Reactive oxygen species

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Problem-Based Learning: An Approach to Medical Education

Nuclear factor E2–related factor 2 (Nrf2) is a transcription factor known to induce expression of a variety of cytoprotective and detoxification genes. Several of the genes commonly regulated by Nrf2 have been implicated in protection from neurodegenerative conditions. Work from several laboratories has uncovered the potential for Nrf2-mediated transcription to protect from neurodegeneration resulting from mechanisms involving oxidative stress. For this reason, Nrf2 may be considered a therapeutic target for conditions that are known to involve free radical damage. Because common mechanisms of neurodegeneration, such as mitochondrial dysfunction and build-up of reactive oxygen species, are currently being uncovered, targeting Nrf2 may be valuable in combating conditions with variable causes and etiologies. Most effectively to target this protein in neurodegenerative conditions, a description of the involvement of Nrf2 and potential for neuroprotection must come from laboratory models. Herein, we ...

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The Nrf2/ARE Pathway as a Potential Therapeutic Target in Neurodegenerative Disease

We aim to quantitatively synthesise available epidemiological evidence on the prevalence rates of workplace violence (WPV) by patients and visitors against healthcare workers. We systematically searched PubMed, Embase and Web of Science from their inception to October 2018, as well as the reference lists of all included studies. Two authors independently assessed studies for inclusion. Data were double-extracted and discrepancies were resolved by discussion. The overall percentage of healthcare worker encounters resulting in the experience of WPV was estimated using random-effects meta-analysis. The heterogeneity was assessed using the I2 statistic. Differences by study-level characteristics were estimated using subgroup analysis and meta-regression. We included 253 eligible studies (with a total of 331 544 participants). Of these participants, 61.9% (95% CI 56.1% to 67.6%) reported exposure to any form of WPV, 42.5% (95% CI 38.9% to 46.0%) reported exposure to non-physical violence, and 24.4% (95% CI 22.4% to 26.4%) reported experiencing physical violence in the past year. Verbal abuse (57.6%; 95% CI 51.8% to 63.4%) was the most common form of non-physical violence, followed by threats (33.2%; 95% CI 27.5% to 38.9%) and sexual harassment (12.4%; 95% CI 10.6% to 14.2%). The proportion of WPV exposure differed greatly across countries, study location, practice settings, work schedules and occupation. In this systematic review, the prevalence of WPV against healthcare workers is high, especially in Asian and North American countries, psychiatric and emergency department settings, and among nurses and physicians. There is a need for governments, policymakers and health institutions to take actions to address WPV towards healthcare professionals globally.

https://oem.bmj.com/content/oemed/76/12/927.full.pdf

Prevalence of workplace violence against healthcare workers: a systematic review and meta-analysis.

Aging is a complex phenomenon and its impact is becoming more relevant due to the rising life expectancy and because aging itself is the basis for the development of age-related diseases such as cancer, neurodegenerative diseases and type 2 diabetes. Recent years of scientific research have brought up different theories that attempt to explain the aging process. So far, there is no single theory that fully explains all facets of aging. The damage accumulation theory is one of the most accepted theories due to the large body of evidence found over the years. Damage accumulation is thought to be driven, among others, by oxidative stress. This condition results in an excess attack of oxidants on biomolecules, which lead to damage accumulation over time and contribute to the functional involution of cells, tissues and organisms. If oxidative stress persists, cellular senescence is a likely outcome and an important hallmark of aging. Therefore, it becomes crucial to understand how senescent cells function and how they contribute to the aging process. This review will cover cellular senescence features related to the protein pool such as morphological and molecular hallmarks, how oxidative stress promotes protein modifications, how senescent cells cope with them by proteostasis mechanisms, including antioxidant enzymes and proteolytic systems. We will also highlight the nutritional status of senescent cells and aged organisms (including human clinical studies) by exploring trace elements and micronutrients and on their importance to develop strategies that might increase both, life and health span and postpone aging onset.

Happily (n)ever after: Aging in the context of oxidative stress, proteostasis loss and cellular senescence.

