Arsenic interferes with spermatogenesis involving Rictor/mTORC2-mediated blood-testis barrier disruption in mice.

Ingestion of arsenic interferes with spermatogenesis and increases the risk of male infertility, but the underlying mechanism remines unclear. In this study, we investigated spermatogenic injury with a focus on blood-testis barrier (BTB) disruption by administrating 5 mg/L and 15 mg/L arsenic orally to adult male mice for 60 d. Our results showed that arsenic exposure reduced sperm quality, altered testicular architecture, and impaired Sertoli cell junctions at the BTB. Analysis of BTB junctional proteins revealed that arsenic intake downregulated Claudin-11 expression and increased protein levels of ß-catenin, N-cadherin, and Connexin-43. Aberrant localization of these membrane proteins was also observed in arsenic-treated mice. Meanwhile, arsenic exposure altered the components of Rictor/mTORC2 pathway in mouse testis, including inhibition of Rictor expression, reduced phosphorylation of protein kinase Cα (PKCα) and protein kinase B (PKB), and elevated matrix metalloproteinase-9 (MMP-9) levels. Furthermore, arsenic also induced testicular lipid peroxidative damage, inhibited antioxidant enzyme (T-SOD) activity, and caused glutathione (GSH) depletion. Our findings suggest that disruption of BTB integrity is one of the main factors responsible for the decline in sperm quality caused by arsenic. PKCα-mediated rearrangement of actin filaments and PKB/MMP-9-increased barrier permeability jointly contribute to arsenic-induced BTB disruption.

Arsenic intake-induced gastric toxicity is blocked by grape skin extract by modulating inflammation and oxidative stress in a mouse model.

Arsenic (As) is known to induce toxic responses in many organs of human beings and animals. However, research concerning toxicity in the stomach is limited. In this study, arsenic-induced gastric toxicity was investigated in a mouse model, and grape skin extract (GSE) was confirmed to have protective effects against arsenic toxicity. Our experimental results showed that exposure to 10 mg/l arsenic via drinking water for 56 days caused oxidative damage and inflammatory responses. The H2O2 and malondialdehyde (MDA) contents were significantly increased, accompanied by significant decreases in total superoxide dismutase (T-SOD) activity and glutathione (GSH) content in the gastric tissue of arsenic-treated mice. Two inflammatory signalling pathways, i.e., TLR2/MyD88/NF-κB and IL-6/STAT-3, were activated, along with inflammatory cell infiltration and the elevated mRNA expression of pro-inflammatory cytokines (TNF-α, IL-1ß and IFN-γ) and myeloperoxidase (MPO) in the gastric tissue of mice exposed to arsenic. Meanwhile, the mRNA levels of the ZO-1, ZO-2 and occludin genes, which encode the key components of tight junction (TJ) complexes, were downregulated. However, the application of GSE (300 mg/kg bw) significantly inhibited the arsenic-induced increases in H2O2 and MDA contents and the decreases in T-SOD activity and GSH content. The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-α, IL-1ß and IFN-γ), MPO and IL-6/STAT3 and TLR2/MyD88/NF-κB pathways was found down-regulated. Moreover, the arsenic-induced inflammatory cell infiltration and inhibition of TJ genes transcription were markedly attenuated in the As+GSE (300 mg/kg bw) group. Based on the present findings, arsenic intake appears to cause gastric toxicity via oxidative stress and inflammation, and the application of GSE offers significant protection against arsenic toxicity in a mouse model by attenuating the oxidative stress and inflammatory response. Our results suggest that GSE by oral administration might function as a candidate therapeutic supplement to antagonize arsenic toxicity.

Enhancement of drought tolerance in Arabidopsis plants induced by sulfur dioxide.

