Can l-ascorbic acid and trans-resveratrol protect HaCaT cells from fine particulate matter toxicity?

Continuous exposure of human skin to air pollution can result in a range of undesirable skin conditions. In our recent study, UV and visible light were found to increase cytotoxicity of fine particulate matter (PM2.5 ) against human keratinocytes. Since it is impossible to avoid exposure of human skin to PM2.5 , effective strategies are needed to reduce their damaging effects. l-ascorbic acid and resveratrol were tested as potential topical agents against pollution-related skin impairment. Although these agents were previously found to ameliorate PM-dependent damage, the effect of light and seasonal variation of particles were not previously studied. EPR spin-trapping, DPPH assay, and singlet oxygen phosphorescence were used to determine the scavenging activities of the antioxidants. MTT, JC-10 and iodometric assays were used to analyze the effect on PM2.5 -induced cytotoxicity, mitochondrial damage and oxidation of lipids. Live-cell imaging was employed to examine wound-healing properties of cells. Light-induced, PM2.5 -mediated oxidative damage was examined by immunofluorescent staining. Both antioxidants effectively scavenged free radicals and singlet oxygen produced by PM2.5 , reduced cell death and prevented oxidative damage to HaCaT cells. l-ascorbic acid and resveratrol, especially when applied in combination, can protect HaCaT cells against the dark and light induced toxicity of PM2.5 .

Do urban air pollutants induce changes in the thallus anatomy and affect the photosynthetic efficiency of the nitrophilous lichen Physcia adscendens?

Lichens are symbiotic organisms that are generally sensitive to air pollution due to their specific biological and physiological features. Physcia adscendens is a nitrophilous lichen well-known for being resistant to air pollution associated with progressive anthropopressure. The aim of this study was to investigate the effect of nitrogen oxides and suspended particulate matter (PM10 and PM2.5) on anatomical structure of the thallus and photobiont's photosynthetic efficiency in P. adscendens inhabiting sites that differ in terms of air pollution level and thereby to determine the relevance of these pollutants for shaping the structure of the thallus and the physiological condition of the photosynthetic partner. We found that P. adscendens from polluted sites had increased thickness of the algal layer and the larger size of the algae cells, but a much lower ratio of the algal layer to the whole thallus. Lichens from highly polluted sites had also higher photosynthetic efficiency, which indicates a relatively good physiological condition of the photobiont. This indicates that the photobiont of P. adscendens is well-adapted to function under air pollution stress which may contribute to its success in colonizing polluted sites. Both changes in the anatomy of the lichen thallus and the efficiency of photosynthesis may be related to the enrichment of the environment with nitrogen. The increased photosynthetic efficiency as well as investment in the size of photobiont cells and growth mycobiont hyphae confirms that P. adscendens is well-adapted to urban conditions; however, the mechanism behind those adaptations needs more focus in the context of global environmental changes.

Berberine hydrochloride ameliorates PM2.5-induced pulmonary fibrosis in mice through inhibiting oxidative stress and inflammatory.

Elevated levels of respirable particulate matter (PM) have been strongly linked to disease incidence and mortality in population-based epidemiological studies. Berberine hydrochloride (BBR), an isoquinoline alkaloid found in Coptis chinensis, exhibits antipyretic, anti-inflammatory, and antioxidant properties. However, the protective effects and underlying mechanism of BBR against pulmonary fibrosis remain unclear. This study aimed to investigate the protective effect of BBR on lung tissue damage using a mouse model of PM2.5-induced pulmonary fibrosis. SPF grade C57BL/6 mice were randomly assigned to four groups, each consisting of 10 mice. The mice were pretreated with BBR (50 mg/kg) by gavage for 45 consecutive days. A tracheal drip of PM2.5 suspension (8 mg/kg) was administered once every three days for a total of 15 times to induce lung fibrosis. Moreover, the results demonstrated that PM2.5 was found to inhibit the PPARγ signaling pathway, increase ROS expression, upregulate protein levels of IL-6, IL-1ß, TNF-α, as well as regulation of gene expression of STAT3 and SOCS3. Importantly, PM2.5 induced lung fibrosis by promoting collagen deposition, upregulating gene expression of fibrosis markers (TGF-ß1, FN, α-SMA, COL-1, and COL-3), and downregulating E-cadherin expression. Remarkably, our findings suggest that these injuries could be reversed by BBR pretreatment. BBR acts as a PPARγ agonist in PM2.5-induced pulmonary fibrosis, activating the PPARγ signaling pathway to mitigate oxidative and inflammatory factor-mediated lung injury. This study provides valuable insights for the future prevention and treatment of pulmonary fibrosis.

