Diesel Exhaust Particulate Matter Research Articles

Diesel exhaust particulate matter induces GC-1 spg cells oxidative stress by KEAP1-NRF2 pathway and inhibition of ATP5α1 S-sulfhydration

Diesel exhaust particle (DEP) exposure induces a variety of toxicological effects through oxidative stress and inflammation responses. This research investigated the mechanisms underlying DEP-induced GC-1spg cells oxidative stress by examining ROS accumulation, antioxidant defense systems activation, mitochondrial dysfunction, and the Nrf2/Keap1/HO-1 pathway response. Subsequently, we further evaluated the ATP levels, ATP5α synthase activity and ATP5α synthase S-sulfhydrated modification in DEP-exposed GC-1 spg cells. The results showed that DEP exposure significantly inhibited cell proliferation and viability, increased intracellular ROS production, decreased MMP, down-regulated antioxidant capacity, activated the Nrf2/Keap1/HO-1 pathway. However, DEP-induced oxidative stress was partially alleviated by GSH and exogenous H2S. In addition, DEP exposure induced ATP depletion and ATP5α synthase inactivity in GC-1 spg cells, accompanied by ATP5α synthase S-sulfhydrated modification. In conclusion, our research showed that DEP may incapacitate mitochondria through oxidative stress injury, leading to GC-1 spg cells oxidative stress. This process may be associated with the reduction of ATP5α1 S-sulfhydrated modification. It provides a new perspective for the research of the mechanism related to male reproductive toxicity due to air pollution.

Inhalation of diesel exhaust particulate matter accelerates weight gain via regulation of hypothalamic appetite-related genes and gut microbiota metabolism

Mice exposed to diesel exhaust particulate matter (DEPM) exhibited accelerated weight gain. Several hypothalamic genes, hormones (serum Hypothalamic-Pituitary-Adrenal (HPA) axis hormones and gastrointestinal peptide tyrosine tyrosine (PYY)), metabolites (intrahepatic triglyceride (IHTG) and fecal short-chain fatty acids (SCFAs)), and gut microbiota structure, which may influence obesity and appetite regulation, were examined. The result suggested that DEPM-induced accelerated weight gain may be associated with increased expression of hypothalamic Gamma-aminobutyric acid (GABA) type B receptor, tight junction protein, and orexin receptors, in addition with decreased IHTG and repressed HPA axis. Moreover, changes in the structure of intestinal microbiota are also related to weight changes, especially for phylum Firmicutes, genus Lactobacillus, and the ratio of relative abundance of Firmicutes and Bacteroidetes (F/B). DEPM exposure also caused widespread increase in the levels of intestinal SCFAs, the concentrations of propionic acid and isobutyric acid were associated with weight gain rate and the abundance of some bacteria. Although DEPM exposure caused changes in expression of hypothalamic serotonin, NPY, and melanocortin receptors, they were not associated with weight changes. Furthermore, no significant difference in gastrointestinal PYY and expression of hypothalamic receptors for leptin, insulin, and glucagon-like peptide 1 receptors was observed between DEPM-exposed and control mice.

Inhalation of diesel exhaust particulate matter induces locomotor hyperactivity and its relationship with brain and gut metabolism

Diesel exhaust particulate matter (DEPM) are important components of urban air pollution worldwide. Recent studies proved that airborne DEPM can enter the human brain, which was associated with brain and mental diseases. In this study, we investigated the effects of DEPM exposure on behavior, and explored potential mechanisms from the perspective of metabolism in specific brain regions and short chain fatty acids (SCFAs) in the gut using mice. The results showed that inhalation of DEPM induced locomotor hyperactivity and a tendency for memory decline in mice. Exposure to DEPM disrupted motor behavior generation related cerebellar Purkinje cells, induced widespread reduction of neurotransmitters in the frontal cortex, and downregulated expression of genes encoding Brain-derived neurotrophic factor (BDNF) and involved in the Brain-blood-barrier (BBB) in the hippocampus. Moreover, there was a DEPM dose-dependent increase in fecal SCFA levels. Correlation analysis showed that DEPM-induced locomotor hyperactivity was mainly associated with decreased neurotransmission in the frontal cortex and increased gut SCFAs, and those associations were discussed. This study provides new insights into the mechanisms underpinning behavioral changes caused by air pollution, and extends our knowledge on the toxicity and health effects of airborne pollutants.