Sulfur dioxide (SO2) is a common air pollutant that has multiple effects on plants. In the present study, the improvement of drought tolerance in Arabidopsis plants by SO2 fumigation was investigated. The results showed that pre-exposure to 30 mg/m3 SO2 for 72 h could reduce water loss, stomatal conductance (Gs) and the transpiration rate (Tr) but increased the net photosynthetic rate (Pn), water use efficiency (iWUE) and photosynthetic pigment contents under drought conditions. The activities of superoxide dismutase (SOD) and peroxidase (POD) were significantly increased, while the contents of hydrogen peroxide (H2O2) and malondialdehyde (MDA) were decreased in SO2-pretreated Arabidopsis plants under drought stress. Additionally, the activity of o-acetylserine(thio)lyase (OASTL) and the content of cysteine (Cys), the rate-limiting enzyme and the first organic product of sulfur assimilation, were significantly increased in drought-stressed plants after SO2 pretreatment, along with increases in other thiol-containing compounds, such as glutathione (GSH) and nonprotein thiol (NPT). Meanwhile, SO2 pre-exposure induced a higher level of proline accumulation, with increased activity of proline synthase P5CS and decreased activity of proline dehydrogenase ProDH. Consistent with the changes in enzyme activity, their corresponding gene expression patterns were different after SO2 treatment. Overall, the enhanced drought tolerance afforded by SO2 might be related to the improvement of plant photosynthesis, antioxidant defense, sulfur assimilation and osmotic adjustment. These findings provide new insights into the role of SO2 in plant adaptation to environmental stress.

Sulfur dioxide enhance drought tolerance of wheat seedlings through H2S signaling.

Drought is one of the most common factors that limit plant growth and productivity. Sulfur dioxide (SO2) has recently been found to play a benefical role in protection of plants against environmental stress. In this study, we investigated the effect of SO2 on the physiological and molecular response of wheat seedlings to drought stress. Pretreatment with 10 mg/m3 SO2 significantly increased the survival rate and relative water content (RWC) of wheat seedlings under drought stress, indicating that pre-exposure to appropriate level of SO2 could enhance drought tolerance of plants. These responses were related to the enhanced proline accumulation in the drought-treated wheat seedlings that induced by SO2 pretreatment. Meanwhile, SO2 pretreatment increased the activities of superoxide dismutase (SOD) and peroxidase (POD), and effectively reduced the content of hydrogen peroxide (H2O2) and malondialdehyde (MDA) in drought-treated wheat seedlings, suggesting SO2 could alleviate drought-induced oxidative damage by enhancing antioxidant defense system in plants. Expression analysis of transcription factor genes also showed that SO2 pretreatment decreased the expression of TaNAC69, but the expression of TaERF1 and TaMYB30 changed slightly and maintained at higher levels in wheat seedlings in response to drought stress. Furthermore, SO2 pretreatment triggered marked accumulation of hydrogen sulfide (H2S) in wheat seedlings under drought stress. When scavenged H2S by spraying Hypotaurine (HT), the activities of antioxidant enzymes and the expression of transcription factor genes were decreased, and the content of H2O2 and MDA increased to the level of drought treatment alone, suggesting a regulatory role of SO2-induced H2S in plant adaptation to drought stress. Together, this study indicated that SO2 enhanced drought tolerance of wheat seedlings through H2S signaling, and provided new strategy for enhancing plant tolerance to drought stress.

Sulfur dioxide-induced exacerbation of airway inflammation via reactive oxygen species production and the toll-like receptor 4/nuclear factor-κB pathway in asthmatic mice.

Sulfur dioxide (SO2) is a common air pollutant that can exacerbate asthmatic airway inflammation. The mechanisms underlying these effects are not yet fully understood. In this study, we investigated the effects of SO2 exposure (10 mg/m3) on asthmatic airway inflammation in ovalbumin-induced asthmatic mice. Our results showed that SO2 exposure alone induced slight airway injury, decreased superoxide dismutase activity, and increased nuclear factor-κB (NF-κB) expression in the lungs of mice. Moreover, SO2 exposure in asthmatic mice induced marked pathological damage, significantly increased the counts of inflammatory cells (e.g., macrophages, lymphocytes, and eosinophils) in bronchoalveolar lavage fluid, and significantly enhanced malondialdehyde and glutathione levels in the lungs. Moreover, the expression of toll-like receptor 4 (TLR4), NF-κB, pro-inflammatory cytokines (e.g., tumor necrosis factor α and interleukin-6), and type II T-helper cell (Th2) cytokines was found to be elevated in the mice exposed to SO2 and ovalbumin compared to those exposed to ovalbumin alone. These results suggest that SO2 amplifies Th2-mediated inflammatory responses, which involve reactive oxygen species and TLR4/NF-κB pathway activation; these can further enhance Th2 cytokine expression and eosinophilic inflammation. Thus, our findings provide important evidence to understand a potential mechanism through which SO2 may exacerbate airway asthmatic inflammation.

