Effects of Fluoride and/or Sulfur Dioxide on Morphology and DNA Integrity in Rats’ Hepatic Tissue

This study was aimed to evaluate the toxic effects of fluoride (F) and/or sulfur dioxide (SO₂) on morphology and DNA integrity in liver of male rats. For this, 96 Wistar rats (12-week-old) were randomly divided into four groups after 1-week adaptive breeding: the control group, treated with deionized water; the NaF group, administered high F (100 mg NaF/L in the drinking water); the SO₂ group, with sulfur dioxide in ambient air (15 ppm SO₂, 4 h/day); and NaF + SO₂ group, treated with high F and sulfur dioxide together for 8 consecutive weeks. The body weight, liver organ coefficient, morphology, and DNA damage in the liver of rats were examined. The results showed that the body weight and liver organ coefficient were not significantly changed; however, significant pathological changes of liver tissues were observed in the NaF + SO₂ group compared with the individual treated groups and control group. Furthermore, comet assay indicated that DNA damage in liver was significantly increased in the F and/or SO₂ treatment groups at 2, 4, 6, and 8 weeks, especially at 4 weeks. These results indicate that the liver morphology and DNA integrity of rats are adversely affected by F and/or SO₂ exposure.     

Curing raisins with sulfur dioxide suppresses population growth of Indian meal moth,Plodia interpunctella (Hubner) (Lepidoptera: Pyralidae)

A sulfur dioxide treatment is often used to preserve the color and flavor of raisins. We used a life table approach to examine the effects of residual sulfites on Plodia interpunctella (Hubner) when larvae fed on raisins under controlled laboratory conditions. Raisins were fumigated with 66 g/m³ or 133 g/m³ SO₂ for either three or six hours, or received no SO₂ exposure (control). A two sex life table was constructed for insects in each treatment (n = 70 per treatment). Total immature mortality exceeded 90% in 66 g/m³ SO₂ treatments, and 80% in 133 g/m³ SO₂ treatments, compared to 28.6% in controls. Sulfur dioxide treatments significantly extended developmental time relative to controls, again more so in the 66 g/m³ SO₂ treatments than in the 133 g/m³ treatments, but did not affect the adult longevity of survivors. All SO₂ treatments reduced the fecundity of surviving female moths to a small fraction of controls, without significant differences among them. These effects combined to result in significantly diminished life table parameters in all treatments relative to controls, although generation times were increased more in the 66 g/m³ SO₂ treatments than in the 133 g/m³ treatments. These inverse dosage-dependent effects may reflect increased feeding avoidance of sulfite residues in the higher dose treatments that resulted in reduced consumption. We conclude that residual sulfur and sulfites deposited on fruit surfaces during SO₂ treatment provide substantial control of P. interpunctella, and should effectively suppress the proliferation of moths within bulk stores of dried raisins.     

Sulfur accumulation in western wheatgrass exposed to three controlled SO2 concentrations

Summary Sulfur concentrations of western wheatgrass tillers and individual leaves were measured from plants exposed to four SO₂ concentrations (9, 52, 105 and 183 g·m^–3). Sulfur concentration of plants was a linear function of either time of exposure or concentration.Young leaves and the youngest portion of leaves contained less sulfur than their older counterparts irregardless of whether they had or had not been exposed to SO₂.Current hypotheses which relate plant sensitivity to amount of sulfur taken up do not apply for western wheatgrass.     

Photosynthesis,carbon allocation,and growth of sulfur dioxide ecotypes ofGeranium carolinianum L.

