Free radicals and cell chemiluminescence

Abstract

Application of chemiluminescence (CL) for study of free-radical reactions in human and animal cells and tissues is considered in this review. Historically, the study of intrinsic (ultraweak) luminescence gave place to the measurement of CL in the presence of chemical activators (CL probes) and physical activators (sensitizers) of luminescence, which made the method much more sensitive and specific. The methods of CL and EPR are direct methods of radical investigation, though the advantage of the CL method consists in the fact that CL intensity is directly proportional to a steady-state concentration of the radicals responsible for luminescence (first of all, lipid and oxygen radicals) irrespective the activity of these radicals. The mechanisms of CL reactions in the absence of activators and in the presence of luminol and lucigenin are considered. Examples of various applications of the CL method in medical, biological, and clinical investigations are given including those for estimation of the phagocytic activity of cells, antioxidant activity, determination of toxicity, and other purposes.

Nickel-induced Epithelial-Mesenchymal Transition by Reactive Oxygen Species Generation and E-cadherin Promoter Hypermethylation

“…Hypochlorite anion (OCl Ϫ ) is a natural compound that forms from the reaction catalyzed by myeloperoxidase, an enzyme present only in innate immune cells (31). Both OCl Ϫ and OH ⅐ can be detected in photocatalytic ROS production using 3Ј-(p-aminophenyl) fluorescein.…”

Plastic deformation and spall fracture of structural 12CR18NI10TI steel

“…The first-group samples were cut from the 40-mm diameter steel rods. These samples were studied both prior to (as-received, AR1 samples) and after the austenization treatment [6] (T1 samples). More than 10 experiments with each thickness provided the detailed data that allowed us to construct a reliable dependenceσ sp (P max ).…”

Antioxidant defenses in diabetes mellitus: a clinical and molecular approach

“…When oxygen, nitrogen or chlorine reactive species are excessively formed in cells and tissues they are implicated in many pathophysiological and disease events, including diabetes mellitus (DM) [1,2]. As a consequence of the oxidative and nitrosative stresses occurs lipid peroxidation (measured by biomarkers like malonaldehyde, 4-hydroxynonenal, and conjugated dienes), protein and aminoacid oxidation (evaluated by protein carbonyls), nucleic acid oxidation (quantifyied by DNA oxidized bases) and carbohydrate oxidation (measured by glycosilation products like glycated hemoglobin [HbA1] and advanced glycation end products [AGEs] commonly found in DM animal models and human patients [3][4][5][6][7][8].…”

“…During at least four decades, an extensive number of research groups have been studied the oxidative and nitrosative stress biomarkers as well as the different antioxidant defense mechanisms by measuring the antioxidant enzymes (superoxide dismutase [SOD], catalase, glutathione reductase [GSH], glutathione peroxidase [GPx], ceruloplasmin, metallothioneins) [1,2,9]. In DM patients its well established that oxidative and nitrosative stress decreases cell antioxidant enzyme defenses, especially the GSH, and increase the SOD activity in order to detoxify the superoxide anion mitochondrial overload [7,8,10,11].…”