Personal exposure to ultrafine particles from PVC welding and concrete work during tunnel rehabilitation

Objectives

To investigate the exposure to number concentration of ultrafine particles and the size distribution in the breathing zone of workers during rehabilitation of a subsea tunnel.

Methods

Personal exposure was measured using a TSI 3091 Fast Mobility Particle Sizer (FMPS), measuring the number concentration of submicrometre particles (including ultrafine particles) and the particle size distribution in the size range 5.6–560 nm. The measurements were performed in the breathing zone of the operators by the use of a conductive silicone tubing. Working tasks studied were operation of the slipforming machine, operations related to finishing the verge, and welding the PVC membrane. In addition, background levels were measured.

Results

Arithmetic mean values of ultrafine particles were in the range 6.26x10⁵–3.34x10⁶. Vertical PVC welding gave the highest exposure. Horizontal welding was the work task with the highest maximum peak exposure, 8.1x10⁷ particles/cm³. Background concentrations of 4.0x10⁴–3.1x10⁵ were found in the tunnel. The mobility diameter at peak particle concentration varied between 10.8 nm during horizontal PVC welding and during breaks and 60.4 nm while finishing the verge.

Conclusions

PVC welding in a vertical position resulted in very high exposure of the worker to ultrafine particles compared to other types of work tasks. In evaluations of worker exposure to ultrafine particles, it seems important to distinguish between personal samples taken in the breathing zone of the worker and more stationary work area measurements. There is a need for a portable particle-sizing instrument for measurements of ultrafine particles in working environments.

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Caveolin-1protects against hepatic ischemia/reperfusion injury through ameliorating peroxynitrite-mediated cell death

Publication date: Available online 25 March 2016
Source:Free Radical Biology and Medicine
Author(s): Lei Gao, Xingmiao Chen, Tao Peng, Dan Yang, Qi Wang, Zhiping Lv, Jiangang Shen
Nitrative stress is considered as an important pathological process of hepatic ischemia and reperfusion injury but its regulating mechanisms are largely unknown. In this study, we tested the hypothesis that caveolin-1 (Cav-1), a plasma membrane scaffolding protein, could be an important cellular signaling against hepatic I/R injury through inhibiting peroxynitrite (ONOO⁻)-induced cellular damage. Male wild-type miceand Cav-1 knockout (Cav-1^-/-) were subjected to 1hour hepatic ischemia following 1, 6 and 12hours of reperfusion by clipping and releasing portal vessels respectively. Immortalized human hepatocyte cell line (L02) was subjected to 1hour hypoxia and 6hour reoxygenation and treated with Cav-1 scaffolding domain peptide. The major discoveries included: (1) the expression of Cav-1 in serum and liver tissues of wild-type mice was time-dependently elevated during hepatic ischemia-reperfusion injury. (2) Cav-1 scaffolding domain peptide treatment inhibited cleaved caspase-3 expression in the hypoxia-reoxygenated L02 cells; (3) Cav-1 knockout (Cav-1^-/-) mice had significantly higher levels of serum transaminases (ALT&AST) and TNF-α, and higher rates of apoptotic cell death in liver tissues than wild-type mice after subjected to 1hour hepatic ischemia and 6hour reperfusion; (4) Cav-1^-/-mice revealed higher expression levels of iNOS, ONOO⁻and 3-nitrotyrosine (3-NT) in the liver than wild-type mice, and Fe-TMPyP, a representative peroxynitrite decomposition catalyst (PDC), remarkably reduced level of ONOO⁻and 3-NT and ameliorated the serum ALT, AST and TNF-α levels in both wild-typeand Cav-1^-/-mice. Taken together, we conclude that Cav-1 could play a critical role in preventing nitrative stress-induced liver damage during hepatic ischemia-reperfusion injury.

Graphical abstract

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Exercise training as a drug to treat age associated frailty

Publication date: Available online 25 March 2016
Source:Free Radical Biology and Medicine
Author(s): Jose Viña, Andrea Salvador-Pascual, Francisco Jose Tarazona-Santabalbina, Leocadio Rodriguez-Mañas, Mari Carmen Gomez-Cabrera
Exercise causes an increase in the production of free radicals [1]. As a result of a hormetic mechanism antioxidant enzymes are synthesized and the cells are protected against further oxidative stress. Thus, exercise can be considered as an antioxidant [2]. Age-associated frailty is a major medical and social concern as it can easily lead to dependency.In this review we describe that oxidative stress is associated with frailty and the mechanism by which exercise prevents age-associated frailty. We propose that individually tailored multicomponent exercise programmes are one of the best ways to prevent and to treat age-associated frailty.