Summary This study investigated ways in which genetically determined differences in SO₂ susceptibility resulting from ecotypic differentiation inGeranium carolinianum were expressed physiologically. The SO₂-resistant and SO₂-sensitive ecotypes were exposed to a combination of short- and long-term SO₂ exposures to evaluate the responses of photosynthesis, H₂S efflux from foliage (sulfur detoxification), photoassimilate retention, leaf-diffusive resistance to CO₂, and growth. When exposed to SO₂, both ecotypes re-emit sulfur in a volatile, reduced form, presumably as H₂S. Because H₂S efflux rates at various SO₂ concentrations were comparable between ecotypes, genetic differences inG. carolinianum could not be attributed to a re-emission of excess sulfur as H₂S. Incipient SO₂ effects on photosynthesis were observed as cumulative SO₂ flux into the leaf interior excecded 0.40 nmol·m^–2 in the resistant ecotype and 0.26 nmol·m^–2 in the sensitive ecotype. Although initial SO₂-induced changes in photosynthesis in both ecotypes were mediated through an increase in stomatal resistance to CO₂, the ecotype-specific patterns as a function of pollutant concentration and exposure time were associated with marked increases in residual resistance to CO₂. Patterns in photosynthesis, photoassimilate retention, and growth following long-term SO₂ exposures were also ecotype-specific. Although physiological accommodation of SO₂ stress was observed in both ecotypes, it was more pronounced in the resistant ecotype. The physiological mechanisms underlying genetic differences inG. carolinianum in response to SO₂ stress were concluded to be (1) dissimilar threshold levels of response to SO₂ and/or its toxic derivatives and (2) differences in homeostatic processes governing the rate of repair or compensation for physiological injury.Research sponsored by the Office of Health and Environmental Research, U.S. Department of Energy, under contract No. DEAC05-840R21400 with Martin Marietta, Energy Systems, Inc. and the U.S. Environmental Protection AgencyPublication No. 2610, Environmental Sciences Division, Oak Ridge National Laboratory     

Simultaneous detection of SO2 and viscosity in drug-induced inflammation in live cells and zebrafish

The viscosity within cells is a crucial microenvironmental factor, and sulfur dioxide (SO₂) has essential functions in regulating cellular apoptosis and inflammation. Some evidence has been confirmed that changes in viscosity and overexposure of SO₂ within the cell may cause detrimental effects including, but not limited to, respiratory and cardiovascular illnesses, inflammation, fatty liver, and various types of cancer. Therefore, precise monitoring of SO₂ and viscosity in biological entities holds immense practical importance. Therefore, in this research, we developed a versatile fluorescent TCF-Cou that enables the dual detection of SO₂ and viscosity in the living system. Probe TCF-Cou possessed a response to viscosity and SO₂ through red and green emissions. The alteration of SO₂ and viscosity levels in live cells and zebrafish were also monitored using probe TCF-Cou. We hope that this fluorescent probe could be a potential tool for revealing the related pathological and physiological processes through monitoring the changes in SO₂ and viscosity.     

Effects of long-term open-air exposure to fluoride,nitrogen compounds and SO2 on visible symptoms,pollutant accumulation and ultrastructure of Scots pine and Norway spruce seedlings

 Effects of SO₂, aqueous fluoride (NaF) and a solution of nitrogen compounds (NH₄NO₃) on the visible symptoms, pollutant accumulation and ultrastructure of Scots pine (Pinus sylvestris L.) and Norway spruce [Picea abies (L.) Karst.] seedlings were studied in an open-air experiment lasting for 3 consecutive years. Visible injury symptoms were most pronounced in combination exposures and whenever F was applied. Visible symptoms correlated well with needle pollutant concentrations. Exposure to NaF increased needle F contents particularly when F was applied with SO₂ or NH₄NO₃. This suggests that a reduction in N or SO₂ emissions, in F polluted areas, could improve the condition of conifers via decreased accumulation of phytotoxic F in the needles. Norway spruce needles accumulated 2 – 10 times as much S and F as those of Scots pine. Microscopic observations showed various changes in the needle mesophyll cell ultrastructure. In both species, exposure to SO₂ increased significantly the amount of cytoplasmic vacuoles, suggesting detoxification of excess sulphate or low pH. F treatments resulted in a significant enlargement of plastoglobuli in Scots pine and a darkening of plastoglobuli in Norway spruce. All exposures enhanced the accumulation of lipid bodies. An increased portion of translucent plastoglobuli was most pronounced in N treatments. Many of the ultrastructural changes and visible symptoms appeared only as number of years exposed increased, indicating that long-term experiments are needed. Both visible symptoms and ultrastructural changes pointed to the more pronounced sensitivity of Norway spruce compared to Scots pine. Ultrastructural results mostly supported earlier qualitative observations of F, N and SO₂ effects on needle mesophyll cell ultrastructure. However, no reduction of thylakoids in SO₂ containing exposure or curling of thylakoids in F exposure could be detected in the present study. Received: 5 December 1994 / Accepted: 28 April 1995     