Astaxanthin protected against the adverse effects induced by diesel exhaust particulate matter via improving membrane stability and anti-oxidative property

Diesel exhaust particulate matter (DPM), which has been clarified as a Group I carcinogenic agent, is still challenging in its detoxification due to the complex composition and toxic mechanisms. Astaxanthin (AST) is a pleiotropic small biological molecule widely used in medical and healthcare with surprising effects and applications. The present study aimed to investigate the protective effects of AST on DPM-induced injury and the underlying mechanism. Our results indicated that AST significantly suppressed the generation of phosphorylated histone H2AX (γ-H2AX, marker of DNA damage) and inflammation caused by DPM both in vitro and in vivo. Mechanistically, AST prevented the endocytosis and intracellular accumulation of DPM via regulating the stability and fluidity of plasma membranes. Moreover, the oxidative stress elicited by DPM in cells could also be effectively inhibited by AST, together with protecting the structure and function of mitochondria. These investigations provided clear evidence that AST notably reduced DPM invasion and intracellular accumulation by modulating the membrane-endocytotic pathway, which eventually reduced intracellular oxidative stress caused by DPM. Our data might provide a novel clue for curing and treating the harmful effects of particulate matter.

Influence of vehicular emissions and meteorological factors towards anionic surfactants in the urban atmospheric aerosol of Kuala Lumpur, Malaysia

This study aimed to determine the influence of vehicular emissions and meteorological factors on the level of surfactants in urban atmospheric aerosol from Kuala Lumpur city center, Malaysia. Aerosol samples were collected using a high-volume sampler equipped with the cascade impactor to separate fine mode (< 1.5 µm) and coarse mode (> 1.5 µm) particles. Besides, the exhaust particulate matter from various diesel and petrol vehicles was collected using a soft brush during dry weather. Colorimetric analysis was performed to determine the concentration of anionic surfactants as methylene blue active substances (MBAS), and the absorption was determined by using a UV spectrophotometer at a wavelength of 650 nm. Correlation analysis was conducted to determine the influence of vehicular emissions (NOx, SO2, CO and O3), and exhaust particulate matter on the level of surfactants. Results showed that surfactants as MBAS in fine particles showed the dominant values. Correlation analysis showed that the MBAS was positively correlated with NOx (p <0.05) and SO2 (p <0.01), and negatively correlated with O3 (p <0.01), which indicated that the traffic-related air pollutant may influence the anionic surfactants level. It is supported by the high level of MBAS in diesel exhaust particulate matter, particularly from the construction machinery, followed by lorries and buses.

Diesel exhaust particulate matter impairs Toll-like receptor signaling and host defense against staphylococcal cutaneous infection in mice

Air pollution is an emerging cause of mortality, affecting nearly 5 million people each year. Exposure to diesel exhaust fine particulate matter (PM2.5) aggravates respiratory and skin conditions. However, its impact on the protective immunity of the skin remains poorly understood. This study aimed to investigate the underlying molecular mechanism for adverse effects of PM2.5 on the host protective immunity using in vitro cell and in vivo mouse model. Intracellular translocation of Toll-like receptor 9 (TLR9) and CpG-DNA internalization were assessed in dendritic cells without or with PM2.5 treatment using immunofluorescence staining. Cytokine and nitric oxide production were measured in dendritic cells and macrophages without or with PM2.5 treatment. NF-κB and MAPK signaling was determined using western blotting. Skin disease severity, bacterial loads, and cytokine production were assessed in cutaneous Staphylococcus aureus (S. aureus) infection mouse model. PM2.5 interfered with TLR9 activation by inhibiting both TLR9 trafficking to early endosomes and CpG-DNA internalization via clathrin-mediated endocytosis. In addition, exposure to PM2.5 inhibited various TLR-mediated nitric oxide and cytokine production as well as MAPK and NF-κB signaling. PM2.5 rendered mice more susceptible to staphylococcal skin infections. Our results suggest that exposure to PM impairs TLR signaling and dampens the host defense against staphylococcal skin infections. Our data provide a novel perspective into the impact of PM on protective immunity which is paramount to revealing air pollutant-mediated toxicity on the host immunity.

