ABSTRACT
Circadian rhythms in metabolically active tissues are crucial for maintaining physical health. Circadian disturbance (CD) can cause various health issues, such as metabolic abnormalities and immune and cognitive dysfunctions. However, studies on the role of CD in immune cell development and differentiation, as well as the rhythmic expression of the core clock genes and their altered expression under CD, remain unclear. Therefore, we exposed C57bl/6j mice to repeated reversed light-dark cycles for 90 days to research the effects of CD on bone marrow (BM) hematopoietic function. We also researched the effects of CD on endogenous circadian rhythms, temporally dependent expression in peripheral blood and myeloid leukocytes, environmental homeostasis within BM, and circadian oscillations of hematopoietic-extrinsic cues. Our results confirmed that when the light and dark cycles around mice were frequently reversed, the circadian rhythmic expression of the two main circadian rhythm markers, the hypothalamic clock gene, and serum melatonin, was disturbed, indicating that the body was in a state of endogenous CD. Furthermore, CD altered the temporally dependent expression of peripheral blood and BM leukocytes and destroyed environmental homeostasis within the BM as well as circadian oscillations of hematopoietic-extrinsic cues, which may negatively affect BM hematopoiesis in mice. Collectively, these results demonstrate that circadian rhythms are vital for maintaining health and suggest that the association between CD and hematopoietic dysfunction warrants further investigation.
Subject(s)
Bone Marrow , Circadian Clocks , Mice , Animals , Bone Marrow/metabolism , Photoperiod , Circadian Rhythm/physiology , Hematopoietic Stem Cells/metabolism , Mice, Inbred C57BL , Circadian Clocks/geneticsABSTRACT
Previous studies have shown that early-life exposure to fine particulate matter (PM2.5) is associated with an increasing risk of autism spectrum disorder (ASD), however, the specific sensitive period of ASD is unknown. Here, a model of dynamic whole-body concentrated PM2.5 exposure in pre- and early-postnatal male offspring rats (MORs) was established. And we found that early postnatal PM2.5 exposed rats showed more typical ASD behavioral characteristics than maternal pregnancy exposure rats, including poor social interaction, novelty avoidance and anxiety disorder. And more severe oxidative stress and inflammatory responses were observed in early postnatal PM2.5 exposed rats. Moreover, the expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN) was down-regulated and the ratios of p-PI3K/PI3K and p-AKT/AKT were up-regulated in early postnatal PM2.5 exposed rats. This study suggests that early postnatal exposure to PM2.5 is more susceptible to ASD-like phenotype in offspring than maternal pregnancy exposure and the activation of PI3K-AKT signaling pathway may represent underlying mechanisms.
Subject(s)
Autism Spectrum Disorder , Particulate Matter , Animals , Female , Male , Pregnancy , Rats , Autism Spectrum Disorder/chemically induced , Autism Spectrum Disorder/metabolism , Particulate Matter/toxicity , Phenotype , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Signal TransductionABSTRACT
Micro(nano)plastic, as a new type of environmental pollutant, have become a potential threat to the life and health of various stages of biology. However, it is not yet clear whether they will affect brain development in the fetal stage. Therefore, this study aims to explore the potential effects of nanoplastics on the development of fetal rat brains. To assess the allocation of NPs (25â¯nm and 50â¯nm) in various regions of the fetal brain, pregnant rats were exposed to concentrations (50, 10, 2.5, and 0.5â¯mg/kg) of PS-NPs. Our results provided evidence of the transplacental transfer of PS-NPs to the fetal brain, with a prominent presence observed in several cerebral regions, notably the cerebellum, hippocampus, striatum, and prefrontal cortex. This distribution bias might be linked to the developmental sequence of each brain region. Additionally, we explored the influence of prenatal exposure on the myelin development of the cerebellum, given its the highest PS-NP accumulation in offspring. Compared with control rats, PS-NPs exposure caused a significant reduction in myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG) expression, a decrease in myelin thickness, an increase in cell apoptosis, and a decline in the oligodendrocyte population. These effects gave rise to motor deficits. In conclusion, our results identified the specific distribution of NPs in the fetal brain following prenatal exposure and revealed that prenatal exposure to PS-NPs can suppress myelin formation in the cerebellum of the fetus.