Age-related changes in antioxidant enzyme activities and lipid peroxidation in lungs of control and sulfur dioxide exposed rats

Antioxidant defenses within the lung are pivotal in preventing damage from oxidative toxicants. There have also been several reports with conflicting results on the antioxidant system during aging. In this study, we attempted to investigate age-related alterations in both antioxidant enzyme activities and thiobarbituric acid-reactive substances (TBARS), a product of lipid peroxidation, in the whole lung of control and sulfur dioxide (SO₂) exposed rats of different age groups (3-, 12-, and 24-months-old). Swiss-Albino Male rats were exposed to 10 ppm SO₂ 1 hr/day, 7 days/week for 6 weeks. The antioxidant enzymes examined include Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione S-transferase (GST). A mixed pattern of age-associated alterations in antioxidant activities was observed. SOD, GSH-Px and GST activities were increased with age, but CAT activity was decreased. Lung SOD, GSH-Px and GST activities were also increased in response to SO₂. The level of TBARS was increased with age. SO₂ exposure stimulated lipid peroxide formation in the lung as indicated by an increase in the level of TBARS. These findings suggest that both aging and SO₂ exposure may impose an oxidative stress to the body. We conclude that the increase in the activities of the antioxidant enzymes of the lung during aging, could be interpreted as a positive feedback mechanism in response to rising lipid peroxidation.     

The pH dependence of SO2 damage to lichens

Summary In order to determine the influence of the hydrogen-ion concentration on the damage exerted to lichens by sulfur dioxide gas, thalli of the species Hypogymnia physodes and Xanthoria parietina were submerged in buffer solutions of pH 2 to pH 8 and subsequently exposed to SO₂ gas. Net photosynthesis was employed as a criterion of vitality.The degree of damage to the lichens after exposure to 4 mg of SO₂/m³ air for 14 hrs is dependent on the pH of the buffer solutions. Hypogymnia physodes shows the least damage at pH 7, Xanthoria parietina at pH 5 to pH 7. The degree of damage increases with increasing acidity. After exposure to SO₂ gas at pH 3 no apparent photosynthesis is achieved.The different degrees of impairment are due to the fact that the concentration of the toxic products, resulting from the reaction of SO₂ and water, is dependent on the pH value.The mere shift of the pH into the strong acid range of pH 3 and pH 2 damages the lichens with Xanthoria parietina being more seriously damaged than Hypogymnia physodes. Basicity, however, is already harmful to the lichens under test in the low range of pH 8. Here Xanthoria parietina is less affected than Hypogymnia physodes.     

Effect of Sulphur Dioxide and Ascorbic Acid on the Plastid Ultrastructure of Azadirachta indica Leaves

Saplings of Azadirachta indica Juss. were exposed to sulphurdioxide (SO₂) and some of the exposed saplings were treatedwith ascorbic acid (AA). The SO₂ exposure alone inflicted heavydamage to the chloroplasts and cytoplasm in palisade cells.The degeneration of chloroplasts was followed by the rupturingof the outer envelope and the extrusion of plastoglobuli andstarch into the cytoplasm. AA treatment counteracted to a certainextent the toxic effects of SO₂ on the ultrastructure of chloroplasts. Azadirachta indica, Sulphur dioxide, ascorbic acid, chloroplast, mitigation     

The effects of sulfur dioxide and A2 influenza virus on pneumonia and weight reduction in mice: an analysis of stimulus-response relationships

Using a mouse-influenza model, mice were exposed in exposure chambers to various doses of influenza A₂ virus and sulfur dioxide, each alone and in combination. Temperature, relative humidity and length of exposure were all controlled. Control animals were in the same setting, but did not have influenza virus or sulfur dioxide exposure. The two responses measured were: the amount of pneumonia produced and the amount of weight reduction produced by the exposure stimuli. A stimulus-response method of analysis was utilized.Virus exposure produced pneumonia even at low dose. Sulfur dioxide produced pneumonia at higher doses, but appeared to have an inverse effect at lower doses when compared to control animals. The two combined produced more pneumonia than either one did separately. Sulfur dioxide produced more weight reduction than influenza virus, and combination exposures produced more weight reduction than either stimulus did separately. Dosage effects (correlations) were seen in both the production of pneumonia and the production of weight reduction. The stimulus-response method clarified and quantified the relationships found.     

