Home About us Contact
|
Home About us Contact | ||
|
|
||
Reactive Oxygen Species Levels (reactive + oxygen_species_level)
Selected AbstractsDetermination of Reactive Oxygen Species in Myringotomized Tympanic Membranes: Effect of Vitamin E TreatmentTHE LARYNGOSCOPE, Issue 4 2004Senol Polat MD Abstract Objectives/Hypothesis Recent studies have established a strong relationship between the development of myringosclerosis and reactive oxygen species (ROS). The aims of the present study were to directly detect ROS in the tympanic membrane and middle ear mucosa of rats by measuring luminol amplified chemiluminescence, to evaluate the changes in the levels of ROS after treatment with vitamin E, and to examine the possible changes in the tympanic membranes otomicroscopically and histologically. Study Design Prospective controlled animal study. Methods Forty healthy Sprague-Dawley rats were divided into five groups of eight animals each. Animals in all groups except group 1 were bilaterally myringotomized. Group 2 received no treatment, group 3 was treated with topical olive oil, group 4 received topical vitamin E, and group 5 received intramuscular vitamin E. After 24 hours of myringotomy, tympanic membranes were examined otomicroscopically; thereafter, tympanic membranes and middle ear mucosa were peeled off. The right ears of the animals were used for biochemical assay, and the left ears were used for histological study. Results Reactive oxygen species levels were significantly decreased in group 4 with topical application of vitamin E compared with untreated and myringotomized animals in group 2. Reactive oxygen species levels were also decreased in group 5, although the decrease was not statistically significant when compared with groups 2 and 3. Histological studies confirmed sclerotic changes in the untreated myringotomized animals. The tympanic membranes of animals in groups 2 and 3 showed a white, chalk-like pattern of sclerotic changes, whereas animals in groups 4 and 5, with the exception of two animals in group 5, lacked these changes. Conclusion Although the relationship between the development of myringosclerosis and ROS had been well documented previously, the present study is the first that has directly measured the levels of ROS in the tympanic membrane and middle ear mucosa. These results are relevant because they correlate with histological findings. It has also been demonstrated that topically applied vitamin E is effective in decreasing the ROS levels. [source] Neuroprotection by baicalein in ischemic brain injury involves PTEN/AKT pathwayJOURNAL OF NEUROCHEMISTRY, Issue 6 2010Chao Liu J. Neurochem. (2010) 112, 1500,1512. Abstract Recently more evidences support baicalein (Bai) is neuroprotective in models of ischemic stroke. This study was conducted to determine the molecular mechanisms involved in this effect. Either permanent or transient (2 h) middle cerebral artery occlusion (MCAO) was induced in rats in this study. Permanent MCAO led to larger infarct volumes in contrast to transient MCAO. Only in transient MCAO, Bai administration significantly reduced infarct size. Baicalein also markedly reduced apoptosis in the penumbra of transient MCAO rats. Additionally, oxygen and glucose deprivation (OGD) was used to mimic ischemic insult in primary cultured cortical neurons. A rapid increase in the intracellular reactive oxygen species level and nitrotyrosine formation induced by OGD was counteracted by Bai, which is parallel with attenuated cell injury. The reduction of phosphorylation Akt and glycogen synthase kinase-3, (GSK3,) induced by OGD was restored by Bai, which was associated with preserved levels of phosphorylation of PTEN, the phophatase that negatively regulates Akt. As a consequence, Bcl-2/Bcl-xL-associated death protein phosphorylation was increased and the protein level of Bcl-2 in motochondria was maintained, which subsequently antagonize cytochrome c released in cytosol. LY294002 blocked the increase in phospho-AKT evoked by Bai and abolished the associated protective effect. Together, these findings provide evidence that Bai protects neurons against ischemia injury and this neuroprotective effect involves PI3K/Akt and PTEN pathway. [source] Anti-angiogenic, antinociceptive and anti-inflammatory activities of Lonicera japonica extractJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 6 2008Hye-Jung Yoo This study aimed to elucidate some novel pharmacological activities of Lonicera japonica (Caprifoliaceae), which is widely used in Oriental folk medicine. The ethanolic extract of L. japonica (LJ) dose dependently