Photosynthetic responses of Arabidopsis to SO2 were related to photosynthetic pigments, photosynthesis gene expression and redox regulation.

Sulfur dioxide (SO2) is one of the most common and harmful air pollutants. High concentrations of SO2 can induce a series of defensive responses in Arabidopsis plants. However, the role of photosynthesis in the plant response to SO2 stress is not clear. Here, we report the photosynthetic responses of Arabidopsis plants to SO2 stress. Exposure to 30 mg/m3 SO2 decreased stomatal conductance (Gs) and transpiration rate (Tr) but increased photosynthetic pigments and net photosynthetic rate (Pn). The contents of carbohydrates and sucrose were not altered. The transcript levels of most genes related to photosystem II (PSII), cytochrome b6/f (Cytb6f), photosystem I (PSI) and carbon fixation were upregulated, revealing one important regulatory circuit for the maintenance of chloroplast homeostasis under SO2 stress. Exposure to SO2 triggered reactive oxygen species (ROS) generation, accompanied by increases in superoxide dismutase (SOD) activity and the contents of cysteine (Cys), glutathione (GSH) and non-protein thiol (NPT), which maintained cellular redox homeostasis. Together, our results indicated that chloroplast photosynthesis was involved in the plant response to SO2 stress. The photosynthetic responses were related to photosynthetic pigments, photosynthesis gene expression and redox regulation.

Enhanced drought tolerance of foxtail millet seedlings by sulfur dioxide fumigation.

Recently, sulfur dioxide (SO2) has been considered to be a beneficial bio-regulator in animals. However, the positive roles of SO2 in plant adaptation to drought stress are still unclear. In this study, we investigated the physiological and molecular changes that are induced by SO2 fumigation to improve the drought tolerance of foxtail millet seedlings. The relative water content in the leaves of drought-stressed seedlings was significantly improved by pre-exposure to 30 mg/m3 SO2. These responses might be related to decreased stomatal apertures and a reduced leaf transpiration rate, which were induced by SO2 under drought conditions. In addition, the SO2 pretreatment markedly enhanced proline accumulation in the leaves of drought-stressed seedlings, which was supported by increased Δ1-pyrroline-5-carboxylate synthetase (P5CS) activity, decreased proline dehydrogenase (ProDH) activity, and the corresponding transcripts. Moreover, the SO2 application upregulated the enzyme activity of catalase (CAT) and peroxidase (POD) in the leaves of drought-stressed plants, as well as their transcripts, which contributed to the scavenging of hydrogen peroxide (H2O2) and alleviated drought-induced oxidative damage, as indicated by the decreased malondialdehyde (MDA) level in SO2-pretreated plants. Together, these results indicate that the application of SO2 might enhance drought tolerance by reducing stomatal apertures, increasing proline accumulation, and promoting antioxidant defence in foxtail millet seedlings. This study presents new insight into the beneficial roles of SO2 in plant responses to drought stress.

SO2 derivatives and As co-exposure promote liver cancer metastasis through integrin αvß3 activation.

Arsenic (As) and sulfur dioxide (SO2) are two environmental pollutants that have been shown to promote the development of human cancer. In recent years, due to increased pollution, humans are often exposed to SO2, in addition to As. Despite the development and implementation of standards for environment and air quality, cases of disease caused by As or SO2 continue to rise alarmingly. It is currently unknown whether simultaneous exposure to As and SO2 results in increased cancer promoting activity. In this study, concentrations of As and SO2 below the limits established by the world health organization (WHO) in force environmental standards (concentrations of As should be lower than 1×10-2 mg/L and SO2 should be lower than 50 µg/m3), were employed to investigate possible, long-term, synergistic effects of As and SO2, by using cell-based assays. We found that co-exposure to these pollutants significantly promotes HepG2 cancer cell migration, while As or SO2 alone have no remarkable effects. Integrins αvß3 play a key role in this process, as cilengitide, an integrin αvß3 inhibitor, substantially prevented As and SO2-induced cell migration. MMPs, IL-8, and TGF-ß were also involved in the induced cell migration. In summary, combined exposure to As and SO2 promotes integrin-dependent cell migration and may be of relevance for the activation of mechanisms underlying liver cancer progression.