Sulfur dioxide,a double-faced molecule in mammals

Sulfur dioxide (SO₂) is a common air pollutant and is detrimental to many organs. Its toxic effects including oxidative damage, deoxyribonucleic acid (DNA) damage and inflammation have been extensively studied. However, recent studies showed that SO₂ can be generated endogenously in mammals. In contrast to the toxic effects of SO₂, protective effects have also been found in mammals. Endogenous SO₂ has antioxidant, anti-inflammatory, anti-hypertension, and anti-atherogenic effects and regulates vascular tone and cardiac function in mammals. SO₂ may have a dual role in regulating physiological and pathophysiological effects in mammals. The biological effects of SO₂ in mammals are reviewed in this study.     

Enhanced bronchoconstriction responses to prostaglandin F2α following inhalation of sulfur dioxide

The effect of chronic sulfur dioxide (SO₂) inhalation was investigated in pharmacologic-induced bronchoconstruction in beagle dogs. Increase in pulmonary resistance (R_L) and decrease in dynamic lung compliance (C_DYN) were observed with i.v. and aerosol administration of prostaglandin F_2α (PGF_2α). After control historical data were accumulated, the animals received exposures of 500 ppm of SO₂ for two hours twice a week. After six months of chronic SO₂ exposure, a significant enhancement in the R_L response to i.v. and aerosolized PGF_2α was observed as compared to pre-SO₂ data. Tracheobronchial inflammation, as observed by fiberoptic bronchoscopy, occurred as a result of the chronic inhalation of SO₂; however, only a small increase in mucous production was observed visually. In additon, hypercapnic and acidotic changes in blood gas profiles were found. Therefore, beagle dogs chronically exposed to SO₂, developed hyperactive airways as seen by increased sensitivity to PGF_2α. This model appears to reflect many of those changes observed in clinical bronchial hyperreactivity and may provide an additional insight into obstructive disease.     

Lung epithelium injury biomarkers in workers exposed to sulphur dioxide in a non-ferrous smelter

Serum Clara cell protein (CC16) and surfactant-associated protein D (SP-D) were measured in 161 workers exposed to sulphur dioxide (SO₂) in a non-ferrous smelter. Seventy workers from a blanket manufacture served as referents. Exposure to SO₂ and tobacco smoking were associated with a decrease of CC16 and an increase of SP-D in serum. Tobacco smoking and exposure SO₂ interacted synergistically to decrease serum CC16 but not to increase serum SP-D. While further illustrating the potential of serum CC16 and SP-D, our study confirms that SO₂ can cause airways damage at exposure levels below current occupational exposure limits.     

Aphid response to elevated ozone and CO2

Numerous reports indicate that pollution stress caused by sulphur dioxide (SO₂), oxies of nitrogen or fluorides promote aphid growth on herbaceous and woody plants. At SO₂ exposures, the response curve of aphids is bell-shaped having the peak at 100 ppb. This curvilinear response is related to physiological stress responses of host plants exposed to pollutants. On the other hand, observations of aphid performance on ozone-exposed (O₃) or elevated carbon dioxide-exposed (CO₂) plants have given very variable results. Depending on the duration and concentration of O₃ or elevated CO₂ exposure or the age of the exposed plants, aphid growth on the same plants either decreased or increased in comparison to growth on control plants grown in filtered air. The results of these studies suggest that there is no general air pollution-induced plant stress that triggers aphid outbreaks on plants. Plants grown in elevated CO₂ usually have higher C/N ratios than plants grown in current ambient CO₂ atmosphere. A reduced proportion of nitrogen in the plant foliage decreases growth of chewing herbivorous insects, but the few studies of elevated CO₂ effects on sucking insects such as aphids have not yielded similar consistent effects. The present paper reviews recent studies of elevated CO₂ effects on aphids and discusses the effects of combined elevated O₃ and CO₂ exposures on aphid performance on woody plants using pine and birch aphids as examples.     