inhibited chick chorioallantoic membrane angiogenesis. The antinociceptive activity of LJ was assessed using the acetic acid-induced constriction model in mice. LJ showed anti-inflammatory activity in two in-vivo models: the vascular permeability and air pouch models. LJ suppressed the production of nitric oxide via down-regulation of inducible nitric oxide synthase in lipopolysaccharide-stimulated RAW264.7 macrophage cells. However, LJ was unable to suppress induction of cyclooxygenase-2 in the stimulated macrophage cells. LJ decreased the reactive oxygen species level in the stimulated macrophage cells. In brief, the flowers of L. japonica possess potent anti-angiogenic and antinociceptive activities, in addition to anti-inflammatory activity, which partly supports its therapeutic efficacy. [source] Protective Effect of Ebselen on Aflatoxin B1 -Induced Cytotoxicity in Primary Rat HepatocytesBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2000Cheng-Feng Yang Recent studies have shown that aflatoxin B1 enhances reactive oxygen species formation and causes oxidative damage, which may ultimately contribute to the cytotoxicity and carcinogenic effect of aflatoxin B1. Ebselen, 2-phenyl-1,2-benzoisoseleazol-3(H)-one, a synthetic seleno-organic compound has been shown to possess glutathione peroxidase-like activity and free radical scavenging ability. Thus present study was designed to investigate the protective effect of ebselen on aflatoxin B1 -induced cytotoxicity in primary rat hepatocytes. Aflatoxin B1 -induced cytotoxicity and lipid peroxidation were determined by lactate dehydrogenase leakage and malondialdehyde generation, respectively. Intracellular reactive oxygen species level was measured using the fluorescent probe 2,,7,-dichlorofluorescin diacetate, and the intracellular reduced glutathione concentration was determined with a fluorometric method. Ebselen was found to display a dose-dependent protective effect on lactate dehydrogenase leakage and malondialdehyde generation caused by aflatoxin B1 exposure. The results also demonstrate that ebselen efficiently inhibits the intracellular reactive oxygen species formation in aflatoxin B1 -treated hepatocytes in a dose and time-dependent manner. It was also noted that ebselen was able to increase the intracellular reduced glutathione concentration, both in the control and in aflatoxin B1 -treated hepatocytes. The protection of ebselen against aflatoxin B1 cytotoxicity, however, was not affected by lowering the concentration of intracellular reduced glutathione. The overall data indicate that ebselen possesses a potent protective effect against aflatoxin B1 -induced cytotoxicity, and the main mechanism involved in the protection may be its strong capability in inhibiting intracellular reactive oxygen species formation and preventing oxidative damage. [source] Varicocelectomy reduces reactive oxygen species levels and increases antioxidant activity of seminal plasma from infertile men with varicoceleINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 5 2001T. Mostafa Several theories have been advanced to explain the mechanisms by which varicocele impairs male fertility. These theories include scrotal hyperthermia, retrograde flow of adrenal or renal metabolites, Leydig cell dysfunction and hypoxia. Varicocele is reported to be associated with elevated reactive oxygen species (ROS) production in spermatozoa and diminished seminal plasma antioxidant activity. The aim of this study was to investigate whether surgical correction of varicocele might reduce ROS or increase the antioxidant capacity of seminal plasma from infertile patients with varicocele. The study group consisted of 68 infertile males, selected from patients scheduled for varicocelectomy at Cairo University Hospital during the year 1999. Seminal plasma levels of two ROS [malondialdehyde (MDA), hydrogen peroxide (H2O2)] and one ROS radical [nitric oxide (NO)] were estimated as well as six antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), vitamin C (Vit C), vitamin E (Vit E), albumin) on the day prior to varicocelectomy. For comparison, the same parameters were measured again 3 and 6 months post-operatively. A statistically significant reduction in the 3 month post-operative levels of MDA, H2O2 and NO was observed when compared with the pre-operative values. A further significant reduction took place during the following 3 months. Four of the six antioxidants tested (SOD, CAT, GPx, and Vit C) showed a significant increase in seminal levels when comparing 3-month post-operative with pre-operative values. A further significant