Effects of Hyposalinity on Osmoregulation, Oxidative Stress, and Microbial Disruption in Chromis notata (Temminck & Schlegel, 1843).

The reactive advanced glycation end product (AGE) precursor methylglyoxal (MGO) and MGO-derived AGEs are associated with diabetic vascular complications and also with an increase in oxidative stress. Glyoxalase-I (GLO-I) transgenic rats were used to explore whether overexpression of this MGO detoxifying enzyme reduces levels of AGEs and oxidative stress in a rat model of diabetes. Rats were made diabetic with streptozotocin, and after 12 weeks, plasma and multiple tissues were isolated for analysis of AGEs, carbonyl stress, and oxidative stress. GLO-I activity was significantly elevated in multiple tissues of all transgenic rats compared with wild-type (WT) littermates. Streptozotocin treatment resulted in a 5-fold increase in blood glucose concentrations irrespective of GLO-I overexpression. Levels of MGO, glyoxal, 3-deoxyglucosone, AGEs, and oxidative stress markers nitrotyrosine, malondialdehyde, and F2-isoprostane were elevated in the diabetic WT rats. In diabetic GLO-I rats, glyoxal and MGO composite scores were significantly decreased by 81%, and plasma AGEs and oxidative stress markers scores were significantly decreased by ∼50%. Hyperglycemia induced a decrease in protein levels of the mitochondrial oxidative phosphorylation complex in the gastrocnemius muscle, which was accompanied by an increase in the lipid peroxidation product 4-hydroxy-2-nonenal, and this was counteracted by GLO-I overexpression. This study shows for the first time in an in vivo model of diabetes that GLO-I overexpression reduces hyperglycemia-induced levels of carbonyl stress, AGEs, and oxidative stress. The reduction of oxidative stress by GLO-I overexpression directly demonstrates the link between glycation and oxidative stress.

Role of Phagocyte Oxidase in UVA-Induced Oxidative Stress and Apoptosis in Keratinocytes

Chronic glaucoma is a multifactorial disease among which oxidative stress may play a major pathophysiological role. We conducted a systematic review and meta-analysis to evaluate the levels of oxidative and antioxidative stress markers in chronic glaucoma compared with a control group. The PubMed, Cochrane Library, Embase and Science Direct databases were searched for studies reporting oxidative and antioxidative stress markers in chronic glaucoma and in healthy controls using the following keywords: “oxidative stress” or “oxidant stress” or “nitrative stress” or “oxidative damage” or “nitrative damage” or “antioxidative stress” or “antioxidant stress” or “antinitrative stress” and “glaucoma”. We stratified our meta-analysis on the type of biomarkers, the type of glaucoma, and the origin of the sample (serum or aqueous humor). We included 22 case-control studies with a total of 2913 patients: 1614 with glaucoma and 1319 healthy controls. We included 12 studies in the meta-analysis on oxidative stress markers and 19 on antioxidative stress markers. We demonstrated an overall increase in oxidative stress markers in glaucoma (effect size = 1.64; 95%CI 1.20–2.09), ranging from an effect size of 1.29 in serum (95%CI 0.84–1.74) to 2.62 in aqueous humor (95%CI 1.60–3.65). Despite a decrease in antioxidative stress marker in serum (effect size = –0.41; 95%CI –0.72 to –0.11), some increased in aqueous humor (superoxide dismutase, effect size = 3.53; 95%CI 1.20–5.85 and glutathione peroxidase, effect size = 6.60; 95%CI 3.88–9.31). The differences in the serum levels of oxidative stress markers between glaucoma patients and controls were significantly higher in primary open angle glaucoma vs primary angle closed glaucoma (effect size = 12.7; 95%CI 8.78–16.6, P < 0.001), and higher in pseudo-exfoliative glaucoma vs primary angle closed glaucoma (effect size = 12.2; 95%CI 8.96–15.5, P < 0.001). In conclusion, oxidative stress increased in glaucoma, both in serum and aqueous humor. Malonyldialdehyde seemed the best biomarkers of oxidative stress in serum. The increase of some antioxidant markers could be a protective response of the eye against oxidative stress.

P-836: Oxidative stress induced caspase activation and associated toxicity in human sperm

Albumin-bound fatty acids induce mitochondrial oxidant stress and impair antioxidant responses in proximal tubular cells

Circulating levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) play an important role in the development and progression of atherosclerosis. We hypothesized that the inflammatory marker C-reactive protein (CRP) might stimulate sLOX-1 release by activating tumor necrosis factor-α converting enzyme (TACE). Macrophages differentiated from THP-1 cells were stimulated with TNF-α and further treated with CRP in the absence or presence of specific inhibitors or small interfering RNA (siRNA). Our results showed that CRP increased sLOX-1 release from activated macrophages in a dose-dependent manner and that these effects were regulated by Fc γ receptor II (FcγRII)-mediated p47(phox) phosphorylation, reactive oxygen species (ROS) production, and TACE activation. CRP also enhanced sLOX-1 release from macrophages derived from peripheral blood mononuclear cells (PBMC) of patients with acute coronary syndrome (ACS). Pretreatment with antibody against FcγRII or with CD32 siRNA, p47(phox) siRNA, apocynin, N-acetylcysteine, tumor necrosis factor-α protease inhibitor 1 (TAPI-1) or TACE siRNA attenuated sLOX-1 release induced by CRP. CRP also elevated serum sLOX-1 levels in a rabbit model of atherosclerosis. Thus, CRP might stimulate sLOX-1 release, and the underlying mechanisms possibly involved FcγRII-mediated p47(phox) phosphorylation, ROS production, and TACE activation.