Effects of sulfur dioxide and ozone on intact leaves and isolated mesophyll cells of groundnut plants (Arachis hypogaea L.)

Difference between effects of sulfur dioxide (SO₂) and ozone (O₃) on groundnut plants (Arachis hypogaea L.) was studied by use of an exposure system of enzymatically-isolated mesophyll cells. SO₂ inhibited photosynthesis of intact groundnut leaves but induced no visible injury on leaves. SO₂ also inhibited photosynthesis of isolated mesophyll cells but did not kill the cells, suggesting that SO₂ inhibits photosynthesis by attacking rather specifically the photosynthetic apparatus in chloroplasts. O₃ inhibited photosynthesis of intact leaves and at the same time induced visible injury corresponding to the extent of photosynthesis inhibition. O₃ also inhibited photosynthesis of isolated mesophyll cells and killed the cells to the extent corresponding to photosynthesis inhibition, suggesting that O₃ inhibits photosynthesis not directly by attacking the photosynthetic apparatus but indirectly by killing cells. Since the response of intact leaves to each pollutant resembled that of isolated mesophyll cells, the difference between responses of intact leaves to both pollutants may considerably reflect that of mesophyll cells.     

Direct Observation of Reversible and Irreversible Stomatal Responses of Attached Sunflower Leaves to SO(2)

The effects of SO₂ on stomatal aperture of attached sunflower leaves were observed with a remote-control light microscope system that permitted continuous observation of stomatal responses over periods of several hours. The relationship between actual stomatal aperture and stomatal conductance, measured with a porometer, also was examined on leaves before and after exposure to SO₂.

A distinction between uninjured and injured regions was clearly visible on leaves after exposure to 1.5 microliters per liter SO₂ for less than an hour. During the exposure, the mean value of apertures for many stomata, which indicates stomatal conductance and transpiration rate, tended to decrease simultaneously in the uninjured and injured regions. However, the rate of decrease in the injured region was slower than that in the uninjured region because of a transient opening induced by water-soaking in the injured region. The transient opening was less common in stomata near veins and veinlets.

There was a good correlation between pore width and stomatal conductance measured with a porometer before exposure to SO₂. This correlation continued in leaves exposed to SO₂ until visible, irreversible injury occurred, but then it disappeared.

The results of these experiments indicate the necessity of continuous observation of individual stomata under the microscope to understand the effects of air pollutants such as SO₂ on stomatal behavior.

     

Estuarine sediment hydrocarbon-degrading microbial communities demonstrate resilience to nanosilver

Little is currently known about the potential impact of silver nanoparticles (AgNPs) on estuarine microbial communities. The Colne estuary, UK, is susceptible to oil pollution through boat traffic, and there is the potential for AgNP exposure via effluent discharged from a sewage treatment works located in close proximity. This study examined the effects of uncapped AgNPs (uAgNPs), capped AgNPs (cAgNPs) and dissolved Ag₂SO₄, on hydrocarbon-degrading microbial communities in estuarine sediments. The uAgNPs, cAgNPs and Ag₂SO₄ (up to 50 mg L⁻¹) had no significant impact on hydrocarbon biodegradation (80–92% hydrocarbons were biodegraded by day 7 in all samples). Although total and active cell counts in oil-amended sediments were unaffected by silver exposure; total cell counts in non-oiled sediments decreased from 1.66 to 0.84 × 10⁷ g⁻¹ dry weight sediment (dws) with 50 mg L⁻¹ cAgNPs and from 1.66 to 0.66 × 10⁷ g⁻¹ dws with 0.5 mg L⁻¹ Ag₂SO₄ by day 14. All silver-exposed sediments also underwent significant shifts in bacterial community structure, and one DGGE band corresponding to a member of Bacteroidetes was more prominent in non-oiled microcosms exposed to 50 mg L⁻¹ Ag₂SO₄ compared to non-silver controls. In conclusion, AgNPs do not appear to affect microbial hydrocarbon-degradation but do impact on bacterial community diversity, which may have potential implications for other important microbial-mediated processes in estuaries.     

