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

Paraquat has been suggested to induce apoptosis by generation of reactive oxygen species (ROS). However, little is known about the mechanism of paraquat-induced apoptosis. Here, we demonstrate that extracellular signal-regulated protein kinase (ERK) is required for paraquat-induced apoptosis in NIH3T3 cells. Paraquat treatment resulted in activation of ERK, and U0126, inhibitors of the MEK/ERK signaling pathway, prevented apoptosis. Moreover, paraquat-induced apoptosis was associated with cytochrome C release, which could be prevented by treatment with the MEK inhibitors. Taken together, our findings suggest that ERK activation plays an active role in mediating paraquat-induced apoptosis of NIH3T3 cells.
Apoptosis* ; Cytochromes c* ; Negotiating ; Paraquat* ; Protein Kinases ; Reactive Oxygen Species

BACKGROUND: Reoxygenation of an ischemic heart causes a decrease in the cardiac function, which is known as reperfusion injury that is associated with an increase in the concentration of reactive oxygen species (ROS). This study examined the effect of the propofol concentration on the generation of ROS during reoxygenation in rat embryonic heart H9c2 cells. METHODS: Cultured H9c2 cells were examined in the following sequences: Prehypoxic, Hypoxic and Reoxygenation period. Each period required 60 minutes. The cells were exposed to propofol at the beginning of the prehypoxic period. Thirty minutes later, DCFH-DA (dichlorofluorescin diacetate) 10 micrometer was added to detect the ROS. The propofol concentrations used were 0, 5, 25, 50, 250 micrometer in the first experiment and 0, 1, 2, 3, 4, 5 micrometer in the second experiment. The ROS level was estimated using a fluorometer at 5-minute intervals from 5 to 60 minutes after reoxygenation. RESULTS: When the propofol concentrations was > 5 micrometer, the ROS levels were significantly lower than those of the untreated group (P0) (P < 0.05). At propofol concentrations < 5 micrometer, the ROS levels 35 to 60 minutes after reoxygenation were significantly lower that in the untreated group (P < 0.05). Between 5 and 30 minutes after reoxygenation, the cells exposed to 1, 4 and 5 micrometer propofol also showed lower ROS levels than the untreated group P0. However, 2 and 3 micrometer propofol did not show any significant difference in ROS values to those observed in the untreated group except for 2 micrometer at 25 minutes after reoxygenation. CONCLUSIONS: During the reoxygenation period in H9c2 cells, propofol concentrations > 5 micrometer inhibited ROS production over the whole period, and even 1micrometer showed some inhibition of ROS.
Animals ; Heart* ; Propofol* ; Rats* ; Reactive Oxygen Species* ; Reperfusion ; Reperfusion Injury