Chronic Kidney Disease (CKD) is one of the most important health challenges faced by the world today, with new cases being added at an alarming rate. Controlling traditional risk factors has not been effective in bringing down the incidence of the disease. CKD is associated with inflammation, morbidity, poor quality of life, decreased life-expectancy and death. Oxidative stress represents the imbalance between pro- oxidants and antioxidants in our body. Though a number of studies have focussed on the association between CKD and oxidative stress, majority of them are based on patients on hemodialysis. Moreover, there is confusion about the way the levels of some of these biomarkers vary in response to oxidative stress. This study was designed to study the biomarker of inflammation (CRP), MDA as a marker of oxidative stress, and SOD, GPx and TAC as parameters of antioxidant activity in controls and patients in different stages of CKD. We found that CRP and MDA values increase as disease progresses while there is decrease in the levels of SOD and GPx. The TAC values in patients do not vary much from that of controls. Efforts should be made to identify and reduce large funds to face this challenge, people in the developing countries are reeling under the tremendous financial, psychological and emotional burden of the disease due to insufficient infrastructure and resources available to deal with the disease. Scientists are looking at not just traditional risk factors but also non-traditional ones to help in early detection of the disease so as to initiate treatment early and probably try to reverse this condition or at least delay adverse outcomes. Reactive Oxygen Species (ROS) are free radicals which are constantly being produced in our body during various metabolic processes. When healthy, our body is endowed with the ability to deal with these attackers with the help of antioxidant mechanisms. Trouble starts brewing when the subtle balance tilts in favour of the free radicals. They gain an upper hand while the defence mechanism lags behind. Cellular antioxidants are overwhelmed by repeated oxidative insults. The production of ROS soon cascades leading to a scenario of tissue damage, cell death and disease. ROS cause tissue damage by a variety of different mechanisms which include DNA & protein damage, lipid peroxidation, stimulating release of pro-inflammatory cytokines, etc. (2) This disturbance in the delicate equilibrium of pro-oxidants:antioxidants in favour of the pro-oxidants is termed as oxidative stress. In short, oxidative stress represents an imbalance between the production and manifestation of ROS and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. Oxidative stress may be the sole cause of some disease but more often it weakens the immune system and makes the body vulnerable to diseases caused by other factors. It may also worsen existing conditions and slow down healing process. CKD is associated with increased inflammation. (3) Chronic inflammation in the body is measured by the elevated levels of inflammatory markers and CRP is the marker of choice in monitoring the acute phase response as it increases to a relatively high concentration compared to basal concentration.

Unlike a high-fat diet model, mitochondrial ROS production does not appear to contribute to bed rest-induced insulin resistance.

Relative contributions of mitochondria and NADPH oxidase to deoxycorticosterone acetate-salt hypertension in mice

The Relationship between the Aging- and Photo-Dependent T414G Mitochondrial DNA Mutation with Cellular Senescence and Reactive Oxygen Species Production in Cultured Skin Fibroblasts

Influencing mitochondrial membrane composition and bioenergetics through omega-3 supplementation.

Muscle dysfunction is a common complication and an important prognostic factor in chronic obstructive pulmonary disease (COPD). As therapeutic strategies are still needed to treat this complication, gaining more insight into the process that leads to skeletal muscle decline in COPD appears to be an important issue. This review focuses on mitochondrial involvement in limb skeletal muscle alterations (decreased muscle mass, strength, endurance and power and increased fatigue) in COPD. Mitochondria are the main source of energy for the cells; they are involved in production of reactive oxygen species and activate an important pathway that leads to apoptosis. In COPD patients, skeletal muscles are characterized by decreased mitochondrial density and biogenesis, impaired activity and coupling of mitochondrial respiratory chain complexes, increased mitochondrial production of reactive oxygen species and, possibly, increased apoptosis. Of particular interest, a sedentary lifestyle, hypoxia, hypercapnia, tobacco smoking, corticosteroid therapy and, possibly, inflammation participate in this mitochondrial dysfunction, which is accessible to conventional therapies, such as exercise and tobacco cessation, as well as, potentially, to more innovative approaches, such as antioxidant treatment and supplementation with polyunsaturated fatty acids.

p47phox contributes to albuminuria and kidney fibrosis in mice

HIV infection increases the oxidative stress process, and antiretroviral combination therapy increases protein oxidation and preexistent oxidative stress. The latter induces production of reactive oxygen species. Lipid peroxidation (LPO) is a means of determining oxidative stress. There is also a deficiency of glutathione in HIV infection. Persistent oxidative load leads to an accelerated rate of consumption of glutathione (GSH). This study measured LPO and GSH levels in plasma of HIV-infected individuals with or without therapy and compared these with healthy controls. One hundred HIV-infected individuals and 30 healthy controls were included in the study. LPO and GSH levels were measured in plasma according to previously described methods. The mean level of LPO in HIV-infected individuals was 0.7 +/- 0.1 micromol/ml (range, 0.5-0.9 micromol/ml), whereas the mean LPO level in controls was 0.3 +/- 0.1 micromol/ml (range, 0.2-0.4 micromol/ml). The mean LPO levels were significantly higher in HIV-infected individuals as compared to healthy controls (p value <0.0001). The mean GSH level in HIV-infected individuals was 0.06 +/- 0.01 micromol/ml (range, 0.03-0.08). The mean GSH level in healthy controls was 0.09 +/- 0.01 micromol/ml (range, 0.05-0.1). The mean glutathione level in HIV-infected individuals was significantly lower in compared to healthy controls (p value < 0.0001). There was a significant positive correlation between absolute CD4 cells and GSH levels (rho = 0.182, p = 0.045). There is increased oxidative stress in HIV-infected patients. Whether supplementation with antioxidants will reduce this oxidative stress is still unknown.

Iron oxide nanoparticles induced cytotoxicity, oxidative stress, cell cycle arrest, and DNA damage in human umbilical vein endothelial cells