Temporary disturbance of translocation of assimilates in douglas firs caused by low levels of ozone and sulfur dioxide

Douglas firs (Pseudotsuga menziesii [Mirb.] Franco) are suffering strongly from air pollution in western Europe. We studied the effect of low concentrations of ozone (200 micrograms per cubic meter during 3 days) and sulfur dioxide (53 micrograms per cubic meter during 28 days) on translocation of assimilates in 2 year old Douglas firs. The trees were exposed to the pollutants and afterward transferred to a growth chamber adapted to the use of ¹⁴CO₂. Root/soil respiration was measured daily. The results showed a significant decrease of the ¹⁴CO₂ root/soil respiration during the first 1 to 2 weeks after exposure to either ozone or sulfur dioxide. The ultimate level of ¹⁴CO₂ root/soil respiration did not differ significantly, which suggests a recovery of the exposed trees during the first weeks after exposure.     

Alterations of gene expression profiles induced by sulfur dioxide in rat lungs

Sulfur dioxide (SO₂) is a ubiquitous air pollutant, presents in low concentrations in urban air and in higher concentrations in working environment. Few data are available on the effects of being exposed to this pollutant on the molecular mechanism, although some biochemical changes in lipid metabolism, intermediary metabolism and oxidative stress have been detected. The present investigation aimed at analyzing the gene expression profiles of the lungs of Wistar rats short-term (20 ppm, 6 h/day, for seven days) and long-term (5 ppm, 1 h/day, for 30 days) exposed to SO₂ by Affymetrix GeneChip (RAE230A) analysis. It was found that 31 genes, containing 18 known genes and 13 novel genes, were up-regulated, and 31 genes, containing 20 known genes and 11 novel genes, were down-regulated in rats short-term exposed to SO₂ compared with control rats. While there were 176 genes, containing 82 known genes and 94 novel genes, were up-regulated, and 85 genes, containing 46 known genes and 39 novel genes, were down-regulated in rats long-term exposed to SO₂ compared with control rats. It is suggested that: (1) SO₂ exerts its effects by different mechanisms in vivo at high-dose short-term inhalation and at low-dose long-term inhalation; (2) a notable feature of the gene expression profile was the decreased expression of genes related to oxidative phosphorylation in lungs of rats short-term exposed to SO₂, which shows high-dose short-term exposed to SO₂ may cause the deterioration of mitochondrial functions; (3) discriminating genes in lungs of rats long-term exposed to SO₂ included those involved in fatty acid metabolism, immune, inflammatory, oxidative stress, oncogene, tumor suppresser and extracellular matrix. The mechanism of low-dose long-term exposed to SO₂ is more complex. __________ Translated from Journal of Shanxi University (Nat Sci Ed), 2006, 29(3): 225–236 [译自: 山西大学学报(自然科学版)]     

The role of reactive oxygen species in silicon dioxide nanoparticle-induced cytotoxicity and DNA damage in HaCaT cells

The increasing applications of silicon dioxide (SiO₂) nanomaterials have been widely concerned over their biological effects and potential hazard to human health. In this study, we explored the effects of SiO₂ nanoparticles (15, 30, and 100 nm) and their micro-sized counterpart on cultured human epidermal Keratinocyte (HaCaT) cells. Cell viability, cell morphology, reactive oxygen species (ROS), DNA damage (8-OHdG, γH2AX and comet assay) and apoptosis were assessed under control and SiO₂ nanoparticles exposed conditions. As observed in the Cell Counting Kit-8 (CCK-8) assay, exposure to 15, 30 or 100 nm SiO₂ nanoparticles at dosage levels between 0 and 100 μg/ml decreased cell viability in a concentration- and size dependent manner and the IC50 of 24 hour exposure was 19.4 ± 1.3, 27.7 ± 1.5 and 35.9 ± 1.6 μg/ml for 15, 30 and 100 nm SiO₂ nanoparticles, respectively. Morphological examination revealed cell shrinkage and cell wall missing after SiO₂ nanoparticle exposure. Increase in intracellular ROS level and DNA damage as well as apoptosis were also observed in SiO₂ nanoparticle-exposed HaCaT cells. Exposure to SiO₂ nanoparticles results in a concentration- and size-dependent cytotoxicity and DNA damage in cultural HaCaT cells which is closely correlated to increased oxidative stress.