Cumulative Oxidative Stress Research Articles

Facile construction of dual-response super-resolution probes for tracking organelles dynamics.

Super-resolution imaging techniques, such as structured illumination microscopy (SIM), have enabled researchers to obtain nanoscale organelle-level outputs in living systems, but they impose additional stringent requirements on fluorescence probes. However, high-performance, custom-designed SIM probes that can explain underlying biological processes remain unavailable. Herein, a customizable engineering toolkit is developed for the facile assembly of SIM probes suitable for subcellular component detection. This toolkit is used to customize a fluorescent molecule, CPC (coumarin-phenylhydrazine-carboxyl), capable of simultaneously monitoring peroxynitrite (ONOO-) and polarity distribution in mitochondria and lipid droplets (LDs), respectively, through functional ON-OFF mechanisms. The customized CPC molecule demonstrated excellent imaging capabilities under SIM, enabled the successful localization of multiple organelles, and reliably tracked the distribution of different components, thus facilitating the study of the interplay between organelles. Using CPC, the physical transition of intracellular LDs is demonstrated from heterogeneity to homogeneity. This was specifically observed during ferroptosis where the polarity of the LDs increased and their morphology became more contracted. Furthermore, the loss of LDs functionality could not counteract the accumulation of ONOO- within the mitochondria, leading to the decoupling of mitochondrial LDs during ferroptosis. These results confirmed the potential mechanism of LDs dysfunction and decoupling triggered via cumulative mitochondrial oxidative stress during ferroptosis. To summarize, this toolkit will be a powerful tool for examining subtle variations among components during the interplay between different organelles, thus offering novel avenues for understanding and treating related diseases.

Biosafe Polydopamine-Decorated MnO2 Nanoparticles with Hemostasis and Antioxidative Properties for Postoperative Adhesion Prevention.

Surgical bleeding and cumulative oxidative stress are significant factors in the development of postoperative adhesions, which are always associated with adverse patient outcomes. However, effective strategies for adhesion prevention are currently lacking in clinical practice. In this study, we propose a solution using polydopamine-decorated manganese dioxide nanoparticles (MnO2@PDA) with rapid hemostasis and remarkable antioxidant properties to prevent postsurgical adhesion. The PDA modification provides MnO2@PDA with enhanced tissue adhesiveness and hemocompatibility with negligible hemolysis. Furthermore, MnO2@PDA exhibits impressive antioxidant and free radical scavenging properties, protecting cells from the negative effects of oxidative stress. The hemostatic activity of MnO2@PDA is evaluated in a mouse truncated tail model and a liver injury model, with results demonstrating reduced bleeding time and volume. The in vivo test on a mouse cecal abrasion model shows that MnO2@PDA exhibits excellent antiadhesion properties coupled with alleviated inflammation around the damaged tissue. Therefore, MnO2@PDA, which exhibits high biosafety, rapid hemostasis, and beneficial antioxidant capacity, displays exceptional antiadhesion performance, holding great potential for clinical applications to prevent postoperative adhesion.

Prenatal exposure to air pollution and BWGA Z-score: Modifying effects of placenta leukocyte telomere length and infant sex

BackgroundAir pollutants, such as fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3), have been associated with adverse birth outcomes, including low birth weight, often exhibiting sex-specific effects. However, the modifying effect of placental telomere length (TL), reflecting cumulative lifetime oxidative stress in mothers, remains unexplored. MethodUsing data from a Northeastern U.S. birth cohort (n = 306), we employed linear regression and weighted quantile sum models to assess trimester-average air pollution exposures and birth weight for gestational age (BWGA) z-scores. Placental TL, categorized by median split, was considered as an effect modifier. Interactions among air pollutants, placental TL, infant sex, and BWGA z-score were evaluated. ResultsWithout placental TL as a modifier, only 1st trimester O3 was significantly associated with BWGA z-scores (coefficient: 0.33, 95% CI: 0.03, 0.63). In models considering TL interactions, a significant modifying effect was observed between 3rd trimester NO2 and BWGA z-scores (interaction p-value = 0.02). Specifically, a one interquartile range (1-IQR) increase in 3rd trimester NO2 was linked to a 0.28 (95% CI: 0.06, 0.52) change in BWGA z-score among shorter placental TL group, with no significant association among longer TL group. Among male infants, there were significant associations between 3rd trimester PM2.5 exposure and BWGA z-scores in the longer TL group (coefficient: −0.34, 95% CI: −0.61, −0.02), and between 1st trimester O3 exposure and BWGA z-scores among males in the shorter TL group (coefficient: 0.59, 95% CI: 0.06, 1.08). For females, only a negative association in 2nd trimester mixture model was observed within the longer TL group (coefficient: −0.10, 95% CI: −0.21, −0.01). ConclusionThese findings highlight the need to consider the complex interactions among prenatal air pollutant exposures, placental TL, and fetal sex to better elucidate those at greatest risk for adverse birth outcomes.