Therapeutic Efficacy of Weissella cibaria CMU and CMS1 on Allergic Inflammation Exacerbated by Diesel Exhaust Particulate Matter in a Murine Asthma Model.

Background and Objectives: Diesel exhaust particulate matter (DEPM) is an air pollutant that is associated with asthma. In this study, the therapeutic efficacy of Weissella cibaria strains CMU (Chonnam Medical University) and CMS (Chonnam Medical School) 1, together with the drug Synatura, an anti-tussive expectorant, was investigated in a murine asthma model exacerbated by DEPM. Materials and Methods: BALB/c mice were sensitized with ovalbumin (OVA) before intranasal challenge with OVA and DEPM. W. cibaria CMU, CMS1, and Synatura were administered orally for 21 days. Results: Neither Synatura nor W. cibaria strains affected spleen, liver, or lung weights. W. cibaria strains CMU and CMS1 significantly reduced the levels of interleukin (IL)-4, OVA-specific immunoglobulin E (IgE), and total lung collagen in bronchoalveolar lavage fluid (BALF), similar to those with Synatura, regardless of the oral dose concentration (p < 0.05). In addition, the W. cibaria CMU strain significantly alleviated IL-1β, IL-6, IL-12, monocyte chemotactic protein-1, and tumor necrosis factor-α in BALF, whereas the CMS1 strain significantly alleviated IL-10 and IL-12 in BALF (p < 0.05); however, Synatura did not show any statistical efficacy against them (p > 0.05). All concentrations of W. cibaria CMU and low concentrations of W. cibaria CMS1 significantly reduced lung bronchiolar changes and inflammatory cell infiltration. Conclusions: In conclusion, W. cibaria CMU in asthmatic mice showed better efficacy than W. cibaria CMS1 in improving asthma exacerbated by DEPM exposure, as well as better results than pharmaceuticals.

Potential hazards associated with interactions between diesel exhaust particulate matter and pulmonary surfactant

Long term exposure to diesel exhaust particulate matter (DEPM) can induce numerous adverse health effects to the respiratory system. Understanding the interaction between DEPM and pulmonary surfactant (PS) can be an essential step toward preliminary evaluation of the impact of DEPM on pulmonary health. Herein, DEPM was explored for its interaction with 1,2-dipalmitoyl-sn-glycerol-3-phosphocholine (DPPC), the major component of PS. The results indicated that the surface pressure-area (π-A) isotherms of DPPC monolayers shifted toward lower molecular areas and the compression modulus (CS−1) reduced in the presence of DEPM. Atomic force microscopy image showed that DEPM can disrupt the ultrastructure of DPPC monolayers along with the direction of lateral compression. In addition, DPPC can in turn condition the surface properties of DEPM, permitting its agglomeration in aqueous media, which was attributed to the adsorption of DEPM to DPPC. Furthermore, the particle-bound polycyclic aromatic hydrocarbons (PAHs) could be desorbed from DEPM by the solubilization of DPPC and it was positively correlated with the hydrophobicity of PAHs. These findings revealed the toxicity of DEPM-associated PAHs and the role of DPPC in facilitating the removal of the inhaled particles, which can provide a new insight into the potential hazards of airborne particles on lung health.

Investigation on the adsorption characteristics and influencing factors of diesel engine exhaust particulate matter.

