Oxidative stress implication in a new phenotype of amyotrophic quadricipital syndrome with cardiac involvement due to lamin A/C mutation

This study aimed at evaluating OS in an amyotrophic quadricipital syndrome with cardiac impairment in a family of 80 members with a mutation in lamin A/C gene. Twelve patients had cardiac involvement (5 cardiac and skeletal muscles impairment). OS was evaluated in blood samples (thiobarbituric acid-reactive substances (TBARS), carbonylated proteins (PCO)) 6 “affected patients” with phenotypic and genotypic abnormalities without heart failure and 3 “healthy carrier” patients. OS was higher in affected patients than in healthy, as shown by the higher TBARS and PCO values. Patients with cardiac and peripheral myopathy exhibited a higher OS than patients with only cardiac disease (TBARS: 1.73 ± 0.05 vs. 1.51 ± 0.04 mmol/l (p = 0.051), PCO: 2.73 ± 0.34 vs. 0.90 ± 0.10 nmol/mg protein (p = 0.47)), and with healthy carriers patients (TBARS: 1.73 ± 0.05 vs. 1.16 ± 0.14 mmol/l (p = 0.05), PCO: 2.73 ± 0.34 vs. 0.90 ± 0.20 nmol/mg protein (p = 0.47)).

OS may thus contribute to the degenerative process of this laminopathy. ROS production occurs, prior to heart failure symptoms. We suggest that the extent activation may also promote the variable phenotypic expression of the disease.     

Hydrogen peroxide is involved in the sclerotial differentiation of filamentous phytopathogenic fungi

Aims: The purpose of this study was to investigate the role of H₂O₂ and the related oxidative stress markers catalase (CAT) and lipid peroxidation in the sclerotial differentiation of the phytopathogenic filamentous fungi Sclerotium rolfsii, Sclerotinia minor, Sclerotinia sclerotiorum and Rhizoctonia solani. Methods and Results: Using the H₂O₂‐specific scopoletin fluorometric assay and the CAT‐dependent H₂O₂ consumption assays, it was found that the production rate of intra/extracellular H₂O₂ and CAT levels in the sclerotiogenic fungi were significantly higher and lower, respectively, than those of their nondifferentiating counterpart strains. They peaked in the transition between the undifferentiated and the differentiated state of the sclerotiogenic strains, suggesting both a cell proliferative and differentiative role. In addition, the indirect indicator of oxidative stress, lipid peroxidation, was substantially decreased in the nondifferentiating strains. Conclusions: These findings suggest that the differentiative role of H₂O₂ is expressed via induction of higher oxidative stress in the sclerotiogenic filamentous phytopathogenic fungi. Significance and Impact of the Study: This study shows that the direct marker of oxidative stress H₂O₂ is involved in the sclerotial differentiation of the phytopathogenic filamentous fungi S. rolfsii, S. minor, S. sclerotiorum and R. solani, which could have potential biotechnological implications in terms of developing antifungal strategies by regulating intracellular H₂O₂ levels.     

Antioxidant and oxidative stress changes in experimental cor pulmonale

Although right heart failure (RHF) contributes to 20% of all cardiovascular complications, most of the information available on RHF in general is based on the experiences with left heart failure. This study on RHF investigates changes in antioxidants and oxidative stress which are suggested to play a role in the transition from hypertrophy to failure. RHF subsequent to pulmonary hypertension was produced in rats by a single injection of monocrotaline (MCT, 60 mg/kg, i.p.). Based on hemodynamic, clinical and histopathologic observations, the animals were grouped in three functional stages at 1-, 2- and 6-week post-injection periods. In the 1-week group, RV pressure overload and hypertrophy, and a mild increase in antioxidant enzymes was seen. In the 2-week group, compensated HF, a significant increase in antioxidant enzymes, an increase in septal (IVS) wall thickness and leftward displacement of IVS without change in LV free wall were seen. In the 6-week group, lung and liver congestion, RVF and dilation, a decrease in antioxidant enzyme activities, increase in lipid peroxidation and severe bulging of the IVS into the left ventricle were seen. These changes in the hemodynamic, biochemical and histopathologic characteristics suggest that in early stages of MCT-induced pulmonary hypertension at 1 and 2 weeks, RV hypertrophy was accompanied by sustained hemodynamic function and an increase in antioxidant reserve. In the later stage at 6 weeks, clinical RHF was associated with abnormalities of the right heart systolic and diastolic function along with a decrease in antioxidant reserve. These biphasic changes in RV antioxidant enzymes, i.e. an increase during hypertrophy and a decrease in failure may suggest a role of oxidative stress in the pathogenesis of right ventricular dysfunction.     