Prenatal exposure to ambient PM2.5 and its chemical constituents and child intelligence quotient at 6 years of age.

There are limited studies on the associations between prenatal exposure to constituents of fine particulate matter (PM2.5) and children's intelligence quotient (IQ). Our study aimed to explore the associations between prenatal PM2.5 and its six constituents and the IQ levels of 6-year-old children. We included 512 mother-child pairs. We used a satellite-based modelling framework to estimate prenatal PM2.5 and its six constituents (ammonium, sulfate, nitrate, organic carbon, soil dust, and black carbon). We assessed the children's IQ using the short form of the Wechsler Intelligence Scale. Perceptual Reasoning Index (PRI), Verbal Comprehension Index (VCI), and Full Scale IQ (FSIQ) scores were computed. The multiple informant model (MIM) was applied to explore the trimester specific effects of PM2.5 and its six constituents' exposure on children's PRI, VCI, and FSIQ. To examine whether the duration of breastfeeding and physical activity (PA) could modify the effects of PM2.5 on children's IQ, we stratified the analyses according to the duration of breastfeeding (≤6 and >6 months) and time of outdoor activities after school (≤2 and >2 h/week). The first trimester PM2.5 and its five constituents' exposures were inversely associated with FSIQ [ß = -1.34, 95 % confidence interval [CI] (-2.71, 0.04) for PM2.5] and PRI [ß = -2.18, 95 %CI (-3.80, -0.57) for PM2.5] in children. The associations were magnified among boys and those with less outdoor activities or shorter breastfeeding duration. Our results indicate that prenatal PM2.5 and several of its main constituents' exposure may disrupt cognitive development in children aged 6 years. More PA and longer breastfeeding duration may alleviate the detrimental effects of prenatal PM2.5 exposure on children's cognitive function.

Cultivar assortment index (CAI): a tool to evaluate the ozone tolerance of Indian Amaranth (Amaranthus hypochondriacus L.) cultivars.

The adverse impact of climate change on crop yield has accelerated the need for identification of crop cultivars resistant to abiotic stress. In the present study, a cultivar assortment index (CAI) was generated for the evaluation of forty Amaranthus hypochondriacus cultivars response to elevated ozone (EO) concentrations (AO + 30 ppb) in Free Air Ozone Enrichment (FAOE) facility using the parameters viz. foliar injury, gaseous exchange attributes, namely, net photosynthetic rate, stomatal conductance, transpiration rate, intercellular carbon dioxide, and water use efficiency along with above ground biomass and grain yield attributes. The dataset was used to identify key indicator parameters responsive to EO through principal component analysis (PCA) and further transformed to obtain linear score and weighted score. The CAI varied from 70.49 to 193.43. Cultivars having CAI value less than 151 were ozone tolerant (OT) whereas cultivars with CAI values between 150 and 170 were moderately tolerant (MOT). The cultivars exhibiting CAI values above 170 were ozone sensitive (OS). The cultivars exhibited differential sensitivity to EO with IC-5994 (CAI = 187.26) being the most affected cultivar whereas IC-5576 (CAI = 83.38) and IC-5916 (CAI = 70.49) being the least affected ones. The CAI, based on linear score and weighted score, offers easy identification of ozone sensitive (OS) and ozone tolerant (OT) cultivars. This index could help researchers to define a clear and strong basis for identification of OT cultivars which will reduce the time required for preliminary screening and further evaluation of crop cultivars for the development of climate smart crops.

Cardiac Autonomic Impacts of Bushfire Smoke-A Prospective Panel Study.