increase of the four antioxidant levels took place during the following 3 months. No significant change in the level of seminal plasma albumen took place during the first 3 months after varicocelectomy, however, a significant increase was noted during the next 3 months. In contrast to other antioxidants, seminal plasma levels of Vit E showed a significant decrease when comparing 3-month post-operative with pre-operative values. A further significant decrease took place during the following 3 months. It is concluded that varicocelectomy reduces ROS levels and increases antioxidant activity of seminal plasma from infertile men with varicocele. [source] Mitochondrial dysfunction, oxidative stress, regulation of exocytosis and their relevance to neurodegenerative diseasesJOURNAL OF NEUROCHEMISTRY, Issue 2 2008Damien J. Keating Abstract A common feature in the early stages of many neurodegenerative diseases lies in mitochondrial dysfunction, oxidative stress, and reduced levels of synaptic transmission. Many genes associated with neurodegenerative diseases are now known to regulate either mitochondrial function, redox state, or the exocytosis of neurotransmitters. Mitochondria are the primary source of reactive oxygen species and ATP and control apoptosis. Mitochondria are concentrated in synapses and significant alterations to synaptic mitochondrial localization, number, morphology, or function can be detrimental to synaptic transmission. Mitochondrial by-products are capable of regulating various steps of neurotransmission and mitochondrial dysfunction and oxidative stress occur in the early stages of many neurodegenerative diseases. This mini-review will highlight the prospect that mitochondria regulates synaptic exocytosis by controlling synaptic ATP and reactive oxygen species levels and that dysfunctional exocytosis caused by mitochondrial abnormalities may be a common underlying phenomenon in the initial stages of some human neurodegenerative diseases. [source] Chronic exposure to sub-lethal beta-amyloid (A,) inhibits the import of nuclear-encoded proteins to mitochondria in differentiated PC12 cells*JOURNAL OF NEUROCHEMISTRY, Issue 5 2007Daniel Sirk Abstract Studies on amyloid beta (A,|), the peptide thought to play a crucial role in the pathogenesis of Alzheimer's disease, have implicated mitochondria in A,-mediated neurotoxicity. We used differentiated PC12 cells stably transfected with an inducible green fluorescent protein (GFP) fusion protein containing an N,-terminal mitochondrial targeting sequence (mtGFP), to examine the effects of sub-lethal A, on the import of nuclear-encoded proteins to mitochondria. Exposure to sub-lethal A,25,35 (10 ,mol/L) for 48 h inhibited mtGFP import to mitochondria; average rates decreased by 20 ± 4%. Concomitant with the decline in mtGFP, cytoplasmic mtGFP increased significantly while mtGFP expression and intramitochondrial mtGFP turnover were unchanged. Sub-lethal A,1,42 inhibited mtGFP import and increased cytoplasmic mtGFP but only after 96 h. The import of two endogenous nuclear-encoded mitochondrial proteins, mortalin/mtHsp70 and Tom20 also declined. Prior to the decline in import, mitochondrial membrane potential (mmp), and reactive oxygen species levels were unchanged in A,-treated cells versus reverse phase controls. Sustained periods of decreased import were associated with decreased mmp, increased reactive oxygen species, increased vulnerability to oxygen-glucose deprivation and altered mitochondrial morphology. These findings suggest that an A,-mediated inhibition of mitochondrial protein import, and the consequent mitochondrial impairment, may contribute to Alzheimer's disease. [source] Adaptation of the antioxidant defence system in hydrothermal-vent mussels (Bathymodiolus azoricus) transplanted between two Mid-Atlantic Ridge sitesMARINE ECOLOGY, Issue 1 2007Rui Company Abstract The vent mussel Bathymodiolus azoricus is the dominant member of the Northern Mid-Atlantic Ridge (MAR) hydrothermal megafauna, and lives in an environment characterized by temporal and spatial variations in the levels of heavy metals, methane and hydrogen sulphide, substances which are known to increase reactive oxygen species levels in the tissues of exposed organisms. To evaluate the effects of two contrasting hydrothermal environments on the antioxidant defence system of this vent mussel species, a 2-week transplant experiment was carried out involving mussels collected from the relatively deep (2300 m), and chemical rich, Rainbow vent field. These were transplanted to the shallower (1700 m), and relatively less