Differences in oxidative stress markers based on the aetiology of heart failure: Comparison of oxidative stress in patients with and without coronary artery disease

Abstract

Various oxidative stress markers have been measured to evaluate the status of heart failure (HF). However, the relationships between these markers and the aetiology of HF have not been fully investigated. This study compared 8-hydroxy-2′-deoxyguanosine (8-OHdG) and biopyrrins levels in patients with ischemic and non-ischemic HF. Study subjects were divided into a coronary artery disease (CAD) group (n=70), a non-CAD group (n=61) and a control group (n=33). In the CAD group, 8-OHdG and biopyrrins levels increased with the severity of the New York Heart Association (NYHA) functional class and log BNP levels correlated with 8-OHdG and biopyrrins levels. However, non-CAD patients with NYHA class III/IV had significantly lower 8-OHdG levels than CAD patients with NYHA class III/IV and the levels did not correlate with log BNP levels. In the CAD group, 8-OHdG levels reflected the severity of atherosclerosis. These results indicate that the properties of oxidative stress markers should be carefully taken into consideration for the assessment of HF status.     

On the benefit of melatonin in protection against ouabain-induced arrhythmia through modulation of oxidative stress factors in isolated rat atria

Considering the cardioprotective and antioxidant properties of melatonin, in the present experiment, we investigated the possible involvement of oxidative stress factors in antiarrhythmic effects of melatonin in ouabain-induced arrhythmia in isolated rat atria. Male rats were divided into two groups, receiving either of melatonin (2 mg/kg) or vehicle, orally once daily for three weeks. Rats were anesthetized, and atria were isolated and incubated with ouabain in an organ bath. Time of onset of arrhythmia and asystole as well as atrial beating rate and contractile force were recorded. We also measured the activity of superoxide dismutase (SOD) and levels of thiobarbituric acid reactive substances (TBARS) in atria after injection of ouabain to animals. Pretreatment of animals with melatonin could significantly postpone the onset of arrhythmia and asystole compared with vehicle-treated group (P ≤ 0.001). Incubation of ouabain boosted the atrial beating rate in vehicle-treated group (P ≤ 0.01), while this response in melatonin-treated group was not significant (P > 0.05). Injection of ouabain decreased the activity of SOD and increased the levels of TBARS in atria (P ≤ 0.001, P ≤ 0.01, respectively), while pretreatment of animals with melatonin reversed these effects (P ≤ 0.05). It is concluded that melatonin possesses antiarrhythmic properties, and oxidative stress factors might mediate this response.     

Effect of temperature on antioxidant enzymatic activity in the Pacific white shrimp Litopenaeus vannamei in a BFT (Biofloc technology) system

A 10-day trial was conducted to evaluate the effect of temperature on the antioxidant system of Litopenaeus vannamei in a biofloc technology system. Four treatments in triplicate tanks were assigned to the following temperatures: 15, 21, 27 (control), and 33 °C and the water quality parameters were monitored every day. For all enzyme assays, the hemolymph cells lysate of six shrimp per treatment was collected. Lipid peroxidation (LPO) was assessed by determining the content of thiobarbituric acid-reactive substances (TBARS); the activities of catalase (CAT) and glutathione-S-transferase (GST) were also evaluated. The results of TBARS showed that shrimp reared at 15 and 21 °C presented an increase of 407% (240 h) and 339% (120 h), respectively. L. vannamei exposed to 15 °C augmented in 186% (24 h) the activity of CAT. Moreover, shrimp of 21 °C group also increased CAT activity in 228% (6 h). GST presented the strongest variation reaching 1437% in shrimp of 15 °C for 6 h and 1425% of the 21 °C treatment at the same time. All these results were compared to the initial time (27 °C). Moreover, the antioxidant system was not sufficient to counteract LPO; therefore, the animals reared in 15 and 21 °C presented higher enzyme activities, suggesting that cold water can induce the oxidative stress in L. vannamei.     