Subject(s)
Brain , Myelin Sheath , Polystyrenes , Animals , Female , Pregnancy , Brain/drug effects , Brain/embryology , Brain/metabolism , Myelin Sheath/drug effects , Myelin Sheath/metabolism , Rats , Polystyrenes/toxicity , Environmental Pollutants/toxicity , Myelin Basic Protein/metabolism , Maternal Exposure , Nanoparticles/toxicity , Apoptosis/drug effects , Microplastics/toxicity , Rats, Sprague-Dawley , Maternal-Fetal Exchange , Fetus/drug effectsABSTRACT
Ambient ozone (O3) pollution can induce respiratory and cardiovascular toxicity. However, its impact on the metabolome and the underlying mechanisms remain unclear. This study first investigated the serum metabolite changes in rats exposed to 0.5 ppm O3 for 3 months using untargeted metabolomic approach. Results showed chronic ozone exposure significantly altered the serum levels of 34 metabolites with potential increased risk of digestive, respiratory and cardiovascular disease. Moreover, bile acid synthesis and secretion, and arachidonic acid (AA) metabolism became the most prominent affected metabolic pathways after O3 exposure. Further studies on the mechanisms found that the elevated serum toxic bile acid was not due to the increased biosynthesis in the liver, but the reduced reuptake from the portal vein to hepatocytes owing to repressed Ntcp and Oatp1a1, and the decreased bile acid efflux in hepatocytes as a results of inhibited Bsep, Ostalpha and Ostbeta. Meanwhile, decreased expressions of detoxification enzyme of SULT2A1 and the important regulators of FXR, PXR and HNF4α also contributed to the abnormal bile acids. In addition, O3 promoted the conversion of AA into thromboxane A2 (TXA2) and 20-hydroxyarachidonic acid (20-HETE) in the liver by up-regulation of Fads2, Cyp4a and Tbxas1 which resulting in decreased AA and linoleic acid (LA), and increased thromboxane B2 (TXB2) and 20-HETE in the serum. Furthermore, apparent hepatic chronic inflammation, fibrosis and abnormal function were found in ozone-exposed rats. These results indicated chronic ozone exposure could alter serum metabolites by interfering their metabolism in the liver, and inducing liver injury to aggravate metabolic disorders.
Subject(s)
Bile Acids and Salts , Ozone , Rats , Animals , Bile Acids and Salts/metabolism , Bile , Liver/metabolism , Metabolome , Arachidonic Acids/metabolism , Ozone/toxicity , Ozone/metabolismABSTRACT
Oil mist particulate matter (OMPM) causes acute and chronic diseases and exacerbations. Owing to the characteristics of poor ventilation, high oil mist concentration, and a relatively closed working environment, the existence of OMPM in the cabin is inevitable, and its impact on the health of occupations on ships cannot be ignored. However, compared with several studies that summarized the health effects of OMPM from traditional sources, few studies have focused on the occupational exposure risk of OMPM from oil pollution sources in ships. In this study, we collected OMPM from oil pollution in cabins and assessed the exposure to OMPM from oil pollution and the corresponding health risks through acute exposure experiments in rats. OMPM exposure induces protein regulation in the extracellular matrix and immune responses, leading to severe inflammatory responses. The abundance and composition of the lung microbial community changed significantly. It interferes with the lung metabolite levels. However, more research is needed to fully understand the extent of health risks associated with OMPM exposure. Further research on vulnerable groups exposed to OMPM from ships is needed to inform public health interventions.