toxic, Lucky Strike vent field. To achieve this objective, levels of superoxide dismutase, catalase (CAT), total glutathione peroxidase (GPx), selenium-dependent glutathione peroxidase and lipid peroxidation (LPO) were measured in the gills and mantle tissues of resident and transplant mussels before and after the transplant experiment. With the exception of CAT, the gills of the transplanted mussels had significantly higher antioxidant enzyme activity compared with the basal levels in the donor (Rainbow) and recipient (Lucky Strike) populations; whereas the antioxidant enzyme levels in the mantle tissues of the transplants reflected the baseline levels of activity in the native Lucky Strike mussels after 2 weeks. In contrast, LPO levels were significantly higher in both tissue types in the transplants than in either the source or the recipient populations, which suggested a response to hydrostatic pressure change (note, the transplant animals were brought to the surface for transportation between the two vent fields). The fact that the Rainbow mussels survived the transplant experience indicates that B. azoricus has a very robust constitution, which enables it to cope behaviourally, physiologically and genetically with the extreme conditions found in its naturally contaminated deep-sea environment. [source] Correlation of the Mitochondrial Activity of Two-Cell Embryos Produced In Vitro and the Two-Cell Block In Kunming and B6C3F1 MiceTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 5 2009Shie Wang Abstract The correlation between the early embryonic block to development and mitochondrial activity was investigated comparing two-cell embryos produced in vitro from Kunming (KM) and B6C3F1 mice. One-cell embryos were obtained from two species of hybrids (female KM mice mated with KM males and female B6C3F1 mice mated with KM males) and cultured for 84 hr in M16 media. The mitochondrial membrane potential, ATP content, and reactive oxygen species levels were measured in the resulting KM and B6C3F1 two-cell embryos. Mitochondrial membrane potential and ATP content were also determined in KM and B6C3F1 metaphase II eggs. The results showed that the two-cell block was observed in cultured KM embryos but not in B6C3F1 embryos. Mitochondrial membrane potential and ATP content of KM two-cell embryos were significantly lower than in B6C3F1 two-cell embryos (P < 0.01). Interestingly, the reactive oxygen species levels of KM two-cell embryos were significantly lower than their B6C3F1 counterparts (P < 0.01). There was no difference in mitochondrial membrane potential and ATP content between KM and B6C3F1 metaphase II eggs. It is concluded that KM mice have an early two-cell embryo block and that a possible "blocking" mechanism is the lower mitochondrial membrane potential and ATP content in these embryos. The results suggest a new approach for overcoming early embryonic development block, that of manipulating mitochondrial activity. Anat Rec, 292:661,669, 2009. © 2009 Wiley-Liss, Inc. [source] Effects of H2O2 exposure on human sperm motility parameters, reactive oxygen species levels and nitric oxide levelsANDROLOGIA, Issue 3 2010S. S. Du Plessis Summary Research has revealed that reactive oxygen species (ROS) negatively affect sperm function, both in vivo and in vitro. Sperm preparation techniques for assisted reproductive technologies (ART) are potential causes for additional ROS production. This study aimed to correlate the concentration of exogenous H2O2 with sperm motility parameters and intracellular ROS and nitric oxide (NO) levels to reiterate the importance of minimising ROS levels in ART. Human spermatozoa from 10 donors were incubated and exposed to different exogenous H2O2 concentrations (0, 2.5, 7.5 and 15 ,m). Subsequently, motility was determined using computer-aided semen analysis, while ROS (2,7-dichlorofluorescin diacetate) and NO (diaminofluorescein-2/diacetate) were analysed using fluorescence-activated cell sorting. Results showed that H2O2 did affect the sperm parameters. Exogenous H2O2 was detrimental to motility and resulted in a significant increase in overall ROS and NO levels. A significant increase in static cells was seen as well. It is important to elucidate the mechanisms between intracellular ROS levels with sperm motility parameters. While this experiment demonstrated a need to reduce exogenous ROS levels during ART, it did not illustrate the cause and effect relationship of intracellular ROS and NO levels with sperm motility. Further research needs to be conducted to define a pathological level of ROS. [source] | |||||||||||||