Effects of Fetal Bovine Serum on Ferrous Ion-Induced Oxidative Stress in Pheochromocytoma (PC12) Cells

Ferrous ion (Fe²⁺) has been considered to be a cause of neuronal oxidative injury. Since body fluids contain protein and serum is an essential component of tissue culture medium, we have examined the role of serum protein on Fe²⁺-mediated oxidative stress using PC12 cells and rat cerebral cortices. Fe²⁺ or the combination of ascorbate and Fe²⁺ increased concentrations of thiobarbituric acid reactive substances (TBARS) in PC12 cells and cerebrocortical homogenates in medium (RPMI 1640), but did not increase TBARS when the medium was supplemented with 10% fetal bovine serum. Treatment with ascorbate/Fe²⁺ in serum-free medium reduced endogenous glutathione (GSH) concentration in PC12 cells. However, the medium supplemented with serum did not reduce GSH concentrations. PC12 cell death induced by ascorbate/Fe²⁺ was alleviated by increasing serum or bovine albumin concentrations in the medium. These observations indicated that oxidative injury caused by the transition metal ion could be lessened by adding fetal bovine serum to culture medium.     

Doxorubicin-induced thiol-dependent alteration of cardiac mitochondrial permeability transition and respiration

Doxorubicin (DOX) is a highly effective treatment for several forms of cancer. However, clinical experience shows that DOX induces a cumulative and dose-dependent cardiomyopathy that has been ascribed to redox-cycling of the drug on the mitochondrial respiratory chain generating free radicals and oxidative stress in the process. Mitochondrial dysfunction including induction of the mitochondrial permeability transition (MPT) and inhibition of mitochondrial respiration have been implicated as major determinants in the pathogenesis of DOX cardiotoxicity. The present work was aimed at investigating whether the inhibition of mitochondrial respiration occurs secondarily to MPT induction in heart mitochondria isolated from DOX-treated rats and whether one or both consequences of DOX treatment are related with oxidation of protein thiol residues. DOX-induced oxidative stress was associated with the accumulation of products of lipid peroxidation and the depletion of alpha-tocopherol in cardiac mitochondrial membranes. No changes in mitochondrial coenzyme Q9 and Q10 concentrations were detected in hearts of DOX-treated rats. Cardiac mitochondria from DOX-treated rats were more susceptible to diamide-dependent induction of the MPT. Although DOX treatment did not affect state 4 respiration, state 3 respiration was decreased in heart mitochondria isolated from DOX-treated rats, which was reversed in part by adding either cyclosporin A or dithiothreitol, but not Trolox. The results suggest that in DOX-treated rats, (i) induction of the MPT is at least in part responsible for decreased mitochondrial respiration, (ii) heart mitochondria are more susceptible to diamide induced-MPT, (iii) thiol-dependent alteration of mitochondrial respiration is partially reversible ex vivo with dithiothreitol. Collectively, these data are consistent with the thesis that thiol-dependent alteration of MPT and respiration is an important factor in DOX-induced mitochondrial dysfunction.     

Structure-Related Oxidative Damage in Rat Brain After Acute and Chronic Electroshock

The role of oxidative stress in electroconvulsive therapy-related effects is not well studied. The purpose of this study was to determine oxidative stress parameters in several brain structures after a single electroconvulsive seizure or multiple electroconvulsive seizures. Rats were given either a single electroconvulsive shock or a series of eight electroconvulsive shocks. Brain regions were isolated, and levels of oxidative stress in the brain tissue (cortex, hippocampus, striatum and cerebellum) were measured. We demonstrated a decrease in lipid peroxidation and protein carbonyls in the hippocampus, cerebellum, and striatum several times after a single electroconvulsive shock or multiple electroconvulsive shocks. In contrast, lipid peroxidation increases both after a single electroconvulsive shock or multiple electroconvulsive shocks in cortex. In conclusion, we demonstrate an increase in oxidative damage in cortex, in contrast to a reduction of oxidative damage in hippocampus, striatum, and cerebellum.