Subject(s)
Lung Injury , Particulate Matter , Animals , Dysbiosis/chemically induced , Lung , Lung Injury/chemically induced , Particulate Matter/toxicity , Proteomics , RatsABSTRACT
Exposure to PM2.5 can aggravate the occurrence and development of bronchial asthma and fibrosis. Here, we investigated the differences in bronchial injury caused by different exposure modes of PM2.5 (high concentration intermittent exposure and low concentration continuous exposure), and the mechanism of macrophage activation and respiratory immune imbalance induced by PM2.5, leading to bronchial asthma and airway fibrosis using animal and cell models. A "PM2.5 real-time online concentrated animal whole-body exposure system" was used to conduct PM2.5 respiratory exposure of Wistar rats for 12 weeks, which can enhance oxidative stress in rat bronchus, activate epithelial cells and macrophages, release chemokines, recruit inflammatory cells, release inflammatory factors and extracellular matrix, promote bronchial mucus hypersecretion, inhibit the expression of epithelial cytoskeletal proteins, destroy airway barrier, and induce asthma. Furthermore, PM2.5 induced M2 polarization in lung bronchial macrophages through JAK/STAT and PI3K/Akt signaling pathways, and compared with low concentration continuous exposure, high concentration intermittent exposure of PM2.5 could regulate significantly higher expression of TIPE2 protein through promoter methylation of TIPE2 DNA, thereby activating PI3K/Akt signaling pathway and more effectively inducing M2 polarization of macrophages. Additionally, activated macrophages release IL-23, and activated epithelial cells and macrophages released TGF-ß1, which promoted the differentiation of Th17 cells, triggered the Th17 dominant immune response, and activated the TGF-ß1/Smad2 signaling pathway, finally causing bronchial fibrosis. Moreover, when the total amount of PM2.5 exposure was equal, high concentration-intermittent exposure was more serious than low concentration-continuous exposure. In vitro experiments, the co-culture models of PM2.5 with BEAS-2B, WL-38 and rat primary alveolar macrophages further confirmed that PM2.5 could induce the macrophage activation through oxidative stress and TIPE2 DNA methylation, and activate the TGF-ß1/Smad2 signaling pathway, leading to the occurrence of bronchial fibrosis.
Subject(s)
Asthma , Transforming Growth Factor beta1 , Animals , Male , Rats , Asthma/chemically induced , Asthma/genetics , Asthma/metabolism , Epithelial Cells/metabolism , Fibrosis , Macrophage Activation , Methylation , Particulate Matter/toxicity , Particulate Matter/metabolism , Phosphatidylinositol 3-Kinases/genetics , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Rats, Wistar , Transforming Growth Factor beta1/genetics , Transforming Growth Factor beta1/metabolismABSTRACT
The molecular mechanisms of PM2.5 exposure in the male reproductive system, have scarcely been studied. Here, we demonstrate the possible relationship and molecular mechanisms between endoplasmic reticulum stress (ERS), oxidative stress, and reproductive toxicity caused by PM2.5. A "PM2.5 real-time online concentrated animal whole-body exposure system" was employed to expose male Wistar rats to PM2.5 for 12 weeks, which could induce sperm quality decline, apoptosis, inflammation, oxidative stress, ERS, and histopathological damage in the testis. In vitro study on cultured primary testicular spermatogonia and Leydig cells confirmed that treatment with PM2.5 (0-320 µg/mL) for 24 h decreased cell survival rate, increased reactive oxygen species, lactate dehydrogenase and 8-hydroxydeoxyguanosine levels, induced DNA damage, ERS and apoptosis, and inhibit the secretion and synthesis of testosterone in Leydig cells. These results clarified that ERS pathways triggered by oxidative stress could significantly induce CHOP and caspase-12 activation, which are significantly associated with cell apoptosis. However, oxidative stress and ERS inhibitors significantly inhibited the occurrence of these injuries. In conclusion, PM2.5 triggers the ERS pathway and induces DNA damage in rat testicular cells through oxidative stress, ultimately leading to cellular apoptosis. Furthermore, high-concentration intermittent inhalation was more harmful than low-concentration continuous inhalation when the total mass of PM2.5 exposure was the same.
