Arsenic is widely distributed in nature and all organisms possess regulatory mechanisms to evade toxicity and acquire tolerance. Yet, little is known about arsenic sensing and signaling mechanisms or about their impact on tolerance and detoxification systems. Here, we describe a novel role of the S. cerevisiae mitogen-activated protein kinase Hog1p in protecting cells during exposure to arsenite and the related metalloid antimonite. Cells impaired in Hog1p function are metalloid hypersensitive, whereas cells with elevated Hog1p activity display improved tolerance. Hog1p is phosphorylated in response to arsenite and this phosphorylation requires Ssk1p and Pbs2p. Arsenite-activated Hog1p remains primarily cytoplasmic and does not mediate a major transcriptional response. Instead, hog1⌬ sensitivity is accompanied by elevated cellular arsenic levels and we demonstrate that increased arsenite influx is dependent on the aquaglyceroporin Fps1p. Fps1p is phosphorylated on threonine 231 in vivo and this phosphorylation critically affects Fps1p activity. Moreover, Hog1p is shown to affect Fps1p phosphorylation. Our data are the first to demonstrate Hog1p activation by metalloids and provides a mechanism by which this kinase contributes to tolerance acquisition. Understanding how arsenite/antimonite uptake and toxicity is modulated may prove of value for their use in medical therapy.
Abstract. In this paper emission factors (EFs) for particulate matter (PM) and some sub-components as well as gaseous substances were investigated in two onboard measurement campaigns. Emissions from two 4-stroke main engines were measured under stable-load conditions. The impact of varying engine load on the emissions was investigated on one of the engines, and the impact of fuel quality on the other, where heavy fuel oil (HFO) with sulphur content 1% and 0.5% and marine gas oil (MGO) with sulphur content 0.1% were used. Furthermore, emissions from one auxiliary engine were studied. The measured EFs for PM mass were in the range of 0.3 to 2.7 g kg−1 fuel with the lowest values for emissions from the combustion of MGO, and the highest values for HFO with a sulphur content of 1%. The PM mass size distribution was dominated by particles in accumulation mode. Emission factors for particle numbers EF(PN) in the range of 5 × 1015–1 × 1017 # kg−1 fuel were found, the number concentration was dominated by particles in the ultrafine mode and ca. 2/3 of the particle number were non-volatile. The most abundant component of the PM mass was organic carbon, making up 25–60% of the PM. The measured EFs for organic carbon (OC) were 0.6 g kg−1 fuel for HFO and 0.2 g kg−1 fuel for MGO. Elemental carbon (EC) made up 10–38% of the PM mass, with no significant differences between HFO and MGO fuels. The concentrations of metals on sampled filters were investigated with energy dispersive X-ray fluorescence (EDXRF) and the detected metal elements in exhaust when using HFO was concluded to originate from both the fuel (V, Ni, Fe) and the lubricant (Ca, Zn), while for the case of MGO combustion, most of the metals were concluded to originate from the lubricants. The measured emission factors for sulphate particles, EF (SO2−4), were low, ca. 0.1–0.2 g kg−1 fuel for HFO with 1% sulphur, 0.07–0.09 g kg−1 fuel for HFO with 0.5% sulphur and 0.003–0.006 g kg−1 fuel for MGO. This corresponds to 0.1–0.8% and 0.1–0.6% of fuel S converted to PM sulphate for HFO and MGO, respectively. Scanning transmission electron microscopy (STEM) images of the collected PM showed three different types of particles: relatively pure soot; char and char-mineral particles; and amorphous, probably organic particles containing inorganic impurities. The maps of elements obtained from STEM showed a heterogeneous composition of primary soot particles with respect to the trace metals and sulphur. Temperature-programmed oxidation (TPO) of PM showed higher soot oxidation reactivity compared to automotive diesel soot, PM from the HFO exhaust being more reactive than PM from the MGO exhaust. Oxidative potential measured as the rate of consumption of Dithiothreitol (DTT) was for the first time measured on PM from ship exhaust. The obtained values were between 0.01 and 0.04 nmol DTT min−1 μg−1 PM, which is quite similar to oxidative potentials of PM collected at urban and traffic sites. The data obtained during the experiments add information about emission factors for both gaseous and PM-bound compounds from ship engines using different fuels and under different engine-load conditions. Observed variability of the EFs illustrates uncertainties of these emission factors as a result of influences from fuel and lubricant composition, from differences between individual engines and from the differences in sampling conditions.
BackgroundExposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles’ physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures.ResultsWSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved.ConclusionThe toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs.
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