Aggravated gut inflammation in mice lacking the taste signaling protein α-gustducin.

Inflammatory bowel disease (IBD) is a debilitating immune-related condition that affects over 1.4 million Americans. Recent studies indicate that taste receptor signaling is involved in much more than sensing food flavor, and taste receptors have been localized in a variety of extra-oral tissues. One of the newly revealed functions of taste receptors and downstream signaling proteins is modulation of immune responses to microbes and parasites. We previously found that components of the taste receptor signaling pathway are expressed in subsets of the intestinal epithelial cells. α-Gustducin, a key G-protein α subunit involved in sweet, umami, and bitter taste receptor signaling, is expressed in the intestinal mucosa. In this study, we investigated the role of α-gustducin in regulation of gut mucosal immunity and inflammation using α-gustducin knockout mice in the dextran sulfate sodium (DSS)-induced IBD model. DSS is a chemical colitogen that can cause intestinal epithelial damage and inflammation. We analyzed DSS-induced colitis in α-gustducin knockout versus wild-type control mice after administration of DSS in drinking water. Our results show that the knockout mice had aggravated weight loss, diarrhea, intestinal bleeding, and inflammation over the experimental period compared to wild-type mice, concurrent with augmented immune cell infiltration and increased expression of TNF and IFN-γ but decreased expression of IL-13 and IL-5 in the colon. These results suggest that the taste receptor signaling pathway may play critical roles in regulating gut immune balance and inflammation.

Enhanced Arabidopsis disease resistance against Botrytis cinerea induced by sulfur dioxide.

Sulfur dioxide (SO2) is a common air pollutant that has complex impacts on plants. The effect of prior exposure to 30mgm-3 SO2 on defence against Botrytis cinerea (B. cinerea) in Arabidopsis thaliana and the possible mechanisms of action were investigated. The results indicated that pre-exposure to 30mgm-3 SO2 resulted in significantly enhanced resistance to B. cinerea infection. SO2 pre-treatment significantly enhanced the activities of defence-related enzymes including phenylalanine ammonia-lyase (PAL), polyphenol oxidase (PPO), ß-1,3-glucanase (BGL) and chitinase (CHI). Transcripts of the defence-related genes PAL, PPO, PR2, and PR3, encoding PAL, PPO, BGL and CHI, respectively, were markedly elevated in Arabidopsis plants pre-exposed to SO2 and subsequently inoculated with B. cinerea (SO2+ treatment group) compared with those that were only treated with SO2 (SO2) or inoculated with B. cinerea (CK+). Moreover, SO2 pre-exposure also led to significant increases in the expression levels of MIR393, MIR160 and MIR167 in Arabidopsis. Meanwhile, the expression of known targets involved in the auxin signalling pathway, was negatively correlated with their corresponding miRNAs. Additionally, the transcript levels of the primary auxin-response genes GH3-like, BDL/IAA12, and AXR3/IAA17 were markedly repressed. Our findings indicate that 30mgm-3 SO2 pre-exposure enhances disease resistance against B. cinerea in Arabidopsis by priming defence responses through enhancement of defence-related gene expression and enzyme activity, and miRNA-mediated suppression of the auxin signalling pathway.

Sulphur dioxide and arsenic affect male reproduction via interfering with spermatogenesis in mice.

As two potential environmental hazards, sulphur dioxide (SO2) and arsenic have adverse effects on male reproduction, but the mechanism of which and their combined toxicity are not clear. In this study, we investigate male reproductive toxicity with a focus on spermatogenesis by treating mice with 5 mg/m3 SO2 and/or 5 mg/L arsenic. Our results showed that arsenic exposure caused significant decreases in water and food consumption and body weight in mice, whereas these changes were not observed in the SO2-only group. Both SO2 and arsenic reduced sperm counts, increased the percentage of sperm malformation, and induced abnormal testicular pathological changes. Elevated H2O2 and MDA contents, declined T-SOD activity, decreased spermatogenic cell counts, enhanced caspase-3 activity, and increased TUNEL-positive cells were also observed in mice exposed to SO2 and/or arsenic. Moreover, SO2 and arsenic co-exposure changed the mRNA levels of Bax and Bcl-2, decreased serum testosterone levels, and downregulated the expression of steroidogenic-related genes (LHR, StAR, and ABP) in mice. These findings provide a new theoretical basis for understanding how SO2 and arsenic interfere with spermatogenesis leading to infertility. These results also suggest that SO2 and arsenic co-exposure likely result in an additive effect on male reproductive toxicity in mice.