Subject(s)
Endoplasmic Reticulum Stress , Semen , 8-Hydroxy-2'-Deoxyguanosine , Animals , Apoptosis , Caspase 12/metabolism , Lactate Dehydrogenases/metabolism , Male , Oxidative Stress , Particulate Matter/toxicity , Rats , Rats, Wistar , Reactive Oxygen Species/metabolism , TestosteroneABSTRACT
OBJECTIVE: To study the regulatory relationship between ozone-induced mitophagy and pyroptosis in lung epithelial cells. RESULTS: First, type I primary alveolar epithelial cells and male Wistar rats were treated with ozone at different dosages. The ATP content and mitochondrial membrane potential significantly decreased in type I primary alveolar epithelial cells. The mitophagy-related markers and PINK1/Parkin pathway-related proteins, and the co-localization of LC3, Parkin, and mitochondria in type I alveolar epithelial cells indicated that ozone exposure triggered mitophagy. On the other hand, the reactive oxygen species (ROS) inhibitor NAC could significantly alleviate mitophagy in epithelial cells. After treatment with the mitophagy inhibitor MDIVI-1, the levels of the NLRP3 inflammasome, cleaved caspase-1, and N-gasdermin D (N-GSDMD) significantly decreased in the cells. Altogether, these results indicated that mitophagy can be triggered by ozone exposure, and subsequently induces cell death mediated by the NLRP3 inflammasome. Finally, the overexpression and knockdown of NLRP3 confirmed this conclusion. CONCLUSION: Ozone exposure induced oxidative damage, leading to mitochondrial structural and functional damage. Ozone-induced ROS triggered mitophagy through the activation of the PINK1/Parkin signaling pathway, then pyroptosis through activation of the NLRP3 inflammasome.
Subject(s)
Mitophagy , Ozone , Animals , Inflammasomes/metabolism , Lung/metabolism , Male , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Ozone/toxicity , Protein Kinases/metabolism , Pyroptosis/physiology , Rats , Rats, Wistar , Reactive Oxygen Species/metabolism , Ubiquitin-Protein Ligases/metabolismABSTRACT
Non-coding RNAs appear to be involved in the regulation of the nervous system. However, no competing endogenous RNA (ceRNA) network related to PM2.5 damage in the hippocampal function has yet been constructed. Herein, we used whole-transcriptome sequencing technology to systematically study the ceRNA network in rat hippocampi after PM2.5 exposure. We identified 100 circRNAs, 67 lncRNAs, 28 miRNAs, and 539 mRNAs and constructed the most comprehensive ceRNA network to date, to our knowledge. Gene Ontology and KEGG analyses showed that the network molecules are involved in synapses, neural projections, and neural development and involve signal pathways such as the synaptic vesicle cycle. Finally, the expression of the differentially expressed RNAs confirmed by quantitative real-time PCR was consistent with the sequencing data. This study systematically dissected the ceRNA atlas related to cognitive memory function in the hippocampal tissue of PM2.5-exposed rats for the first time, to our knowledge, and promotes the development of potential new treatments for cognitive impairment.
Subject(s)
Air Pollutants/toxicity , Gene Regulatory Networks , Hippocampus/metabolism , Particulate Matter/toxicity , Transcriptome , Animals , HEK293 Cells , Hippocampus/drug effects , Humans , Male , RNA, Circular/genetics , RNA, Circular/metabolism , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Rats , Rats, WistarABSTRACT
N-terminal heptad repeat (NHR)-derived peptide (N-peptide) fusion inhibitors, which are derived from human immunodeficiency virus (HIV) envelope glycoprotein 41 (gp41), are limited by aggregation and unstable trimer conformation. However, they could function as potent inhibitors of viral infection by forming a coiled-coil structure covalently stabilized by interchain disulfide bonds. We previously synthesized N-peptides with potent anti-HIV-1 activity and high stability by coiled-coil fusion and covalent stabilization. Here, we attempted to study the effects of NHRs of chimeric N-peptides by fusing de novo coiled-coil isopeptide bridge-tethered T21 peptides of different NHR lengths. Peptides (T21N23)3 and (T21N36)3 was a more potent HIV-1 fusion inhibitor than (T21N17)3. The site of isopeptide bond formation was precisely controlled and had little influence on N-peptide properties. The N-peptide (T21N36)3, which had a similar conformation as the NHR trimer and interacted well with the C34 peptide, may be useful for screening other C-peptides and small-molecule fusion inhibitors, and for studying the interactions between the NHR trimer and C-terminal heptad repeats.