In the exhaust pipe, the adsorption process of diesel exhaust particulate matter (PM) is affected by the combination of its adsorption capacity and the environment. A diesel exhaust particle collection system was established to collect samples with different environmental conditions. The adsorption capacity of the samples was characterized by an isothermal adsorption test. Changes in sample characteristics were investigated by scanning electron microscope and thermogravimetric analyzer. The correlation analysis of the factors influencing the adsorption process was performed. The results showed that the diesel exhaust particulate matter has adsorption capacity, the pore diameter is distributed continuously in the range of 8 to 80 nm, and the specific surface area and pore structure parameters are similar to carbon black and belong to the category of mesopores and macropores. As the engine speed increased from 1500 to 3600 r·min-1, the specific surface area of samples increased from 65.408 to 101.885 m2·g-1, and the pore volume expanded from 0.093 to 0.152 mL·g-1, with a more complex pore structure and enhanced adsorption capacity. The samples at the outlet of the exhaust pipe had increased box dimension (DB), moisture, and soluble organic fraction (SOF) content compared to the samples at the inlet of the exhaust pipe. The activation energies (E) of the three samples were reduced by 34.77 kJ∙mol-1, 38.88 kJ∙mol-1, and 47.43 kJ∙mol-1, respectively. Among the influencing factors, the increase of hydrocarbon concentration contributes to the increase of adsorption volume and the reduction of E. The increase of the average temperature inhibits the increase of the DB, and the increase of the temperature difference between the inlet and outlet facilitates the adsorption of water and SOF by samples. The reduction of adsorption time is one of the main reasons for delaying the increase of DB. Average pore diameter has the largest positive correlation with the variation amount of DB, and the growth of the specific surface area and pore volume is the dominant reason for the improvement of adsorption capacity and oxidation activity.

Geniposide, a Principal Component of Gardeniae Fructus, Protects Skin from Diesel Exhaust Particulate Matter-Induced Oxidative Damage

Gardeniae Fructus (GF) is the fruit of Gardenia jasminoides Ellis and is traditionally prescribed to treat pyogenic infections and skin ulcers. This study investigated the protective effects of GF and the underlying mechanism responsible for these effects on diesel exhaust particulate matter- (DEP-) induced skin damage. The protective effects of an ethanolic extract of GF (GFE) and its constituents (geniposidic acid, gardenoside, geniposide, chlorogenic acid, and genipin) were examined by analyzing reactive oxygen species (ROS) production, apoptosis, and tight junction (TJ) protein expression in HaCaT cells. Treatment with GFE dose-dependently inhibited intracellular ROS production and apoptosis by regulating the protein expressions of Bax, Bcl-2, and cytochrome C in DEP-stimulated (100 μg/ml) HaCaT cells. Mechanistic studies revealed that the protective effects of GFE were related to its activation of Nrf2 and HO-1 signaling in HaCaT cells. Geniposide, a main constituent of GFE, enhanced the expression of occludin in DEP-stimulated HaCaT cells. Furthermore, topical application of geniposide reduced the expressions of 8-OHdG and Bax and increased the expression of occludin in the dorsal skin lesions of DEP-stimulated mice. Gardeniae Fructus and its main component geniposide are potential candidates for the repair of DEP-induced skin damage due to their antioxidant and antiapoptotic activities.

Glial activation and inflammation in the NTS in a rat model after exposure to diesel exhaust particles

Airway pollution can affect the central nervous system, but whether this causes glial activation and inflammation in the nucleus of solitary tract (NTS) remains unclear. We used a rat model with exposure to diesel exhaust particulate matter (DEP) at 200 μg/m3 (low exposure) and 1000 μg/m3 (high exposure) for 14 days. Activation of microglia and astrocytes in the NTS was assessed using Iba-1 and glial fibrillary acidic protein (GFAP) staining. The expression of neurotrophic factors including brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), and nerve growth factor (NGF) in the NTS were evaluated by immunofluorescence. Changes in the intracellular structure of NTS neurons were observed via electron microscopy. Inflammatory cytokines and oxidant stress levels in the medulla were also measured. Exposure to DEP can cause NTS inflammation as well as airway inflammation, especially in the H-exposure group. We showed that the numbers of microglia and astrocytes in the NTS, as well as NGF expression in the NTS, were significantly higher in both exposure groups than in controls, but BDNF or GDNF expression was not detected. Exposure to DEP induced ultrastructural changes in NTS neurons as reflected by endoplasmic reticulum dilation, ribosomal loss, mitochondrial vacuolization, and a sparse myelin sheath. Medulla inflammation and an imbalance of oxidants and antioxidants also resulted from exposure to DEP. The H-exposure group showed an imbalance of oxidants and antioxidants with decreased levels of SOD and GSH and increased levels of MDA and ROS compared to the control group (both p < 0.01) in the medulla. Inflammatory cytokines (IL-1β, IL-6, and TNF-α) were also significantly increased in the H-exposure group. Fourteen days of exposure to DEP can affect the NTS neurons in rat. Glial activation and inflammation may play important roles in the response of the NTS to DEP.