Living organisms are surrounded with heavy metals such as methylmercury, manganese, cobalt, cadmium, arsenic, as well as pesticides such as deltamethrin and paraquat, or atmospheric pollutants such as quinone. Extensive studies have demonstrated a strong link between environmental pollutants and human health. Redox toxicity is proposed as one of the main mechanisms of chemical-induced pathology in humans. Acting as both a sensor of oxidative stress and a positive regulator of antioxidants, the nuclear factor erythroid 2-related factor 2 (NRF2) has attracted recent attention. However, the role NRF2 plays in environmental pollutant-induced toxicity has not been systematically addressed. Here, we characterize NRF2 function in response to various pollutants, such as metals, pesticides and atmospheric quinones. NRF2 related signaling pathways and epigenetic regulations are also reviewed.

Redox toxicology of environmental chemicals causing oxidative stress.

Transcription factor Nrf2 activation by deltamethrin in PC12 cells: Involvement of ROS.

Manganese has been known to induce neurological disorders similar to Parkinson's disease. One of the features of manganese-induced neurotoxicity is oxidative stress. Accumulating data implicate NF-E2-related factor 2 (Nrf2) as a key regulator in the adaptive survival response to oxidative stress. Recent studies suggest that the activation of Nrf2 is induced by manganese in PC12 cells. In the present study, we investigated possible links between reactive oxygen species (ROS), proteasome or mitogen-activated protein kinase (MAPK) signaling and Nrf2/HO-1 activation in manganese-treated PC12 cells. After MnCl(2) treatment, there was an increase in nuclear localization and subsequent binding of Nrf2 to the antioxidant-responsive element (ARE) and upregulation of heme oxygenase-1 (HO-1) protein in PC12 cells. Pretreatment with N-acetyl cysteine, a scavenger of reactive oxygen species, suppressed MnCl(2) -induced Nrf2 activation, increase in Nrf2-ARE binding and subsequent upregulation of HO-1 expression. However, pretreatment with lactacystin, an inhibitor of proteasome activity, enhanced MnCl(2) -induced Nrf2 activation, increase in Nrf2-ARE binding and subsequent upregulation of HO-1 expression. Pretreatment of cells with a pharmacological inhibitor of MAPK (ERK inhibitor PD 98059, P38 inhibitor SB203580 or JNK inhibitor SP600125) did not affect the MnCl(2) -induced Nrf2 activation, increase in Nrf2-ARE binding or subsequent upregulation of HO-1 expression. These results suggest that Nrf2/HO-1 activation by Mn in PC12 cells is associated with ROS and the ubiquitin-proteasome pathway, not MAPK signaling.

Nrf2/HO-1 pathway activation by manganese is associated with reactive oxygen species and ubiquitin-proteasome pathway, not MAPKs signaling.

The present study was conducted to investigate workplace violence and to examine how it is associated with quality of life (QOL) among medical professionals in China. A total of 2,464 medical professionals were selected from Fujian Province and Henan Province by using stratified cluster-sampling method. A Chinese version of the workplace violence scale was used to measure the incidence of workplace violence. The Short Form-36 Health Survey was employed to assess their QOL. Approximately 50% of the participants reported at least one type of workplace violence occurring in the previous 12 months. The multivariate analysis demonstrated workplace violence as a significant predictor for QOL among medical professionals, after controlling for other potential predictors. It suggests that the implementation of violence prevention policies and strategies to reduce workplace violence may improve QOL of medical professionals in China.

A study on workplace violence and its effect on quality of life among medical professionals in China.

The present study was to evaluate workplace violence and examine its effect on job burnout and turnover attempt among medical staff in China. A total of 2,020 medical employees were selected from Fujian province by using stratified cluster sampling method. The Chinese version of the Workplace Violence Scale and the Maslach Burnout Inventory-General Survey were used to measure the workplace violence and job burnout, respectively. Other potential influencing factors for job burnout and turnover attempt were collected using a structured questionnaire. The incidence of workplace violence among medical staff was 48.0%. Workplace violence had a positive correlation with emotional exhaustion and cynicism and a negative correlation with professional efficacy. Workplace violence, marital status, employment type, working time (≥ 10 h/day), performance recognition, and life satisfaction were significant predictors for turnover attempt among Chinese medical staff.

Huangyuan Li

Papers

Redox toxicology of environmental chemicals causing oxidative stress.

Transcription factor Nrf2 activation by deltamethrin in PC12 cells: Involvement of ROS.

Nrf2/HO-1 pathway activation by manganese is associated with reactive oxygen species and ubiquitin-proteasome pathway, not MAPKs signaling.

A study on workplace violence and its effect on quality of life among medical professionals in China.

Workplace violence and its effect on burnout and turnover attempt among Chinese medical staff