Subject(s)
Anti-HIV Agents/pharmacology , HIV Envelope Protein gp41/pharmacology , HIV Fusion Inhibitors/pharmacology , HIV Infections/drug therapy , HIV-1/drug effects , Peptide Fragments/pharmacology , Anti-HIV Agents/chemical synthesis , Anti-HIV Agents/chemistry , Dose-Response Relationship, Drug , HIV Envelope Protein gp41/chemical synthesis , HIV Envelope Protein gp41/chemistry , HIV Fusion Inhibitors/chemical synthesis , HIV Fusion Inhibitors/chemistry , Humans , Microbial Sensitivity Tests , Molecular Structure , Peptide Fragments/chemical synthesis , Peptide Fragments/chemistry , Structure-Activity RelationshipABSTRACT
Smoking is associated with an increased risk of respiratory diseases, including lung cancer and asthma. However, the mechanisms or diagnostic markers for smoking-related diseases remain largely unknown. Here we investigated the role of cigarette smoke condensate (CSC) in the regulation of human bronchial epithelial cell (BEAS-2B) behavior. We found that exposure to CSC significantly inhibited BEAS-2B cell viability, impaired cell morphology, induced cell apoptosis, triggered oxidative damage, and promoted inflammatory response, which suggests a deleterious effect of CSC on bronchial epithelial cells. In addition, CSC markedly altered the expression of apoptosis-associated protein factors, including p21, soluble tumor necrosis factor receptor 1, and Fas ligand. In sum, our study identified a panel of novel protein factors that may mediate the actions of CSC on bronchial epithelial cells and have a predictive value for the development and progression of smoking-related diseases, thus providing insights into the development of potential diagnostic and therapeutic strategies against these diseases.
Subject(s)
Apoptosis Regulatory Proteins/biosynthesis , Bronchi/metabolism , Cigarette Smoking/metabolism , Epithelial Cells/metabolism , Gene Expression Regulation , Oxidative Stress , Bronchi/pathology , Cell Line , Cigarette Smoking/pathology , Epithelial Cells/pathology , HumansABSTRACT
The presence of disinfection by-products (DBPs) increases the mutagenicity of water and may pose adverse health effects. Gut microbiota exerts a fundamental role on host physiology, and how extrinsic perturbations influence its composition has been increasingly examined. However, the effect of DBPs on gut microbiota is still poorly understood. In the present study, adult zebrafish were exposed to different concentrations of dichloroacetamide (DCAcAm, an emerging nitrogenous DBP) for 30 days. Sequencing of 16S rRNA amplicons revealed a significant change in the richness and diversity of microbiota in the gut of DCAcAm-exposed zebrafish. At the phylum level, the abundance of Proteobacteria decreased and the abundance of Fusobacteria and Firmicutes increased significantly in the gut after exposure to 100 and 500 µg/L DCAcAm. At the genus level, the abundances of several bacteria which are considered pathogens or opportunistic pathogens in fish and closely related to fish metabolism, disease and inflammation (Aeromonas, Stenotrophomonas, Bacteroides and Ralstonia) increased in the DCAcAm-treated groups. Our results reveal that DBPs in drinking water potentially affect gut microbiota composition, which may contribute to the toxicity assessment of DBPs in future and provide new insight into the complex interactions between the DBPs in drinking water and host health.