BACKGROUND: Air pollution is associated with cardiovascular disease and mortality. Most studies have focussed on urban or traffic-related pollution, and less is known about the impacts from bushfire smoke on cardiovascular autonomic function, although it is associated with increased sudden cardiac death and mortality. We sought to investigate its instantaneous and short-term impacts on heart rate variability (HRV). METHODS: Twenty-four (24)-hour Holter electrocardiography (ECG) was repeated twice (during bushfire [Phase 1] and then clean air [Phase 2]) in 32 participants from two Australian towns (Warburton and Traralgon, Victoria) surrounding planned burning areas. This was compared with 10 control participants in another town (Maffra, Victoria) with two clean air assessments during the same periods. The primary HRV parameters assessed were those assessing overall HRV (Standard Deviation of Normal-to-Normal intervals [SDNN]), long-term HRV (Standard Deviation of the Average of Normal Sinus-to-Normal Sinus intervals for each 5-minutes [SDANN]), low frequency [LF]) and short-term HRV (Root Mean Square of Successive Differences between N-N intervals [RMSSD], High Frequency [HF], LF:HF ratio). Average concentrations of particulate matter <2.5 µm in diameter (PM2.5) were measured at fixed site monitors in each location. RESULTS: Mean PM2.5 levels were significantly elevated during bushfire exposure in Warburton (96.5±57.7 µg/m3 vs 4.0±1.9 µg/m3, p<0.001) and Traralgon (12.6±4.9 µg/m3 vs 3.4±3.1 µg/m3, p<0.001), while it remained low in the control town, Maffra, in each phase (4.3±3.2 µg/m3 and 3.9±3.6 µg/m3, p=0.70). Although SDANN remained stable in controls, the exposed cohort showed significant worsening in SDANN during bushfire smoke exposure by 9.6±25.7ms (p=0.039). In univariable analysis, smoke exposure was significantly associated with higher ΔSDNN and ΔSDANN (p=0.03, p=0.01 exposed vs control). The association remained significant in ΔSDANN after adjusting for age, sex and cigarette smoking (p=0.02) and of borderline significance in ΔSDNN (p=0.06). CONCLUSIONS: Exposure to the bushfire smoke was independently associated with reduced overall and long-term HRV. Our findings suggest that imbalance in cardiac autonomic function is a key mechanism of adverse cardiovascular effects of bushfire smoke.

Fish oil blunts lung function decrements induced by acute exposure to ozone in young healthy adults: A randomized trial.

BACKGROUND: Over one-third of the U.S. population is exposed to unsafe levels of ozone (O3). Dietary supplementation with fish oil (FO) or olive oil (OO) has shown protection against other air pollutants. This study evaluates potential cardiopulmonary benefits of FO or OO supplementation against acute O3 exposure in young healthy adults. METHODS: Forty-three participants (26 ± 4 years old; 47% female) were randomized to receive 3 g/day of FO, 3 g/day OO, or no supplementation (CTL) for 4 weeks prior to undergoing 2-hour exposures to filtered air and 300 ppb O3 with intermittent exercise on two consecutive days. Outcome measurements included spirometry, sputum neutrophil percentage, blood markers of inflammation, tissue injury and coagulation, vascular function, and heart rate variability. The effects of dietary supplementation and O3 on these outcomes were evaluated with linear mixed-effect models. RESULTS: Compared with filtered air, O3 exposure decreased FVC, FEV1, and FEV1/FVC immediately post exposure regardless of supplementation status. Relative to that in the CTL group, the lung function response to O3 exposure in the FO group was blunted, as evidenced by O3-induced decreases in FEV1 (Normalized CTL -0.40 ± 0.34 L, Normalized FO -0.21 ± 0.27 L) and FEV1/FVC (Normalized CTL -4.67 ± 5.0 %, Normalized FO -1.4 ± 3.18 %) values that were on average 48% and 70% smaller, respectively. Inflammatory responses measured in the sputum immediately post O3 exposure were not different among the three supplementation groups. Systolic blood pressure elevations 20-h post O3 exposure were blunted by OO supplementation. CONCLUSION: FO supplementation appears to offer protective effects against lung function decrements caused by acute O3 exposure in healthy adults.

Size-based effects of anthropogenic ultrafine particles on activation of human lung macrophages.