Exposure to different fractions of diesel exhaust PM2.5 induces different levels of pulmonary inflammation and acute phase response

AimAmbient fine particulate matter (PM2.5) consists of various components, and their respective contributions to the toxicity of PM2.5 remains to be determined. To provide specific recommendations for preventing adverse effects due to PM2.5 pollution, we determined whether the induction of pulmonary inflammation, the putative pathogenesis for the morbidity and mortality due to PM2.5 exposure, was fractioned through solubility-dependent fractioning. MethodsIn the present study, the water and heptane solubilities-dependent serial fractioning of diesel exhaust particulate matter (DEP), a prominent source of urban PM2.5 pollution, was performed. The pro-inflammatory actions of these resultant fractions were then determined using both an intratracheal instillation mouse model and cultured BEAS-2B cells, a human bronchial epithelial cell line. ResultsInstillation of the water-insoluble, but not -soluble fraction elicited significant pulmonary inflammatory and acute phase responses, comparable to those induced by instillation of DEP. The water-insoluble fraction was further fractioned using heptane, a polar organic solvent, and instillation of heptane-insoluble, but not -soluble fraction elicited significant pulmonary inflammation and acute phase responses. Furthermore, we showed that DEP and water-insoluble DEP, but not water-soluble DEP, activated pro-inflammatory signaling in cultured BEAS-2B cells, ruling out the possibility that the solubility impacts the in vivo distribution and thus the pulmonary inflammatory response.

The Development of Diesel Particulate Filter Technology

With the rapid development of internal combustion engine technology and the widespread popularity of diesel locomotives, the exhaust pollution of internal combustion engines has become a factor that cannot be ignored in air pollution. Particulate matter in diesel engine exhaust is an important culprit in diesel engine exhaust pollution, the harm of which has been widely recognized. This paper introduces the hazards of particulate matter in diesel exhaust, and summarizes DPF for particulate emissions and the regeneration technology of DPF.

Covalent N-arylation by the pollutant 1,2-naphthoquinone activates the EGF receptor

The epidermal growth factor receptor (EGFR) is the most intensively investigated receptor tyrosine kinase. Several EGFR mutations and modifications have been shown to lead to abnormal self-activation, which plays a critical role in carcinogenesis. Environmental air pollutants, which are associated with cancer and respiratory diseases, can also activate EGFR. Specifically, the environmental electrophile 1,2-naphthoquinone (1,2-NQ), a component of diesel exhaust particles and particulate matter more generally, has previously been shown to impact EGFR signaling. However, the detailed mechanism of 1,2-NQ function is unknown. Here, we demonstrate that 1,2-NQ is a novel chemical activator of EGFR but not other EGFR family proteins. We found that 1,2-NQ forms a covalent bond, in a reaction referred to as N-arylation, with Lys80, which is in the ligand-binding domain. This modification activates the EGFR–Akt signaling pathway, which inhibits serum deprivation–induced cell death in a human lung adenocarcinoma cell line. Our study reveals a novel mode of EGFR pathway activation and suggests a link between abnormal EGFR activation and environmental pollutant–associated diseases such as cancer.

