽  
Author(s):  
Iman Kavianinia ◽  
Sung-Hyun Yang ◽  
Harveen Kaur ◽  
Paul W. R. Harris ◽  
Renwick C. J. Dobson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Building Block ◽  
End Products ◽  
Mimetic Peptides ◽  
Collagen Mimetic Peptides ◽  
And Oxidative Stress

Advanced lipid peroxidation end-products (ALEs) accumulate with ageing and oxidative stress-related diseases.

Effect of Dietary Selenite on Hepatic Organic Solvent-Soluble Lipofuscin Pigments

1986 ◽  
Vol 5 (1) ◽  
pp. 79-85 ◽  
Author(s):  
A.S. Csallany ◽  
B.Z. Menken
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Organic Solvent ◽  
Normal Level ◽  
Sodium Selenite ◽  
Basal Diet ◽  
Glutathione Peroxidase Activity ◽  
End Products ◽  
Oxidative Effect

Supplementation of selenium as sodium selenite results in an increase in hepatic organic solvent-soluble lipofuscin pigments, the metabolic end products of lipid peroxidation. Weanling mice fed a basal diet containing 0.05 ppm selenium had a significant increase in hepatic organic solvent-soluble lipofuscin pigments and glutathione peroxidase activity following supplementation of an additional 0.1 ppm selenium as sodium selenite from 5 to 9 months of age. Normal levels of vitamin E (30 mg/kg) were insufficient to protect against the oxidative effect of this increased dose of selenite. However, 10 times the normal level of vitamin E markedly suppressed this oxidative effect.

scholarly journals Lipid Peroxidation: A Signaling Mechanism in Diagnosis of Diseases

2021 ◽  
Author(s):  
Kalpana Sabanna Patil ◽  
Raju Ratan Wadekar
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Clinical Practice ◽  
Oxidation Products ◽  
Signaling Mechanism ◽  
Unsaturated Lipids ◽  
End Products ◽  
Lipid Radicals

Quantification of reactive oxygen species, is perplexing either in vivo or in vitro due to their short half-lives. Consequently, to define the magnitude of oxidative stress, the more stable oxidation products can be measured in biological samples. The oxidative stress leads to the lipid peroxidation that involves the initiation, termination and propagation of lipid radicals, wherein, the process involves the oxygen uptake, rearrangement of the double bonds in unsaturated lipids, that leads to polyunsaturated fatty acid deterioration. Subsequently, the toxic signaling end products are considered as biomarkers of free radicals that act both as signaling molecules and as cytotoxic products cause covalent alteration of lipid peroxidation products. The use of validated signaling mechanism (s) of Lipid peroxidation and products derived thereof exhibits its use clinical practice and basic clinical research as well as in clinical practice has become common place, and their presence as endpoints in clinical trials is now broadly accepted. This knowledge can be used to diagnose disease earlier, or to prevent it before it starts. The signaling markers can be used to excel the effectiveness of the prevailing medicines and to improve the new medicines.

scholarly journals Advanced Glycation end product profile of Diabetic and Non-Diabetic patients with cataract

2021 ◽  
pp. 14-20
Author(s):  
Emma-Okon B.O ◽  
Onakpoya O.H ◽  
Kolawole B.A ◽  
Owolabi F.A ◽  
Akinde M.O ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Lipid Peroxidation ◽  
Advanced Glycation End Products ◽  
Fasting Blood Glucose ◽  
Diabetic Patients ◽  
Healthy Controls ◽  
Reaction Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

The study determined the levels of advanced glycation end-products (AGEs) and malondialdehyde (MDA) in Nigerian cataract patients with and without diabetes mellitus, those with DM but no cataract as well as apparently healthy controls with a view to further elucidating putative pathophysiologic mechanisms for the occurrence of cataracts among our diabetic population. Participants comprised of 30 diabetic patients with operable cataract, 30 non-diabetic patients with operable cataract, 30 diabetic patients without cataract and 17 healthy controls all matched for age and sex, Glycated Haemoglobin levels in whole blood samples were determined using an affinity assay while fasting blood glucose was estimated by the glucose oxidase reaction. AGE was measured using a competitive ELISA kit while the level of lipid peroxidation in plasma was determined by measuring the reaction products between malondialdehyde and thiobarbituric acid. Statistical analysis was carried out using SPSS software (version 23). P<0.05 was taken as significant. The age range of participants was 52-90 years with a mean of 67.2±0.8. Mean levels of AGE were comparable in patients who had diabetes and cataract, those with cataract but no diabetes and those with Diabetes but no cataracts while healthy controls of similar age group had significantly lower levels. Patients with diabetes mellitus and cataract had significantly higher levels of MDA than those with diabetes only. There was positive, significant correlation between AGE and fasting glucose levels. No significant differences existed between AGE and MDA levels in male and female respondents. We conclude that AGE may serve as a useful index of pathologic conditions, including cataract and diabetes. Keywords: Advanced Glycation End-Products; Cataract; Diabetes; Lipid Peroxidation

scholarly journals The ratio of erythrocyte populations in the blood of puppies during postnatal oxidative stress

2019 ◽  
pp. 81-87
Author(s):  
M. Anfiorova ◽  
M. Broshkov ◽  
O. Danchuk
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Key Words ◽  
Schiff Bases ◽  
The Body ◽  
Peroxide Oxidation ◽  
Diene Conjugates ◽  
Lipid Peroxidation Products ◽  
End Products ◽  
Conjugated Trienes

The article presents new scientifi c data on the ratio of erythrocyte populations in puppies' blood during postnatal oxidative stress. It was established that the number of erythrocytes in the blood of one-day-old puppies was 5.64 ± 0.12 T / l, and half of these cells belonged to the population of "mature", 40% - "young" and 10% - "old". In day-old puppies, the content of lipid peroxidation products in erythrocyte hemolysates is quite high, which indicates the development of postnatal oxidative stress. Thus, the content of diene conjugates, ketodienes and Schiff bases is respectively 1,406 ± 0,023 Conv. units, 0.676 ± 0.004 Conv. units and 0.135 ± 0.003 Conv. units. From one to fi ve days age of puppies the number of erythrocytes in the blooddecrease by 1.5 times (p<0.001), mainly due to the decrease in the number of "mature" cells (by 1.6 times; p<0.001). The intensity of peroxide oxidation in the body of puppies even a month after birth is relatively high, as indicated by the content of Schiff bases in the erythrocytes of the blood of these animals - 0.185 ± 0.002 Conv.units. The inverse correlations of the content of Schiff bases in erythrocyte hemolysate with their number in the bloodstream were found to be r = -0.83 (p<0.001). It should also be noted the direct correlation of the content of diene conjugates in the blood of puppies with the number of erythrocytes in their blood (r = 0,58 p <0,05), but the content of ketodienes and conjugated trienes is inversely related to the content of "young" erythroid cells in the puppies' blood (r = -0.57 p <0.05). Consequently, post-natal adaptation of puppies results in the replacement of fetal erythrocytes by postnatal cells, and this process is associated with the intensifi cation of peroxide oxidation and accumulation of the end products of peroxidationin the cells. This process isaccompanied by an acceleration of the process of "aging" of young forms of erythrocytes, as a result of which prerequisites for the development of anemiaare created. Key words: erythrocytes, oxidative stress, puppies, Schiff bases, ketodienes, diene conjugates.

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