Sulfur dioxide derivatives alleviate cadmium toxicity by enhancing antioxidant defence and reducing Cd2+ uptake and translocation in foxtail millet seedlings.

Sulfur dioxide (SO2) was recently proposed as a novel bio-regulator in mammals. However, the possible advantageous effects of SO2 in plant adaptation to heavy metal-contaminated environments are largely unknown. In the present study, using Na2SO3/NaHSO3 derivatives as SO2 donors, we investigated the possible roles and regulation mechanisms of SO2 in alleviating Cd2+ toxicity in foxtail millet seedlings. Exogenous SO2 derivatives (0.5 mM) application significantly reduced the seedling growth inhibition caused by Cd2+ stress. Cd2+-induced oxidative damage was also alleviated by SO2 derivatives, which was supported by the decreased malondialdehyde (MDA) level in the leaves of seedlings pretreated with SO2 derivatives. These responses were related to the enhanced activities of representative antioxidant enzymes, including catalase and superoxide dismutase, as well as the up-regulation of ascorbate-glutathione cycle, which contributed to the scavenging of Cd2+-elicited O2•－ and H2O2 within the leaves of foxtail millet seedlings. Also, SO2 derivative application promoted sulfur assimilation and increased the content of glutathione and phytochelatins, which may help to enhance Cd2+ detoxification capacity in foxtail millet seedlings. Moreover, application of SO2 derivatives caused down-regulation of the transcript expression levels of several genes involved in Cd2+ uptake and translocation, such as NRAMP1, NRAMP6, IRT1, IRT2, HMA2, and HMA4, thus resulting in reduced Cd2+ accumulation in the shoots and roots of Cd2+-stressed seedlings. Collectively, these results suggest that exogenous SO2 derivative application can alleviate oxidative damage and restrict Cd2+ buildup, thereby reducing Cd2+-induced growth inhibition in foxtail millet seedlings upon Cd2+ exposure. This novel finding indicates that the usage of SO2 derivatives may be an effective approach for enhancing Cd2+ tolerance in foxtail millet and other crops.

Reactive oxygen species and Ca2+ are involved in cadmium-induced cell killing in yeast cells.

Cadmium (Cd) is one of the most toxic heavy metals. It is of great environmental concern and its toxicity has been investigated in a variety of cells. In this study, we elucidated the toxic effects of Cd in cells of yeast (Saccharomyces cerevisiae). Our results showed that Cd2+ (0.05-5.0 mmol·L-1) significantly inhibited yeast cell growth, and the inhibitory effect was positively correlated with Cd2+ concentrations. Cd2+ caused loss of yeast cell viability in a concentration- and duration-dependent manner. Intracellular reactive oxygen species (ROS) and Ca2+ levels increased in yeast cells after exposure to 5.0 mmol·L-1 Cd for 6 h. Cd2+-caused cell viability loss was blocked by antioxidants (0.5 mmol·L-1 ascorbic acid or 500 U·mL-1 catalase) or Ca2+ antagonists (0.5 mmol·L-1 ethylene glycol tetraacetic acid or 0.5 mmol·L-1 LaCl3). Moreover, a collapse of mitochondrial membrane potential (ΔΨm) was observed in Cd2+-treated yeast cells. These results indicate that Cd-induced yeast cell killing was associated with the elevation of intracellular ROS and Ca2+ levels and also the loss of ΔΨm.

miR398 and miR395 are involved in response to SO2 stress in Arabidopsis thaliana.

