No abstract available.
Reactive Oxygen Species

In this study, we investigated the antioxidative and antimicrobial activities of red algae Gloiopeltis tenax (GT). GT was extracted with methanol and then further fractionated it into four different types: methanol (GTMM), hexane (GTMH), butanol (GTMB) and aqueous (GTMA) soluble fractions. The antioxidant activity of the fractions from GT was investigated by measuring the scavenging activities of GT against reactive oxygen species (ROS) and reactive nitrogen species (RNS). Among the four fractions of GT, GTMM and GTMB showed a marked scavenging effect against ROS, but they displayed very low levels of the scavenging effect against RNS. The antimicrobial activity was increased in proportion to its concentration by the paper disc method. Among the various solvent layers, the GTMM and GTMB showed strong antimicrobial activities.
Methanol ; Reactive Nitrogen Species ; Reactive Oxygen Species ; Rhodophyta

No abstract available.
Antioxidants* ; Propofol* ; Reactive Oxygen Species* ; Thiopental* ; Vasodilation*

No abstract available.
Nitric Oxide* ; Oxidative Stress* ; Reactive Oxygen Species*

Cardiovascular Diseases ; Ferroptosis ; Humans ; Reactive Oxygen Species

No abstract available.
Endothelins ; Endothelium ; Hypertension ; Reactive Oxygen Species

Macrovascular and microvascular diseases are currently the principal causes of morbidity and mortality in subjects with diabetes. Disorders of the physiological signaling functions of reactive oxygen species (superoxide and hydrogen peroxide) and reactive nitrogen species (nitric oxide and peroxynitrite) are important features of diabetes. In the absence of an appropriate compensation by the endogenous antioxidant defense network, increased oxidative stress leads to the activation of stress-sensitive intracellular signaling pathways and the formation of gene products that cause cellular damage and contribute to the vascular complications of diabetes. It has recently been suggested that diabetic subjects with vascular complications may have a defective cellular antioxidant response against the oxidative stress generated by hyperglycemia. This raises the concept that antioxidant therapy may be of great benefit to these subjects. Although our understanding of how hyperglycemia-induced oxidative stress ultimately leads to tissue damage has advanced considerably in recent years, effective therapeutic strategies to prevent or delay the development of this damage remain limited. Thus, further investigation of therapeutic interventions to prevent or delay the progression of diabetic vascular complications is needed.
Compensation and Redress ; Diabetic Angiopathies ; Hydrogen ; Hyperglycemia ; Nitrogen ; Oxidative Stress ; Oxygen ; Reactive Nitrogen Species ; Reactive Oxygen Species

PURPOSE: The aim of this work was to investigate the beneficial effects of rhamnazin against inflammation, reactive oxygen species (ROS)/reactive nitrogen species (RNS), and anti-oxidative activity in murine macrophage RAW264.7 cells. METHODS: To examine the beneficial properties of rhamnazin on inflammation, ROS/ RNS, and anti-oxidative activity in the murine macrophage RAW264.7 cell model, several key markers, including COX and 5-LO activities, NO•, ONOO-, total reactive species formation, lipid peroxidation, •O₂ levels, and catalase activity were estimated. RESULTS: Results show that rhamnazin was protective against LPS-induced cytotoxicity in macrophage cells. The underlying action of rhamnazin might be through modulation of ROS/RNS and anti-oxidative activity through regulation of total reactive species production, lipid peroxidation, catalase activity, and •O₂, NO•, and ONOO• levels. In addition, rhamnazin down-regulated the activities of pro-inflammatory COX and 5-LO. CONCLUSION: The plausible action by which rhamnazin renders its protective effects in macrophage cells is likely due to its capability to regulate LPS-induced inflammation, ROS/ RNS, and anti-oxidative activity.
Arachidonate 5-Lipoxygenase ; Catalase ; Inflammation* ; Lipid Peroxidation ; Macrophages* ; Nitrogen ; Reactive Nitrogen Species ; Reactive Oxygen Species

No abstract available.
Chemokine CCL2* ; Humans* ; Mesangial Cells* ; Monocytes* ; Reactive Oxygen Species*

BACKGROUND: In order to elucidate toxic mechanism of the oxygen radicals on cultured rat myocardial cells, cytotoxic effect of oxygen radicals was evaluated by MTT assay. In addition protective effect of glutathione(GSH) on oxidant-induced cardiotoxicity was investigated on these cultures. METHODS: Myocardial cells derived from neonatal rats were cultured for 12 hours in the medium containing various concentrations of glucose oxidase(GO). Cell viability was measured by MTT assay and morphological changes of the myocardial cells were observed by light microscope. RESULTS: GO-mediated oxygen radicals remarkably decreased cell viability of cultured myocardial cells in a dose-and time-dependent manner. And also, GSH blicked GO-induced cardiotoxicity in these cultures. CONCLUSION: These results suggest that the oxygen radicals are tixic and the selective antioxidants such as GSH are effective in blocking against the oxidant-induced cardiotoxicity in cultures of the myocardial cells of neonatsl rats.
Animals ; Antioxidants ; Cell Survival ; Glucose ; Glutathione* ; Rats ; Reactive Oxygen Species