Erratum to “Epigallocathechin-3 gallate inhibits cardiac hypertrophy through blocking reactive oxidative species-dependent and -independent signal pathways” [Free Radical Biol. Med. 40 (2006) 1756–1775]

Among the factors associated with the risk of colorectal cancer and other large bowel diseases are gender, with women having lower incidence than men, and free-radical mediated oxidation. Dietary fiber has been attributed a protective role in human gastro-intestinal health. The main aim of this study was to determine the degree of association between dietary fiber consumption and fecal free-radical production in healthy rural and urban Guatemalan women, moreover, to look for associations between gender and fecal reactive oxidative species (ROS) basal production, a marker of in situ colonic free-radical-based oxidation. For this purpose, we assessed the dietary fiber consumption, using two 24-h recalls, in urban and rural females, and compared the baseline data, i.e., of iron-supplement-free periods, in three previous studies. Two of these trials quantified the fecal ROS generation as total hydroxylated products resulting from free-radical attack on salicylic acid along with residual non-heme iron content in stool samples from 27 Fe-replete men. The third study assessed the same variables in 20 rural and 20 urban women, all consuming their respective habitual diets. The average fiber consumption for females was more than double in the rural group than in the urban population. As for the average ROS responses, a 2.5-fold difference was observed between men and women, with men having the higher concentrations of total hydroxylated products. This difference was sex-linked, unaffected by statistically significant differences in dietary fiber intake, nor by different concentrations of residual fecal non-heme iron between rural and urban women. The difference in background ROS production between men and women suggests a gender-related influence on intraintestinal oxidation that may protect women from harmful effects of dietary oxidants, such as iron.

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Abstract 420: Delineating the Caspase-dependent Targets and Signal Pathways That Promote Pathological Cardiac Hypertrophy

Circulation Research ◽

10.1161/res.117.suppl_1.420 ◽

2015 ◽

Vol 117 (suppl_1) ◽

Author(s):

Charis Putinski ◽

Mohammad Abdul-Ghani ◽

Rebecca Stiles ◽

Steve Brunette ◽

Sarah A Dick ◽

...

Keyword(s):

Cardiac Hypertrophy ◽

Pathological Process ◽

Signal Pathways ◽

Caspase Cleavage ◽

Substrate Protein ◽

Cell Death Pathway ◽

Effector Caspase ◽

The Impact

Although cardiac hypertrophy is initially an adaptive response, chronic stress on the heart is a maladaptive process that inevitably leads to end-stage heart failure. Interestingly, this pathological process is also characterized by cell behaviors associated with apoptosis. We previously demonstrated the essential role of the intrinsic cell death pathway during cardiac hypertrophy; however, the caspase-dependent pathways and cleavage targets remain elusive. To this aim, we evaluated a myocyte enhancer factor 2 (MEF2) transcription factor inhibitor, histone deacetylase 3 (HDAC3), and gelsolin as potential caspase cleavage substrates involved in the induction and/or maintenance of cardiac hypertrophy. In vitro cleavage assays were completed with effector caspase and recombinant substrate protein which demonstrated caspase-dependent cleavage. HDAC3 cleavage was observed during early stages of hypertrophy and reduced in the presence of a caspase inhibitor. Luciferase assays demonstrated that the transcriptional activity of MEF2 is dependent on intact caspase function suggesting caspase-directed HDAC3 cleavage may serve as a novel regulatory mechanism to alleviate MEF2 suppression to engage the hypertrophy gene expression program. Unlike HDAC3, caspase mediated gelsolin cleavage occurs at latter stages and is coincident with the cytoskeletal alterations that occur during this process. As gelsolin is a potent actin capping/severing enzyme, we hypothesize that caspase-mediated gelsolin activation acts as a key regulatory step in the structural rearrangements that allow for hypertrophy to occur. We have generated adenoviral vectors containing caspase cleavage mutants and cleaved forms of HDAC3 and gelsolin and will discuss the impact of these modified substrates on the hypertrophy process in vitro and in vivo. Collectively, this work suggests that caspase signalling acts to engage both the transcriptional program and cytoskeletal accommodations that characterize cardiac hypertrophy. Importantly, these observations suggest that identification of inhibitors that suppress caspase activity and/or activity of its cognate substrates may offer novel therapeutic targets to limit the development of pathological hypertrophy.