The anthropogenic particulate matter (PM), suspended air dust that can be inhaled by humans and deposited in the lungs, is one of the main pollutants in the industrialized cities atmosphere. Recent studies have shown that PM has adverse effects on respiratory diseases. These effects are mainly due to the ultrafine particles (PM0.1, PM < 100 nm), which, thanks to their PM size, are efficiently deposited in nasal, tracheobronchial, and alveolar regions. Pulmonary macrophages are a heterogeneous cell population distributed in different lung compartments, whose role in inflammatory response to injury is of particular relevance. In this study, we investigated the effect of PM0.1 on Human Lung Macrophages (HLMs) activation evaluated as proinflammatory cytokines and chemokine release, Reactive Oxygen Species (ROS) production and intracellular Ca2+concentration ([Ca2+]i). Furthermore, PM0.1, after removal of organic fraction, was fractionated in nanoparticles both smaller (NP20) and bigger (NP100) than 20 nm by a properlydeveloped analytical protocol, allowed isolating their individual contribution. Interestingly, while PM0.1 and NP20 induced stimulatory effects on HLM cytokines release, NP100 had not effect. In particular, PM0.1 induced IL-6, IL-1ß, TNF-α, but not CXCL8, release from HLMs. Moreover, PM0.1, NP20 and NP100 did not induce ß-glucuronidase release, a preformed mediator contained in HLMs. The long time necessary for cytokines release (18 h) suggested that PM0.1 and NP20 could induce ex-novo production of the tested mediators. Accordingly, after 6 h of incubation, PM0.1 and NP20 induced mRNA expression of IL-6, TNF-α and IL-1ß. Moreover, NP20 induced ROS production and [Ca2+]i increase in a time-dependent manner, without producing cytotoxicity. Collectively, the present data highlight the main proinflammatory role of NP20 among PM fractions. This is particularly of concern because this fraction is not currently covered by legal limits as it is not easily measured at the exhausts by the available technical methodologies, suggesting that it is mandatory to search for new monitoring techniques and strategies for limiting NP20 formation.

Ozone-Induced Models of Airway Hyperreactivity and Epithelial Injury.

Ozone (O3), a criterion air pollutant produced as a product of internal combustion, generates increased inflammation, lung permeability, and airway hyperreactivity when exposed to rodents in laboratory settings. Airway hyperreactivity is defined as an exaggerated acute obstructive response of the airways to one or more nonspecific stimuli. Lung permeability is a measure of barrier functions that separate internal and external environments to limit access of pathogens and other noxious material. By modeling in vivo O3 exposure in rodents, this allows investigators to explore pulmonary and nonpulmonary O3 effects as a means of understanding its impact on human health and lung function. Furthermore, direct effects of O3 on epithelial permeability can be defined using in vitro exposures to airway epithelial cells. This chapter will focus on methods of generating O3 and then exposing rodents and cultured epithelial cells in laboratory settings.

Effects of exposure to environmental pollutants on mitochondrial DNA copy number: a meta-analysis.

Exposure to environmental pollutants has been associated with alteration on relative levels of mitochondrial DNA copy number (mtDNAcn). However, the results obtained from epidemiological studies are inconsistent. This meta-analysis aimed to evaluate whether environmental pollutant exposure can modify the relative levels of mtDNAcn in humans. We performed a literature search using PubMed, Scopus, and Web of Science databases. We selected and reviewed original articles performed in humans that analyzed the relationship between environmental pollutant exposure and the relative levels of mtDNAcn; the selection of the included studies was based on inclusion and exclusion criteria. Only twenty-two studies fulfilled our inclusion criteria. A total of 6011 study participants were included in this systematic review and meta-analysis. We grouped the included studies into four main categories according to the type of environmental pollutant: (1) heavy metals, (2) polycyclic aromatic hydrocarbons (PAHs), (3) particulate matter (PM), and (4) cigarette smoking. Inconclusive results were observed in all categories; the pooled analysis shows a marginal increase of relative levels of mtDNAcn in response to environmental pollutant exposure. The trial sequential analysis and rate confidence in body evidence showed the need to perform new studies. Therefore, a large-scale cohort and mechanistic studies in this area are required to probe the possible use of relative levels of mtDNAcn as biomarkers linked to environmental pollution exposure.

Epithelial 3D-spheroids as a tool to study air pollutant-induced lung pathology.

Cigarette smoke (CS) and air pollutants (AP) activate pathological processes in bronchial epithelial cells resulting in lung function decline which severely impacts human health. Knowledge about the molecular mechanism(s) by which CS and AP induce pathology is limited. Our previous studies in 2D cultures of human bronchial epithelial (BEAS-2B) cells showed that CS exposure activates transforming growth factor-ß1 (TGF-ß1) release and signaling. Furthermore, CS exposure reduced the expression of E-cadherin, which was prevented by applying a TGF-ß1 neutralizing antibody. Exposure of BEAS-2B cells cultured in 2D to diesel exhaust particles (DEP) increased TGF-ß1 protein expression and reduced the expression of epithelial cell markers, whereas mesenchymal markers are upregulated. Conventional 2D cell culture may, however, not fully reflect the physiology of bronchial epithelial cells in vivo. To simulate the in vivo situation more closely we cultured the bronchial epithelial cells in a 3D environment in the current study. Treatment of epithelial spheroids with TGF-ß resulted in reduced E-cadherin and increased collagen I expression, indicating the activation of epithelial-to-mesenchymal transition (EMT). Similarly, exposure of spheroids to DEP induced and EMT-like phenotype. Collectively, our data indicate AP induces an EMT-like phenotype of BEAS-2B cells in 3D spheroid cultures. This opens new avenues for drug development for the treatment of lung diseases induced by AP. The 3D spheroid cell culture is a novel, innovative and physiologically relevant model for culturing a variety of cells. It is a versatile tool for both high-throughput studies and for identifying molecular mechanisms involved in bronchial epithelial cell (patho)physiology.

