Peroxidation of lipids and degeneration of photoreceptors in the retina of rats with avitaminosis E

1977 ◽  
Vol 83 (4) ◽  
pp. 473-476 ◽  
Author(s):  
V. E. Kagan ◽  
G. V. Barybina ◽  
K. N. Novikov
Keyword(s):  
Peroxidation Of Lipids ◽  
Avitaminosis E

THE INTENSITY OF OXIDATIVE MODIFICATION OF PROTEINS AND PEROXIDATION OF LIPIDS IN THE BLOOD SERUM, BRAIN, LIVER AND PANCREAS TISSUES OF RATS WITH INSULIN RESISTANCE AND CONGENITAL IODINE DEFICIENCY

2019 ◽  
pp. 115-120
Author(s):  
V. B. Stetsevyat ◽  
N. M. Voronych-Semchenko
Keyword(s):  
Insulin Resistance ◽  
Iodine Deficiency ◽  
Thiobarbituric Acid ◽  
Oxidative Modification ◽  
Peroxidation Of Lipids ◽  
Diene Conjugates ◽  
Oxidative Modification Of Proteins ◽  
High Fructose ◽  
Liver And Pancreas ◽  
Dependent Processes

The results of the study about the nature of oxygen-dependent processes in rats that were on a high-fructose diet for 8 weeks under conditions of adequate iodine supply and congenital iodine deprivation is presented in the article. The significant activation of peroxide oxidation of proteins (by increasing the aldo- and keto-derivates of a neutral nature) and lipids (increased of diene conjugates content and products, that are responsible to thiobarbituric acid) of animals with insulin resistance was found. An aggravating factor in the course of these processes is a congenital iodine deficiency. The changes of oxidative modification of proteins in animals with congenital iodine deficiency had multidirectional character, and processes of lipid peroxidation mainly increased. The most pronounced changes of the studied processes were observed in the liver and pancreas of animals with insulin resistance against the background of congenital iodine deficiency.

scholarly journals Cytochemical Demonstration of Oxidative Damage in Alzheimer Disease by Immunochemical Enhancement of the Carbonyl Reaction with 2,4-Dinitrophenylhydrazine

1998 ◽  
Vol 46 (6) ◽  
pp. 731-735 ◽  
Author(s):  
Mark A. Smith ◽  
Lawrence M. Sayre ◽  
Vernon E. Anderson ◽  
Peggy L.R. Harris ◽  
M. Flint Beal ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Oxidative Damage ◽  
Peroxidation Of Lipids ◽  
Bulk Analysis ◽  
Age Related ◽  
Cytochemical Demonstration ◽  
Highly Sensitive ◽  
Metal Catalyzed ◽  
Specific Oxidation ◽  
Cytochemical Technique

Formation of carbonyls derived from lipids, proteins, carbohydrates, and nucleic acids is common during oxidative stress. For example, metal-catalyzed, “site-specific” oxidation of several amino acid side-chains produces aldehydes or ketones, and peroxidation of lipids generates reactive aldehydes such as malondialdehyde and hydroxynonenal. Here, using in situ 2,4-dinitrophenylhydrazine labeling linked to an antibody system, we describe a highly sensitive and specific cytochemical technique to specifically localize biomacromolecule-bound carbonyl reactivity. When this technique was applied to tissues from cases of Alzheimer disease, in which oxidative events including lipoperoxidative, glycoxidative, and other oxidative protein modifications have been reported, we detected free carbonyls not only in the disease-related intraneuronal lesions but also in other neurons. In marked contrast, free carbonyls were not found in neurons or glia in age-matched control cases. Importantly, this assay was highly specific for detecting disease-related oxidative damage because the site of oxidative damage can be assessed in the midst of concurrent age-related increases in free carbonyls in vascular basement membrane that would contaminate biochemical samples subjected to bulk analysis. These findings demonstrate that oxidative imbalance and stress are key elements in the pathogenesis of Alzheimer disease.

scholarly journals Molecular Mechanism of Heavy Metal Toxicity and Tolerance in Plants: Central Role of Glutathione in Detoxification of Reactive Oxygen Species and Methylglyoxal and in Heavy Metal Chelation