Subject(s)
Acetamides/toxicity , Disinfectants/toxicity , Gastrointestinal Microbiome , Water Purification , Zebrafish/microbiology , Animals , Disinfection , Drinking Water/chemistry , RNA, Ribosomal, 16SABSTRACT
Our study determined the toxic effects of zinc oxide (ZnO) particles with different diameters on dopaminergic (DA) neurons, the role of ubiquitin C-terminal hydrolase L1 (UCH-L1) for ZnO particles-induced neurotoxicity, and corresponding molecular mechanisms. We constructed an in vitro cell injury model for DA neurons to analyze the cytotoxicity of ZnO particles using SH-SY5Y cells. Following cell viability assays and flow cytometry, we found that the cytotoxicity of ZnO particles was affected by particle size, time, and dose of exposure. For example, the toxicity of ZnO particles with 50â¯nm or 100â¯nm diameter was stronger than that of ZnO particles with 1000â¯nm diameter. Furthermore, ZnO particles exposure resulted in a significant decrease in UCH-L1 expression in SH-SY5Y; whereas UCH-L1 overexpression led to a significant increase in cell viability and a sharp decrease in ROS level. Western blotting and adenovirus transfection found that exposure to ZnO particles with different diameters all activate the NF-κB signaling in SH-SY5Y cells; whereas UCH-L1 over-expression resulted in increased levels of IκBα, an endogenous inhibitor of NF-κB signaling pathway. ZnO particles with different diameters all induced cytotoxicity in DA neurons, which may be related to the free Zn2+ in the suspension. Regarding the neurotoxic effect of ZnO particles, UCH-L1 protects against and/or alleviates neuronal damage, possibly by deubiquitination of the endogenous inhibitor, IκBα, which leads to activation of NF-κB signaling. Therefore, one possible mechanism for ZnO particle-induced neurotoxicity may be mediated via the down-regulation of UCH-L1 expression in DA cells.
Subject(s)
Dopaminergic Neurons/drug effects , NF-KappaB Inhibitor alpha/metabolism , NF-kappa B/metabolism , Ubiquitin Thiolesterase/metabolism , Zinc Oxide/toxicity , Apoptosis/drug effects , Cell Line, Tumor , Cell Survival/drug effects , Dopaminergic Neurons/metabolism , Dopaminergic Neurons/pathology , Down-Regulation , Humans , NF-KappaB Inhibitor alpha/genetics , Particle Size , Signal Transduction/drug effects , Surface Properties , Zinc Oxide/chemistryABSTRACT
Tris (1,3-dichloro-2-propyl) phosphate (TDCIPP) is one of the widely used organophosphorus flame retardants (OPFRs), which are regarded as suitable substitutes for brominated flame retardants (BFRs). Previously, we have validated the toxicity of TDCIPP in PC12 cells owing to the induced alterations in GAP43, NF-H, CaMK2a/2b, and tubulin α/ß proteins; however, limited information is currently available on the toxicity and mechanism of TDCIPP. In the present study, cytotoxicity effects were evaluated by exposing PC12 cells to different concentrations of TDCIPP (0-50 µM) for 4 days. To explore the possible mechanisms through which cytotoxicity is induced, changes in intracellular [Ca2+ ]i levels and the activation of calmodulin dependent protein kinase 2 (CaMK2), c-Jun N-terminal kinase (JNK), extracellular regulated protein kinases (ERK1/2), and p38 mitogen-activated protein kinases (MAPK) pathways were evaluated. Furthermore, PC12 cells were pretreated with CaMK2 inhibitor KN93 to investigate the relationship between TDCIPP-induced phosphorylation of CaMK2 and activation of JNK, ERK1/2, and p38 MAPK pathways. Our results indicate that TDCIPP-induced toxicity might be associated with the overload of [Ca2+ ]i levels, increased phosphorylation of CaMK2, and activation of the JNK, ERK1/2, and p38 MAPK pathways, the lattermost of which was further demonstrated to be partially elicited by the CaMK2 phosphorylation.