Impact of Hydrogen Sulfide on Mitochondrial and Bacterial Bioenergetics.

This review focuses on the effects of hydrogen sulfide (H2S) on the unique bioenergetic molecular machines in mitochondria and bacteria-the protein complexes of electron transport chains and associated enzymes. H2S, along with nitric oxide and carbon monoxide, belongs to the class of endogenous gaseous signaling molecules. This compound plays critical roles in physiology and pathophysiology. Enzymes implicated in H2S metabolism and physiological actions are promising targets for novel pharmaceutical agents. The biological effects of H2S are biphasic, changing from cytoprotection to cytotoxicity through increasing the compound concentration. In mammals, H2S enhances the activity of FoF1-ATP (adenosine triphosphate) synthase and lactate dehydrogenase via their S-sulfhydration, thereby stimulating mitochondrial electron transport. H2S serves as an electron donor for the mitochondrial respiratory chain via sulfide quinone oxidoreductase and cytochrome c oxidase at low H2S levels. The latter enzyme is inhibited by high H2S concentrations, resulting in the reversible inhibition of electron transport and ATP production in mitochondria. In the branched respiratory chain of Escherichia coli, H2S inhibits the bo3 terminal oxidase but does not affect the alternative bd-type oxidases. Thus, in E. coli and presumably other bacteria, cytochrome bd permits respiration and cell growth in H2S-rich environments. A complete picture of the impact of H2S on bioenergetics is lacking, but this field is fast-moving, and active ongoing research on this topic will likely shed light on additional, yet unknown biological effects.

Biomarkers of DNA Oxidation Products: Links to Exposure and Disease in Public Health Studies.

Environmental exposure can increase the production of reactive oxygen species and deplete cellular antioxidants in humans, resulting in oxidatively generated damage to DNA that is both a useful biomarker of oxidative stress and indicator of carcinogenic hazard. Methods of oxidatively damaged DNA analysis have been developed and used in public health research since the 1990s. Advanced techniques detect specific lesions, but they might not be applicable to complex matrixes (e.g., tissues), small sample volume, and large-scale studies. The most reliable methods are characterized by (1) detecting relevant DNA oxidation products (e.g., premutagenic lesions), (2) not harboring technical problems, (3) being applicable to complex biological mixtures, and (4) having the ability to process a large number of samples in a reasonable period of time. Most effort has been devoted to the measurements of 8-oxo-7,8-dihydro-2'-deoxyguanine (8-oxodG), which can be analyzed by chromatographic, enzymic, and antibody-based methods. Results from validation trials have shown that certain chromatographic and enzymic assays (namely the comet assay) are superior techniques. The enzyme-modified comet assay has been popular because it is technically simpler than chromatographic assays. It is widely used in public health studies on environmental exposures such as outdoor air pollution. Validated biomarker assays on oxidatively damaged DNA have been used to fill knowledge gaps between findings in prospective cohort studies and hazards from contemporary sources of air pollution exposures. Results from each of these research fields feed into public health research as approaches to conduct primary prevention of diseases caused by environmental or occupational agents.

Plant biochemistry influences tropospheric ozone formation, destruction, deposition, and response.

Tropospheric ozone (O3) is among the most damaging air pollutant to plants. Plants alter the atmospheric O3 concentration in two distinct ways: (i) by the emission of volatile organic compounds (VOCs) that are precursors of O3; and (ii) by dry deposition, which includes diffusion of O3 into vegetation through stomata and destruction by nonstomatal pathways. Isoprene, monoterpenes, and higher terpenoids are emitted by plants in quantities that alter tropospheric O3. Deposition of O3 into vegetation is related to stomatal conductance, leaf structural traits, and the detoxification capacity of the apoplast. The biochemical fate of O3 once it enters leaves and reacts with aqueous surfaces is largely unknown, but new techniques for the tracking and identification of initial products have the potential to open the black box.