Diesel exhaust particle role on gut microbiome and onset of Alzheimer disease neuroinflammation

AbstractBackgroundRecent evidence has emerged to show that diesel exhaust particulate (DEP) pollution can double the risk of getting dementia. Evidence suggest that exposure to high levels of air pollution are significantly more likely to develop dementia‐related diseases including Alzheimer’s disease. DEP is primarily composed of polycyclic aromatic hydrocarbons (PAHs) and nitro‐substituted polycyclic aromatic hydrocarbons (n‐PAHs). PAHs have previously been shown to undergo biotransformation through interactions with human colonic microbiota. The goal of the present study is to determine if DEP may influence selective gut microbiota. We will eventually identify gut‐brain‐axis mechanisms associated with DEP mediated neuroinflammatory mechanisms through microbiota dysbiosis.MethodUsing an in vitro model of the human gastrointestinal tract, EBIOME, we are exploring the human gut bacteria exposed to various concentrations of diesel exhaust particulate matter. Bacterial species were quantified over an extended time‐course to monitor log‐scale changes in colony survival and growth. In order to obtain higher resolution of gut microbiome species meta‐genomic analysis will be also conducted.ResultThe current studies have identified concentration dependent changes in microbiome biodiversity. Through ongoing analysis, it is anticipated that altered biodiversity will lead to decreases in the production of brain penetrant metabolites, such as short‐chain fatty acids including butyrate, acetate, and propionate.ConclusionOur studies provide novel information regarding the role of the gut‐brain‐axis in neuroinflammation in Alzheimer’s disease and other forms of dementia.

Lactic Acid Bacteria Ameliorate Diesel Exhaust Particulate Matter-Exacerbated Allergic Inflammation in a Murine Model of Asthma.

Several air pollution components such as sulfur dioxide, ozone, nitrogen dioxide, and diesel exhaust particulate matter (DEPM) have been linked to the development of asthma. In this study, we investigated the therapeutic potential of three lactic acid bacteria species, Lactobacillus plantarum GREEN CROSS Wellbeing (GCWB)1001, Pediococcus acidilactici GCWB1085, and Lactobacillus rhamnosus GCWB1156, in preventing DEPM-exacerbated asthma in mice. BALB/c mice were first sensitized with ovalbumin (OVA) and were either challenged with OVA or DEPM (DEPM-exacerbated asthma model) by intranasal instillation. All three strains showed no hemolytic activity, suggesting a good safety profile. Oral administration of lactic acid bacteria reduced OVA + DEPM-induced inflammatory infiltration, goblet cell hyperplasia, airway remodeling, and the levels of proinflammatory cytokines and chemokines in bronchoalveolar lavage fluid (BALF). The probiotics also attenuated OVA + DEPM-induced immunoglobulin E (IgE) levels in serum and in BALF, and significantly reduced caspase-3 activity, total collagen level, and matrix metalloproteinase (MMP)-9 activity. In conclusion, lactic acid bacteria such as L. plantarum GCWB1001, P. acidilactici GCWB1085, and L. rhamnosus treatment in mice with asthma showed significant efficacy in preventing lung inflammation exacerbated by DEPM administration.

Evidence for the presence of air pollution nanoparticles in placental tissue cells

Inhaled particulate matter (PM) from combustion- and friction-sourced air pollution adversely affects organs distant from the lung. A putative mechanism for the remote effect of inhaled PM is that ultrafine, nano-sized fraction (<100 nm) translocates across the air-tissue barrier, directly interacting with phagocytic tissue cells. Although PM is reported in other tissues, whether it is phagocytosed by non-respiratory tissue resident cells is unclear.Using the placenta as an accessible organ for phagocytic cells, we sought to seek evidence for air pollution-derived PM in tissue resident phagocytes. Macrophage-enriched placental cells (MEPCs) were isolated, and examined by light and electron microscopy. MEPC carbon was assessed by image analysis (mean μm2/1000 cells); particle composition and numbers were investigated using magnetic analyses and energy dispersive X-ray spectroscopy. MEPCs phagocytic capacity was assessed by culture with diesel exhaust PM in vitro.Fifteen placentas were analysed. Black inclusions morphologically compatible with inhaled PM were identified within MEPCs from all samples (mean ± SEM carbon loading, 1000 MEPCs/participant of 0.004 ± 0.001 μm2). High resolution scanning/transmission electron microscopy revealed abundant nano-sized particle aggregates within MEPCs. MEPC PM was predominantly carbonaceous but also co-associated with a range of trace metals, indicative of high temperature (i.e. exogenous) generation. MEPCs contained readily-measurable amounts of iron-rich, ferrimagnetic particles, in concentrations/particle number concentrations ranging, respectively, from 8 to 50 ng/g and 10 to 60.107 magnetic particles/g (wet wt) MEPCs. Extracted MEPCs (n = 20/ placenta) were phagocytic for PM since all cells showed increased carbon area after culture with diesel PM in vitro (mean ± SEM increase 7.55 ± 1.26 μm2 carbon PM).These findings demonstrate that inhaled, metal-bearing, air pollution-derived PM can not only translocate to distant organs, but is taken up by tissue resident phagocytes in vivo. The human placenta, and hence probably the fetus, thus appears to be a target for such particles.