Subject(s)
Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism , Flame Retardants/toxicity , MAP Kinase Signaling System/drug effects , Organophosphorus Compounds/toxicity , Animals , Cell Survival/drug effects , Enzyme Activation/drug effects , JNK Mitogen-Activated Protein Kinases/metabolism , Mitogen-Activated Protein Kinase 3/metabolism , Mitogen-Activated Protein Kinases/metabolism , PC12 Cells , Phosphorylation , Protein Serine-Threonine Kinases/metabolism , Rats , p38 Mitogen-Activated Protein Kinases/metabolismABSTRACT
Rapid social and industrial development has resulted in an increasing demand for fossil fuel energy, which increases particulate matter (PM) pollution. In this study, we employed a simple one-step electrospinning technique to fabricate polysulfone (PSF) fiber membranes for PM filtration. A 0.3 g/mL polymer solution with an N,N-dimethylformamide:tetrahydrofuran volume ratio of 3:1 yielded uniform and bead-free PSF fibers with a diameter of approximately 1.17 µm. The PSF fiber membrane exhibited excellent hydrophobicity and mechanical properties, including a tensile strength of 1.14 MPa and an elongation at break of 116.6%. Finally, the PM filtration performance of the PSF fiber membrane was evaluated. The filtration efficiencies of the membrane for PM2.5 and PM1.0 were approximately 99.6% and 99.2%, respectively. The pressure drops were 65.0 and 65.2 Pa, which were significantly lower than those of commercial air filters. Using this technique, PSF fiber membrane filters can be easily fabricated over a large area, which is promising for numerous air filtration systems.
ABSTRACT
BACKGROUND: Moringa oleifera leaves are rich in bioactive substances. PURPOSE: The purpose of this study was to evaluate the effects of Moringa oleifera leaf aqueous extract supplements on energy metabolism and antioxidant function in young male adults. METHODS: Forty-four young male adults (26.3 ± 3.5 years) were randomly assigned to two groups: a supplement group (n = 23) receiving aqueous extract of Moringa oleifera leaves and a placebo group (n = 21). The supplementation period lasted for 30 days. Baseline measurements were taken at the beginning of the study, and further measurements were taken at the end of the supplementation period. Changes in upper- and lower-body strength, treadmill endurance, and certain blood biochemical parameters were evaluated. RESULTS: After 30 days of supplementation, participants in the supplement group exhibited enhanced performance in push-ups and treadmill exhaustion tests compared to the placebo group. Levels of glucose, urea, malondialdehyde, and glutathione peroxidase activity in serum were also improved in the supplement group. CONCLUSION: The findings suggest that Moringa oleifera leaf aqueous extracts have the potential to improve post-exercise energy metabolism and antioxidant function in young male adults.
Subject(s)
Antioxidants , Energy Metabolism , Moringa oleifera , Plant Extracts , Plant Leaves , Humans , Moringa oleifera/chemistry , Male , Plant Extracts/pharmacology , Adult , Plant Leaves/chemistry , Antioxidants/pharmacology , Pilot Projects , Young Adult , Energy Metabolism/drug effects , Dietary Supplements , Glutathione Peroxidase/blood , Glutathione Peroxidase/metabolism , Malondialdehyde/blood , Exercise , Blood Glucose/drug effects , Muscle Strength/drug effects , Urea/blood , Exercise Test , Double-Blind MethodABSTRACT
Metabolites produced by the human gut microbiota play an important role in fighting and intervening in inflammatory diseases. It remains unknown whether immune homeostasis is influenced by increasing concentrations of air pollutants such as oil mist particulate matters (OMPM). Herein, we report that OMPM exposure induces a hyperlipidemia-related phenotype through microbiota dysregulation-mediated downregulation of the anti-inflammatory short-chain fatty acid (SCFA)-GPR43 axis and activation of the inflammatory pathway. A rat model showed that exposure to OMPM promoted visceral and serum lipid accumulation and inflammatory cytokine upregulation. Furthermore, our research indicated a reduction in both the "healthy" microbiome and the production of SCFAs in the intestinal contents following exposure to OMPM. The SCFA receptor GPR43 was downregulated in both the ileum and white adipose tissues (WATs). The OMPM treatment mechanism was as follows: the gut barrier was compromised, leading to increased levels of lipopolysaccharide (LPS). This increase activated the Toll-like receptor 4 Nuclear Factor-κB (TLR4-NF-κB) signaling pathway in WATs, consequently fueling hyperlipidemia-related inflammation through a positive-feedback circuit. Our ï¬ndings thus imply that OMPM pollution leads to hyperlipemia-related inflammation through impairing the microbiota-SCFAs-GPR43 pathway and activating the LSP-induced TLR4-NF-κB cascade; our findings also suggest that OMPM pollution is a potential threat to humanmicrobiota dysregulation and the occurrence of inflammatory diseases.