Sulfur dioxide (SO2) is a common air pollutant that has adverse effects on plants. MicroRNAs (miRNAs) are small noncoding RNA that play critical roles in plant development and stress response. In this study, we found that two miRNAs, miR398 and miR395, were differentially expressed in Arabidopsis shoots under SO2 stress. The expression of miR398 was down-regulated, and the transcript levels of its target genes, Cu/Zn superoxide dismutases (CSD1 and CSD2), were increased during SO2 exposure. The activity of superoxide dismutase (SOD), one of the major antioxidant enzymes, was enhanced with the increase in the CSD transcript level, suggesting an important role of miR398 in response to SO2-induced oxidative stress. Meanwhile, the expression of miR395 was increased, and the transcript levels of its target genes, ATP sulfurylases (APS3 and APS4) and a low-affinity sulfate transporter (SULTR2;1), were decreased in Arabidopsis shoots, showing that miR395 played important roles in the regulation of sulfate assimilation and translocation during SO2 exposure. The content of glutathione (GSH), an important sulfur-containing antioxidant, was enhanced with the changes in sulfur metabolism in Arabidopsis shoots under SO2 stress. These results showed that both miR398 and miR395 were involved in protecting plants from oxidative damage during SO2 exposure. Many stress-responsive cis-elements were found in the promoter regions of MIR398 and MIR395, suggesting that these miRNAs might respond to various environmental conditions, including SO2 stress. Overall, our study provides an insight into the regulatory roles of miRNAs in response to SO2 stress in plants, and highlights the molecular mechanisms of plant adaptation to environmental stress.

Manure and mineral fertilization change enzyme activity and bacterial community in millet rhizosphere soils.

Fertilization is a key agricultural practice for increasing millet yields and influencing soil properties, enzyme activities and rhizosphere bacterial communities. High throughput Illumina sequencing of the 16S rDNA was applied to compare the bacterial community structures and diversities among six different soil samples. The experiments involved the following: no fertilizer (CK), phosphate (P) and potassium (K) plus organic manure (M) (PKM), nitrogen (N) and K plus M (NKM), NPM, NPK and NPKM fertilization. The results showed that the NPKM fertilization of the millet field had a maximal yield of 3617 kg ha-1 among the six different treatments. The abundances of the Actinobacteria and Bacteroidetes phyla, especially the Devosia, Mycobacterium, Opitutus and Chitinophaga genera, were higher in NPKM than those in the other samples. Redundancy analysis showed that the soil organic matter (SOM), available phosphorus (AP), and urease (UR) activity were significantly correlated with bacterial communities, while SOM and AP were strongly correlated with soil enzyme activities. Pearson's correlation showed that the available nitrogen was strongly correlated with Devosia and Mycobacterium, and SOM was strongly correlated with Opitutus and Chitinophaga. Besides, catalase was significantly related to Iamia, the UR was significantly related to Devosia, phosphatase was significantly related to Luteimonas and Chitinophaga. Based on the soil quality and millet yield, NPKM treatment was a better choice for the millet field fertilization practices. These findings provide a better understanding of the importance of fertilization in influencing millet yield, soil fertility and microbial diversity, and they lead to a choice of scientific fertilization practices for sustainable development of the agroecosystem.

[Research progress of ellagitannin intestinal metabolite urolithins].

Ellagitannins is a kind of phenolic compounds with many biological activities. Recent studies have found that the effective ingredients of these compounds have close relationship with their colon-derived bacteria metabolites, that is urolithins. The objective of this study was to review the structure characteristics, types and distribution of urolithins, improvement in diseases related to prostate, breast and colon, as well as anti-cancer, anti-oxidation, anti-inflammation and other biological activities. The present review will lay the foundation for development and utilization of urolithins.

Anti-proliferative effects of polyphenols from pomegranate rind (Punica granatum L.) on EJ bladder cancer cells via regulation of p53/miR-34a axis.

miRNAs and their validated miRNA targets appear as novel effectors in biological activities of plant polyphenols; however, limited information is available on miR-34a mediated cytotoxicity of pomegranate rind polyphenols in cancer cell lines. For this purpose, cell viability assay, Realtime quantitative PCR for mRNA quantification, western blot for essential protein expression, p53 silencing by shRNA and miR-34a knockdown were performed in the present study. EJ cell treatment with 100 µg (GAE)/mL PRE for 48 h evoked poor cell viability and caspase-dependent pro-apoptosis appearance. PRE also elevated p53 protein and triggered miR-34a expression. The c-Myc and CD44 were confirmed as direct targets of miR-34a in EJ cell apoptosis induced by PRE. Our results provide sufficient evidence that polyphenols in PRE can be potential molecular clusters to suppress bladder cancer cell EJ proliferation via p53/miR-34a axis.