Metabolic and Lipid Alterations in Mice Brain Cortex after PM2.5 Exposure.

Fine particulate matter (PM2.5) has been reported to be associated with neurological disorders. However, the effects of PM2.5 on changes in metabolic and lipid profile of the brain are unclear. In this study, global metabolomics and lipidomics in mice cortex were investigated from the analyses by ultraperformance liquid chromatography-Orbitrap mass spectrometry. The partial least-squares discriminant analysis showed that the metabolite and lipid profiles were significantly altered by PM2.5 exposure. The changed metabolic pathways including alanine, aspartate, and glutamate metabolism, carnitine metabolism, and glycerophospholipid remodeling pathway were found to be associated with a neurodegenerative process according to their corresponding molecular mechanisms. Our results indicated that PM2.5 exposure could induce neurological damage.

In Utero Exposure to Fine Particles Decreases Early Birth Weight of Rat Offspring and TLR4/NF-κB Expression in Lungs.

Particulate matter (PM2.5) exposure is reported to have deleterious effects on health. Maternal PM2.5 exposure has been confirmed to damage the growth of somatic cells and enhance the incidence of chronic respiratory diseases in children. Here we aim to investigate the impact of in utero PM2.5 exposure on early birth weight and postnatal lung development. Pregnant Sprague-Dawley rats were administered PM2.5 (0.1, 0.5, 2.5, or 7.5 mg/kg) intraperitoneally every 3 days until birth. Maternal and birth outcomes and somatic growth were monitored. Lungs were collected on PND1 (where PND = postnatal day) and PND28; the lung wet-to-dry weight ratio (W/D) was analyzed, and reactive oxygen species (ROS) levels were measured. Expression of Toll-like receptor 4 (TLR4) and NF-κB were evaluated by Western blotting and quantitative RT-PCR. There were no significant intergroup differences for maternal outcomes; however, offspring exposed in utero to 2.5 and 7.5 mg/kg PM2.5 were significantly smaller in litter weight than the controls. In utero exposure to 2.5 and 7.5 mg/kg PM2.5 led to lower body weight after birth and disrupted lung development during infancy. ROS levels were significantly increased in the 7.5 mg/kg PM2.5 group. PM2.5-treated rats showed upregulated pulmonary expression of TLR4 and NF-κB. Maternal PM2.5 exposure enhances the risk of low birth weight and affects lung alveolar development. The underlying molecular mechanisms may involve TLR4/NF-κB signaling.

An assessment of growth, floral morphology, and metabolites of a medicinal plant Sida cordifolia L. under the influence of elevated ozone.

Tropospheric ozone (O3) is a major secondary air pollutant and greenhouse gas, and its impact on growth, yield, and its quality is well established in the case of crop plants. However, the effects of tropospheric O3 have not been comprehensively studied on medicinal plants. Therefore, a field study was planned on a medicinally important Sida cordifolia L. plant (commonly known as country mallow or Bala) to assess the expected changes on the morphology, growth, and leaf injury under elevated O3 (ambient + 20 ppb) by using open-top chambers (OTCs) at 30, 60, and 90 days after treatment (DAT), while leaf and root metabolites were observed at 60 DAT. At all the growth stages, significant leaf damage was recorded as foliar injury symptoms. Most of the growth parameters also showed significant reductions at all the growth stages. Plants under elevated O3 showed a significant negative impact on most of the reproductive parts of the plant. Leaf weight ratio (LWR) showed significant increment at early stages while reduced at 90 DAT; however, root shoot ratio (RSR) showed a significant reduction at 60 DAT. The majority of the steroid metabolites showed an increase in root and leaves under elevated O3, while terpenes showed variable response. Due to O3 stress, most of the major metabolites showed an increase possibly due to their role in defense and other metabolic activities. Based on the outcomes, it is concluded that the future increase in the levels of tropospheric O3 will impact a significant effect on important metabolites of medicinal plants growing in tropical countries like India.

Hydrogen Sulfide Modulates Adult and Reparative Neurogenesis in the Cerebellum of Juvenile Masu Salmon, Oncorhynchus masou.