Chronic exposure to diesel exhaust particulate matter impairs meiotic progression during spermatogenesis in a mouse model

Exposure to ambient PM2.5 may correlate with the decline of semen quality, and the underlying biological mechanism has not been fully understood. In the present study, mice were intratracheally instilled with diesel exhaust PM2.5 (DEP), and its effects on the spermatogenic process as well as the alterations of testicular gene expression profile were assessed. Our results showed that chronic exposure to DEP impaired the fertility of male mice without influencing their libido. Compared with Vehicle-exposed group, the sperm count and motility from DEP-exposed mice were significantly decreased. In addition, immunohistological staining of γH2AX and DMC1, biomarkers for meiotic double strand breaks (DSBs), demonstrated that chronic exposure to DEP comprised the repair of meiotic DSBs, thus disrupting the spermatogenesis. Deep RNA sequencing test showed altered expressions of testicular genes including the GnRH signaling pathway. In summary, our research demonstrated that chronic exposure to DEP may disrupt spermatogenesis through targeting the meiotic recombination, providing a new perspective for the research on the male reproductive system damage caused by air pollution.

Hepatoprotective Effects of Streptococcus thermophilus LM1012 in Mice Exposed to Air Pollutants.

In this study, we explored whether the use of Streptococcus thermophilus LM1012 (TL-LM1012) as a safe probiotic exerts hepatoprotective effects by suppressing oxidative stress and inflammation in vitro and alleviating aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) production in vivo. In a series of safety tests, TL-LM1012 was found to have a negative response to hemolysis and biogenic amines, as well as susceptibility to antibiotics. TL-LM1012 protected cell viability and suppressed cytotoxicity by inhibiting oxidative stress and induced heme oxygenase-1 and superoxide dismutase activity in a dose-dependent manner in diesel exhaust particulate matter (DEPM)-treated HepG2 cells. Moreover, proinflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-6, and IL-1β, were suppressed in DEPM-treated splenocytes. In DEPM-treated mice, oral administration of TL-LM1012 regulated AST, ALT, and LDH production in the serum after 14 days of treatment. These findings indicate that TL-LM1012, a safe probiotic, provides a potent preventive or therapeutic effect against liver disease caused by air pollution.

Investigation of Ceramide involvement in Diesel Exhaust‐Induced Astrocyte Apoptosis

Apoptosis is a complex process involving many different molecules that eventually leads to the programmed death of a cell. Ceramides are believed to function as a second messenger in this process; however, the full involvement of ceramides is under investigation. We are investigating a connection between airborne particulate matter and neurodegenerative processes, including cell death. The primary mission of our research is to better understand how ceramide levels change during apoptosis induced by exposure to diesel exhaust particulate matter (DEP). To track the changing levels of ceramides we performed total lipid extractions on our cell cultures at various timepoints after exposure to DEP. As we gain more understanding on this role of ceramides in apoptosis, we hope to make connections between Alzheimer’s disease and incorrectly functioning ceramide signaling networks. Our current results have indicated a change in ceramide levels during apoptosis at a long timepoint and we continue to work to understand how the ceramide signaling route works.Support or Funding InformationResearch reported in this publication was supported by grant number P20GM103443.