Genome-wide transcriptome analysis of Arabidopsis response to sulfur dioxide fumigation.

Sulfur dioxide (SO2) supplies the basic sulfur element to promote plant growth, yet at the same time it is a harmful air pollutant. Currently, the mechanisms of plant adaptation to SO2 stress are largely unknown. Pathways of SO2 metabolism, a range of networks of interacting regulatory signals and defense mechanisms triggered in resistance to SO2 stress, have not yet been clarified. We performed transcriptome analysis of Arabidopsis plants fumigated with 30 mg m(-3) SO2 for 72 h and untreated controls using microarrays. This identified 2,780 significantly up- or down-regulated genes in plants response to SO2 stress, indicating a possible genome-scale reprogramming of the transcriptome. Significant changes in the transcript abundance of genes that participated in SO2 metabolic pathways indicated that numerous sulfites were involved in sulfur assimilatory pathways directly and away from sulfite oxidative pathways. Furthermore, the up-regulation of components involved in reactive oxygen species generating and scavenging pathways demonstrated altered redox homeostasis. Transcripts encoding key components in nitric oxide biosynthesis pathways were simultaneously up-regulated by SO2 exposure. In addition, transcripts associated with putative biotic stress were also up-regulated. Therefore, SO2 evokes a comprehensive reprogramming of metabolic pathways, consistent with up-regulation of transcripts involved in tolerance and defense mechanisms, in Arabidopsis.

Arsenic exposure induces small intestinal toxicity in mice by barrier damage and inflammation response via activating RhoA/ROCK and TLR4/Myd88/NF-κB signaling pathways.

Numerous studies have shown that arsenic (As) is an important hazardous metalloid that is commonly considered to have systemic toxicity. The main pathway of arsenic exposure is oral; however, many of the events that occur during its passage through the gastrointestinal tract are unclear, and there are few reports on the effect of arsenic on small intestinal mucosal barrier. This study aimed to investigate arsenic-induced mucosal barrier damage in the small intestine of mice induced by oral exposure and its potential mechanisms. In the present study, histomorphometric and immunohistochemical analyses showed that arsenic-treated mice exhibited signs of irregularly arranged and atrophied small intestinal villi, reduced villus lengths, inflammatory cells infiltration, along with up-regulated expression of inflammatory factors TNF-α, IL-6 and IL-1ß in the small intestine of mice. The myeloperoxidase (MPO) activity was also increased in As-exposed mice. Transmission electron microscopy (TEM) analysis demonstrated that intestinal epithelial tight junctions (TJs) were impaired in the small intestines of mice in As group. In addition, arsenic down-regulated mRNA levels of TJ-related genes (ZO-1, ZO-2, occludin, claudin-1, and claudin-7) and protein levels of ZO-1, occludin and claudin-1 were significantly reduced in arsenic-treated groups, while arsenic also increased levels of TLR4, Myd88, NF-κB, RhoA, and ROCK mRNA and protein expression. In summary, these results indicate that the small intestine toxicity in mice evoked by arsenic was correlated with the activation of TLR4/Myd88/NF-κB and RhoA/ROCK pathways.

Sulfur dioxide induced programmed cell death in Vicia guard cells.

Sulfur dioxide (SO(2)) induced nuclear condensation and nuclear fragmentation and rapid loss of guard cell viability in detached epidermis of Vicia leaves at concentrations of 1 mM and higher (3 h exposure). Caspase inhibitors Z-Asp-CH(2)-DCB (0.1 mM) and TLCK (0.1 mM) markedly suppressed SO(2)-induced cell death. The typical nuclear morphological changes and the inhibition effects of caspase inhibitors suggest the activation of a programmed cell death (PCD) pathway. SO(2)-induced cell death can be blocked by either antioxidants (0.1 mM AsA or 200 U/mL CAT) or Ca(2+) antagonists (0.1mM EGTA or LaCl(3)). AsA and CAT also blocked SO(2)-induced ROS production and [Ca(2+)](cyt) increase. However, EGTA and LaCl(3) can inhibit SO(2)-induced [Ca(2+)](cyt) increase, but cannot suppress SO(2)-induced ROS production. Our results indicate that high concentrations of SO(2) induce guard cell death via a PCD pathway through ROS mediating [Ca(2+)](cyt) elevation, which causes harmful effects to plants.