Fish are a convenient model for the study of reparative and post-traumatic processes of central nervous system (CNS) recovery, because the formation of new cells in their CNS continues throughout life. After a traumatic injury to the cerebellum of juvenile masu salmon, Oncorhynchus masou, the cell composition of the neurogenic zones containing neural stem cells (NSCs)/neural progenitor cells (NPCs) in the acute period (two days post-injury) changes. The presence of neuroepithelial (NE) and radial glial (RG) neuronal precursors located in the dorsal, lateral, and basal zones of the cerebellar body was shown by the immunohistochemical (IHC) labeling of glutamine synthetase (GS). Progenitors of both types are sources of neurons in the cerebellum of juvenile O. masou during constitutive growth, thus, playing an important role in CNS homeostasis and neuronal plasticity during ontogenesis. Precursors with the RG phenotype were found in the same regions of the molecular layer as part of heterogeneous constitutive neurogenic niches. The presence of neuroepithelial and radial glia GS+ cells indicates a certain proportion of embryonic and adult progenitors and, obviously, different contributions of these cells to constitutive and reparative neurogenesis in the acute post-traumatic period. Expression of nestin and vimentin was revealed in neuroepithelial cerebellar progenitors of juvenile O. masou. Patterns of granular expression of these markers were found in neurogenic niches and adjacent areas, which probably indicates the neurotrophic and proneurogenic effects of vimentin and nestin in constitutive and post-traumatic neurogenesis and a high level of constructive metabolism. No expression of vimentin and nestin was detected in the cerebellar RG of juvenile O. masou. Thus, the molecular markers of NSCs/NPCs in the cerebellum of juvenile O. masou are as follows: vimentin, nestin, and glutamine synthetase label NE cells in intact animals and in the post-traumatic period, while GS expression is present in the RG of intact animals and decreases in the acute post-traumatic period. A study of distribution of cystathionine ß-synthase (CBS) in the cerebellum of intact young O. masou showed the expression of the marker mainly in type 1 cells, corresponding to NSCs/NCPs for other molecular markers. In the post-traumatic period, the number of CBS+ cells sharply increased, which indicates the involvement of H2S in the post-traumatic response. Induction of CBS in type 3 cells indicates the involvement of H2S in the metabolism of extracellular glutamate in the cerebellum, a decrease in the production of reactive oxygen species, and also arrest of the oxidative stress development, a weakening of the toxic effects of glutamate, and a reduction in excitotoxicity. The obtained results allow us to consider H2S as a biologically active substance, the numerous known effects of which can be supplemented by participation in the processes of constitutive neurogenesis and neuronal regeneration.

Ambient sulfur dioxide could have an impact on testicular volume from a observational study on a population of infertile male.

BACKGROUND: The effect of ambient pollutants on the male reproductive system is controversial. This retrospective study investigated the effect of environmental pollutants on male reproductive health. METHODS: Male patients with primary infertility (n = 282) were identified from a single center between January 2016 and December 2017. Patients were physically examined for the presence of varicocele and for the volume of both testicles. Semen quality was measured in terms of the total sperm count, sperm concentration, and the percentage of sperm cells with motility and normal morphology. Data were acquired on the concentration of ambient pollutants, namely particulate matters of diameter < 2.5 µm, sulfur dioxide (SO2), nitrogen oxides (NOx), and ozone (O3), measured on daily and hourly basis, from the Environmental Protection Administration Executive Yuan, Taiwan. Individual exposure to pollutants was estimated based on the reported residential address of each participant. Statistical analysis indicated the effect of each pollutant on the testicular volume, sex hormone profile, and semen parameters. RESULTS: The mean ± standard deviation of age was 36.7 ± 7.3 years. The average sperm count and concentration were 41.9 million/mL and 34.1 million/mL, respectively. The mean levels of serum testosterone, follicle-stimulating hormone, and luteinizing hormone were 3.57 ± 1.68 ng/mL, 7.59 ± 6.3 IU/L, and 4.68 ± 3.49 IU/L, respectively. According to the multivariate linear regression model, NOx exposure was a risk factor for decreased sperm concentration and motility (p = 0.043 and 0.032). Furthermore, SO2 exposure was negatively associated and testicular volume (p < 0.01). CONCLUSIONS: NO2 and SO2 exposure were negatively associated with the seminal parameter and decreased testicular volume, respectively, in a population of men with infertility. However, additional prospective studies are needed to ascertain the cause-effect relation of current results.