scholarly journals Temporary Disturbance of Translocation of Assimilates in Douglas Firs Caused by Low Levels of Ozone and Sulfur Dioxide

1988 ◽  
Vol 88 (3) ◽  
pp. 559-563 ◽  
Author(s):  
Antonie Gorissen ◽  
Johannes A. van Veen
2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Huilan Yi ◽  
Xin Liu ◽  
Min Yi ◽  
Gang Chen

Sulfur dioxide (SO2) is a major air pollutant and has significant impacts on plant physiology. Plant can adapt to SO2 stress by controlling stomatal movement, gene expression, and metabolic changes. Here we show clear evidences that SO2-triggered hydrogen peroxide (H2O2) production mediated stomatal closure and cell death in Arabidopsis leaves. High levels of SO2 caused irreversible stomatal closure and decline in guard cell viability, but low levels of SO2 caused reversible stomatal closure. Exogenous antioxidants ascorbic acid (AsA) and catalase (CAT) or Ca2+ antagonists EGTA and LaCl3 blocked SO2-induced stomatal closure and decline in viability. AsA and CAT also blocked SO2-induced H2O2 and [Ca2+]cyt elevation. However, EGTA and LaCl3 inhibited SO2-induced [Ca2+]cyt increase but did not suppress SO2-induced H2O2 elevation. These results indicate that H2O2 elevation triggered stomatal closure and cell death via [Ca2+]cyt signaling in SO2-stimulated Arabidopsis guard cells. NADPH oxidase inhibitor DPI blocked SO2-induced cell death but not the stomatal closure triggered by low levels of SO2, indicating that NADPH oxidase-dependent H2O2 production plays critical role in SO2 toxicity but is not necessary for SO2-induced stomatal closure. Our results suggest that H2O2 production and accumulation in SO2-stimulated plants trigger plant adaptation and toxicity via reactive oxygen species mediating Ca2+ signaling.


2001 ◽  
Vol 86 (1) ◽  
pp. 62-67 ◽  
Author(s):  
Jae-Kyoung Park ◽  
Yoon-Keun Kim ◽  
Sang-Rok Lee ◽  
Sang-Heon Cho ◽  
Kyung-Up Min ◽  
...  

2014 ◽  
Vol 132 (6) ◽  
pp. 353-358 ◽  
Author(s):  
Camila Trolez Amancio ◽  
Luiz Fernando Nascimento

CONTEXT AND OBJECTIVE: Little has been discussed about the increased risk of stroke after exposure to air pollutants, particularly in Brazil. The mechanisms through which air pollution can influence occurrences of vascular events such as stroke are still poorly understood. The aim of this study was to estimate the association between exposure to some air pollutants and risk of death due to stroke.DESIGN AND SETTING: Ecological time series study with data from São José dos Campos, Brazil.METHODS: Data on deaths due to stroke among individuals of all ages living in São José dos Campos and on particulate matter, sulfur dioxide and ozone were used. Statistical analysis was performed using a generalized additive model of Poisson regression with the Statistica software, in unipollutant and multipollutant models. The percentage increase in the risk of increased interquartile difference was calculated.RESULTS: There were 1,032 deaths due to stroke, ranging from 0 to 5 per day. The statistical significance of the exposure to particulate matter was ascertained in the unipollutant model and the importance of particulate matter and sulfur dioxide, in the multipollutant model. The increases in risk were 10% and 7%, for particulate matter and sulfur dioxide, respectively.CONCLUSION: It was possible to identify exposure to air pollutants as a risk factor for death due to stroke, even in a city with low levels of air pollution.


1976 ◽  
Vol 59 (6) ◽  
pp. 1404-1408
Author(s):  
Wilson L Brannon ◽  
Walter R Benson ◽  
George Schwartzman

Abstract The feasibility of examining medicinal gases for trace impurities, using an infrared spectrophotometer in conjunction with a 10 m gas cell, was investigated. Many of the impurities for which the USP includes limits were detected and measured at concentrations at or below those permitted by the USP; these include sulfur dioxide, carbon dioxide, carbon monoxide, and water. However, others (hydrogen sulfide, nitric oxide, and nitrogen dioxide) were not detected at these levels by this technique. Methane was found at low levels in some samples.


2021 ◽  
Vol 9 (12) ◽  
pp. 2528
Author(s):  
Patrícia Branco ◽  
Rute Coutinho ◽  
Manuel Malfeito-Ferreira ◽  
Catarina Prista ◽  
Helena Albergaria

The yeast Brettanomyces bruxellensis is one of the most dangerous wine contaminants due to the production of phenolic off-flavors such as 4-ethylphenol. This microbial hazard is regularly tackled by addition of sulfur dioxide (SO2). Nevertheless, B. bruxellensis is frequently found at low levels (ca 103 cells/mL) in finished wines. Besides, consumers health concerns regarding the use of sulfur dioxide encouraged the search for alternative biocontrol measures. Recently, we found that Saccharomyces cerevisiae secretes a natural biocide (saccharomycin) that inhibits the growth of different B. bruxellensis strains during alcoholic fermentation. Here we investigated the ability of S. cerevisiae CCMI 885 to prevent B. bruxellensis ISA 2211 growth and 4-ethylphenol production in synthetic and true grape must fermentations. Results showed that B. bruxellensis growth and 4-ethylphenol production was significantly inhibited in both media, although the effect was more pronounced in synthetic grape must. The natural biocide was added to a simulated wine inoculated with 5 × 102 cells/mL of B. bruxellensis, which led to loss of culturability and viability (100% dead cells at day-12). The conjugated effect of saccharomycin with SO2 was evaluated in simulated wines at 10, 12, 13 and 14% (v/v) ethanol. Results showed that B. bruxellensis proliferation in wines at 13 and 14% (v/v) ethanol was completely prevented by addition of 1.0 mg/mL of saccharomycin with 25 mg/L of SO2, thus allowing to significantly reduce the SO2 levels commonly used in wines (150–200 mg/L).


2008 ◽  
Vol 41 (18) ◽  
pp. 16
Author(s):  
DIANA MAHONEY
Keyword(s):  

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