Subject(s)
Gastrointestinal Microbiome , Hyperlipidemias , Humans , Rats , Animals , NF-kappa B/metabolism , Receptors, G-Protein-Coupled/metabolism , Toll-Like Receptor 4 , Inflammation/chemically induced , Inflammation/metabolism , Signal Transduction , Fatty Acids, Volatile/metabolismABSTRACT
Microplastics have emerged as a prominent global environmental contaminant, and they have been found in both human placenta and breast milk. However, the potential effects and mechanisms of maternal exposure to microplastics at various gestational stages on offspring neurodevelopment remain poorly understood. This investigation delves into the potential neurodevelopmental ramifications of maternal exposure to polystyrene nanoplastics (PS-NPs) during distinct phases of pregnancy and lactation. Targeted metabolomics shows that co-exposure during both pregnancy and lactation primarily engendered alterations in monoamine neurotransmitters within the cortex and amino acid neurotransmitters within the hippocampus. After prenatal exposure to PS-NPs, fetal rats showed appreciably diminished cortical thickness and heightened cortical cell proliferation. However, this exposure did not affect the neurodifferentiation of radial glial cells and intermediate progenitor cells. In addition, offspring are accompanied by disordered neocortical migration, typified by escalated superficial layer neurons proliferation and reduced deep layer neurons populations. Moreover, the hippocampal synapses showed significantly widened synaptic clefts and diminished postsynaptic density. Consequently, PS-NPs culminated in deficits in anxiolytic-like behaviors and spatial memory in adolescent offspring, aligning with concurrent neurotransmitter and synaptic alterations. In conclusion, this study elucidates the sensitive windows of early-life nanoplastic exposure and the consequential impact on offspring neurodevelopment.
Subject(s)
Lactation , Maternal Exposure , Prenatal Exposure Delayed Effects , Animals , Female , Pregnancy , Lactation/drug effects , Maternal Exposure/adverse effects , Hippocampus/drug effects , Hippocampus/growth & development , Polystyrenes/toxicity , Male , Microplastics/toxicity , Rats, Sprague-Dawley , Rats , Neurons/drug effects , Cell Proliferation/drug effects , Neurotransmitter Agents/metabolism , Nanoparticles/toxicity , Brain/drug effects , Brain/growth & developmentABSTRACT
Mitochondria and endoplasmic reticulum (ER) are essential organelles playing pivotal roles in the regulation of cellular metabolism, energy production, and protein synthesis. In addition, these organelles are important targets susceptible to external stimuli, such as environmental pollutants. Exposure to environmental pollutants can cause the mitochondrial damage, endoplasmic reticulum stress (ERS), and oxidative stress, leading to cellular dysfunction and death. Therefore, understanding the toxic effects and molecular mechanisms of environmental pollution underlying these processes is crucial for developing effective strategies to mitigate the adverse effects of environmental pollutants on human health. In the present study, we summarized and reviewed the toxic effects and molecular mechanisms of mitochondrial damage, ERS, and oxidative stress caused by exposure to environmental pollutants as well as interactions inducing the cell apoptosis and the roles in exposure to environmental pollutants.
ABSTRACT
In the original publication [...].