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A look at photodynamic inactivation as a tool for pests and vector-borne diseases control

Laser Physics Letters ◽

10.1088/1612-202x/ac4591 ◽

2022 ◽

Vol 19 (2) ◽

pp. 025601

Author(s):

Alessandra R Lima ◽

Lucas D Dias ◽

Matheus Garbuio ◽

Natalia M Inada ◽

Vanderlei S Bagnato

Keyword(s):

Public Health ◽

Low Cost ◽

Reactive Oxidative Species ◽

Photodynamic Inactivation ◽

Health Issues ◽

Vector Borne Diseases ◽

Control Techniques ◽

The Past ◽

Vector Borne ◽

Oxidative Species

Abstract The control of pests and vector-borne diseases (VDBs) are considered public health issues Worldwide. Among the control techniques and pesticides used so far, photodynamic inactivation (PDI) has been shown as an eco-friendly, low cost, and efficient approach to eliminate pests and VDBs. PDI is characterized using a photosensitizing molecule, light and molecular oxygen (O2) resulting in production of reactive oxidative species which can promote the oxidation of biomolecules on pests and vectors. Herein, we review the past 51 years (1970–2021) regarding the use of photo pesticides, reporting the most important parameters for the protocol applied, the results obtained, and limitations. Moreover, we described the mechanism of action of the PDI, main classes of photopesticides used so far as well as the cell death mechanism resulting from the photodynamic action.

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Abstract 14853: Acute Inhibition of Mitochondrial Reactive Oxidative Species Improves Endothelial SK Channel Function Following Cardioplegic Hypoxia/Reperfusion and Diabetes

Circulation ◽

10.1161/circ.142.suppl_3.14853 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Yi Song ◽

Zhiqi Zhang ◽

Hang Xing ◽

Yixin He ◽

guangbin shi ◽

...

Keyword(s):

Endothelial Cells ◽

Coronary Arteries ◽

Ischemia Reperfusion ◽

Mouse Heart ◽

Reactive Oxidative Species ◽

Sk Channels ◽

Sk Channel ◽

Relaxation Responses ◽

Oxidative Species ◽

Coronary Relaxation

Introduction: Cardioplegic-ischemia/reperfusion (CP-I/R) and diabetes mellitus (DM) are correlated with coronary endothelial dysfunction and inactivated small conductance calcium-activated-potassium (SK) channels. Increased reactive oxidative species (ROS), such as mitochondrial ROS (mROS) may contribute to oxidative injury. Thus, we hypothesized that inhibition of mROS may protect coronary SK channels and endothelial function against CP-I/R-induced injury. Objective: A cardioplegic hypoxia and reoxygenation (CP-H/R) model consisting of coronary endothelial cells and small coronary arteries with or without DM were employed for examining whether MT could protect against coronary endothelial and SK channel dysfunction. Methods: Small coronary arteries (<150μm) and endothelial cells (MHECs) were dissected from the mouse heart with non-diabetes (ND) and DM (n=6/group). The microvessels or MHECs were subjected to hypoxia with cardioplegia and re-oxygenated. The microvessels or MHECs were treated with or without MT (10 -5 M) 5-minutes before and during CP-hypoxia. Microvascular vasodilation function was assessed in vitro by administration of vasoconstrictor, then ADP or NS309,respectively. K + currents of MHECs were measured by whole-cell patch clamp. The levels of endothelial mROS was measured by MitoSox TM . Results: CP-H/R significantly attenuated endothelial SK channels activity and the coronary relaxation responses to ADP and NS309 in the ND and DM groups. Treatment with MT enhanced coronary relaxation responses to ADP or NS309 ( p <0.05, Fig 1. A, B), and similar findings were seen in endothelial SK channel currents in both ND and DM MHECs ( p <0.05, Fig 1. C-F). In addition, treating MHECs with MT reduced CP-H/R-induced mROS in ND and DM groups. Conclusions: Administration of MT improves endothelial SK channels activity which may contribute to its enhancement of endothelium-dependent vasorelaxation following CP-H/R.

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