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Synthesis, Evaluation, and Metabolism of Novel [6]-Shogaol Derivatives as Potent Nrf2 Activators

Publication date: Available online 25 March 2016
Source:Free Radical Biology and Medicine
Author(s): Yingdong Zhu, Pei Wang, Yantao Zhao, Chun Yang, Anderson Clark, TinChung Leung, Xiaoxin Chen, Shengmin Sang
Oxidative stress is a central component of many chronic diseases. The Kelch-like ECH-associated protein 1 (Keap1)-nuclear factor erythroid 2 p45-related factor 2 (Nrf2) system is a major regulatory pathway of cytoprotective genes against oxidative and electrophilic stress. Activation of the Nrf2 pathway plays crucial roles in the chemopreventive effects of various inducers. In this study, we developed a novel class of potent Nrf2 activators derived from ginger compound, [6]-shogaol (6S), using the Tg[glutathione S-transferase pi 1 (gstp1):green fluorescent protein (GFP)] transgenic zebrafish model. Investigation of structure-activity relationships of 6S derivatives indicates that the combination of an α,β-unsaturated carbonyl entity and a catechol moiety in one compound enhances the Tg(gstp1:GFP) fluorescence signal in zebrafish embryos. Chemical reaction and in vivo metabolism studies of the four most potent 6S derivatives showed that both α,β-unsaturated carbonyl entity and catechol moiety act as major active groups for conjugation with the sulfhydryl groups of the cysteine residues. In addition, we further demonstrated that 6S derivatives increased the expression of Nrf2 downstream target, heme oxygenase-1, in both a dose- and time-dependent manner. These results suggest that α,β-unsaturated carbonyl entity and catechol moiety of 6S derivatives may react with the cysteine residues of Keap1, disrupting the Keap1-Nrf2 complex, thereby liberating and activating Nrf2. Our findings of natural product-derived Nrf2 activators lead to design options of potent Nrf2 activators for further optimization.

Graphical abstract

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A SIRT3/AMPK/autophagy network orchestrates the protective effects of trans-resveratrol in stressed peritoneal macrophages and RAW 264.7 macrophages

Publication date: Available online 25 March 2016
Source:Free Radical Biology and Medicine
Author(s): Wen-Jun Duan, Yi-Fang Li, Fang-Lan Liu, Jie Deng, Yan-Ping Wu, Wei-Lin Yuan, Bun Tsoi, Jun-Li Chen, Qi Wang, Shao-Hui Cai, Hiroshi Kurihara, Rong-Rong He
Resveratrol gains a great interest for its strong antioxidant properties, while the molecular mechanisms underlie the beneficial effects on psychosocial stress remain controversial. In this study, we demonstrated that resveratrol protected peritoneal macrophages and RAW 264.7 cells from stress-induced decrease in the total cell count, phagocytic capability, reactive oxygen species generation, monodansylcadaverine and mitochondrial membrane potential in stressed mice. Resveratrol promoted stress-induced autophagy in both models. Modulation of autophagy by rapamycin or 3-methyladenine regulated the protective effect of resveratrol, suggesting a role of autophagy in the protective mechanisms of resveratrol. The comparison studies revealed that distinct mechanisms were implicated in the protective effect of resveratrol and other antioxidants (vitamin C and edaravone). Resveratrol promoted autophagy via upregulating SIRT3 expression and phosphorylation of AMP-activated protein kinase (AMPK). Knockdown of SIRT3 resulted in decreased autophagy and abolished protective effect of resveratrol. SIRT1 was also involved in the protective mechanism of resveratrol, although its effect on autophagy was unnoticeable. Pharmacological manipulation of autophagy modulated the effects of resveratrol on SIRT3 and AMPK, revealing the engagement of a positive feedback loop. In sharp contrast, vitamin C and edaravone effectively protected macrophages from stress-induced cytotoxicity, accompanied by downregulated SIRT3 expression and AMPK phosphorylation, and decreased level of autophagy response. Taken together, we conclude that a SIRT3/AMPK/autophagy network orchestrates in the protective effect of resveratrol in macrophages.

Graphical abstract

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Bayesian Integration and Classification of Composition C-4 Plastic Explosives Based on Time-of-Flight-Secondary Ion Mass Spectrometry and Laser Ablation-Inductively Coupled Plasma Mass Spectrometry

Analytical Chemistry

DOI: 10.1021/acs.analchem.5b04151

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An analysis of baseline data from the PROUD study: an open-label randomised trial of pre-exposure prophylaxis

Pre-exposure prophylaxis (PrEP) has proven biological efficacy to reduce the sexual acquisition of the human immunodeficiency virus (HIV). The PROUD study found that PrEP conferred higher protection than in pl...

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