2012 ◽  
Vol 2012 ◽  
pp. 1-37 ◽  
Author(s):  
Mohammad Anwar Hossain ◽  
Pukclai Piyatida ◽  
Jaime A. Teixeira da Silva ◽  
Masayuki Fujita
Keyword(s):  
Reactive Oxygen Species ◽  
Heavy Metal ◽  
Antioxidant Defense ◽  
Plant Cells ◽  
Reactive Oxygen ◽  
Antioxidant Defense System ◽  
Peroxidation Of Lipids ◽  
Oxygen Species ◽  
Defense System ◽  
Glyoxalase System

Heavy metal (HM) toxicity is one of the major abiotic stresses leading to hazardous effects in plants. A common consequence of HM toxicity is the excessive accumulation of reactive oxygen species (ROS) and methylglyoxal (MG), both of which can cause peroxidation of lipids, oxidation of protein, inactivation of enzymes, DNA damage and/or interact with other vital constituents of plant cells. Higher plants have evolved a sophisticated antioxidant defense system and a glyoxalase system to scavenge ROS and MG. In addition, HMs that enter the cell may be sequestered by amino acids, organic acids, glutathione (GSH), or by specific metal-binding ligands. Being a central molecule of both the antioxidant defense system and the glyoxalase system, GSH is involved in both direct and indirect control of ROS and MG and their reaction products in plant cells, thus protecting the plant from HM-induced oxidative damage. Recent plant molecular studies have shown that GSH by itself and its metabolizing enzymes—notably glutathione S-transferase, glutathione peroxidase, dehydroascorbate reductase, glutathione reductase, glyoxalase I and glyoxalase II—act additively and coordinately for efficient protection against ROS- and MG-induced damage in addition to detoxification, complexation, chelation and compartmentation of HMs. The aim of this review is to integrate a recent understanding of physiological and biochemical mechanisms of HM-induced plant stress response and tolerance based on the findings of current plant molecular biology research.

A Histochemical Study of Embryonic Rat Liver in Avitaminosis E

1967 ◽  
Vol 91 (2) ◽  
pp. 159-173 ◽  
Author(s):  
Dorothy Wei King ◽  
Kusum Verma
Keyword(s):  
Rat Liver ◽  
Histochemical Study ◽  
Avitaminosis E

scholarly journals The Role of Acrolein and NADPH Oxidase in the Granulocyte-Mediated Growth-Inhibition of Tumor Cells

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 292 ◽  
Author(s):  
Morana Jaganjac ◽  
Tanja Matijevic Glavan ◽  
Neven Zarkovic
Keyword(s):  
Nadph Oxidase ◽  
Tumor Cell ◽  
Signaling Pathways ◽  
Tumor Cells ◽  
Redox Homeostasis ◽  
Peroxidation Of Lipids ◽  
Tlr4 Expression ◽  
Antitumor Effects ◽  
Reactive Aldehydes

: Although granulocytes are the most abundant leukocytes in human blood, their involvement in the immune response against cancer is not well understood. While granulocytes are known for their “oxidative burst” when challenged with tumor cells, it is less known that oxygen-dependent killing of tumor cells by granulocytes includes peroxidation of lipids in tumor cell membranes, yielding formation of reactive aldehydes like 4-hydroxynonenal (4-HNE) and acrolein. In the present work, we investigate the role of reactive aldehydes on cellular redox homeostasis and surface toll-like receptor 4 (TLR4) expression. We have further study the granulocyte-tumor cell intercellular redox signaling pathways. The data obtained show that granulocytes in the presence of 4-HNE and acrolein induce excessive ROS formation in tumor cells. Acrolein was also shown to induce granulocyte TLR4 expression. Furthermore, granulocyte-mediated antitumor effects were shown to be mediated via HOCl intracellular pathway by the action of NADPH oxidase. However, further studies are needed to understand interaction between TLR4 and granulocyte-tumor cell intercellular signaling pathways.

Sign in / Sign up

Export Citation Format

Share Document