Research efficacy of gaseous ozone therapy as an adjuvant to periodontal treatment on oxidative stress mediators in patients with type 2 diabetes: a randomized clinical trial

BackgroundChronic inflammation and cumulative oxidative stress have been theorized as two common pathways of the interconnection between periodontitis and diabetes. Improvement in oxidizing status has been demonstrated in periodontal patients with diabetes treated with proper non-surgical periodontal treatment. In addition to periodontal treatment, Gaseous ozone therapy has been reported to possess anti-inflammatory properties and the ability to stimulate the endogenous antioxidant defence mechanism. To date, the antioxidant effect of gaseous ozone, in addition with periodontal treatment in diabetic patients, has been examined in only one study. The aim of this study was to determine the efficacy of gaseous ozone therapy as an alternative approach to supporting non-surgical periodontal therapy (NSPT), aimed at improving antioxidant machinery and interfering with ROS production on plasma levels in diabetic individuals diagnosed with moderate or severe periodontitis.MethodsOne hundred and eighty patients with periodontitis and type 2 diabetes mellitus were randomly assigned to receive non-surgical periodontal treatment (NSPT) plus gaseous ozone therapy (A) NSPT alone (B). Clinical and periodontal parameters -Bleeding on probing (BOP), Periodontal pocket depth (PPD), and Clinical attachment Level (CAL)- and plasma levels of oxidant-antioxidant (TOS- TAOS) levels, glutathione (GSH), and malondialdehyde (MDA) were recorded at baseline and at 3- (T1) and at 6-months (T2) after treatment.ResultsBoth treatments were efficacious in reducing clinical parameters. However, there were no significant differences regarding oxidative stress parameters in group A compared to group B.ConclusionsIn the present study, gaseous ozone therapy did not enhance the effect of periodontal treatment in reducing oxidative stress in plasma levels of periodontitis patients with type II diabetes.Trial registrationThe study was registered with ISRCTN1728169 (23/07/2022).

Mechanism of nephrotoxicity induced by chronic exposure of bisphenol A in mice based on oxidative stress and cell apoptosis

Bisphenol A (BPA) is widely used to produce epoxy resin and polycarbonate plastic products. In severe cases, these plastics may release BPA, which then infiltrates into the environment. Various concentrations of BPA have been found in most biological fluid. Its presence has been well shown to be closely related to many chronic diseases, including chronic kidney disease (CKD). However, little is known regarding the adverse effects of BPA exposure and its succedent cellular events on CKD. Hence, in the current in vivo study, we aimed to assess the effects of chronic exposure to BPA on animal nephrotoxicity through investigating oxidative stress and apoptosis. Upon exposure to BPA at 0.01, 0.1, and 1 mg/L via drinking water for four weeks, the mated and pregnant females were continuously exposed to BPA until weaning. Subsequently, three weeks old F1-male neonates were also orally challenged with the same three doses of BPA for ten weeks. The results showed that the kidneys of 0.1 and 1 mg/L BPA-treated mice were seriously damaged; the contents of serum renal function indexes and lipid peroxidation products were significantly increased, including urea nitrogen, creatinine, uric acid, and thiobarbituric acid reactive substances; the morphological structure of mouse kidneys was impaired; the expressions of antioxidant-related genes at mRNA and protein levels from mouse kidneys were markedly diminished, including glutathione-S-transferase, superoxide dismutase, and catalase; the expressions of genes and proteins related to apoptosis index (ratio of Bax/Bcl-1 and Caspase-3) were significantly enhanced. The data manifested that cumulative oxidative stress and apoptosis might play an essential role in the animal nephrotoxicity induced by chronic exposure to BPA.

817 Encapsulated activated-grape seed extract (E-AGSE): A novel liposome-based formulation that promotes anti-aging, brightening and hydration in human skin

Protein phosphatase 2A (PP2A) is a critical target to control cumulative oxidative stress and chronic inflammation during skin aging by reversible methylation of the C-terminal leucine of the PP2A catalytic subunit (PP2Ac). A novel, proprietary Activated-Grape Seed Extract (AGSE), enriched for PP2A-activating flavonoids, was recently developed, and has demonstrated potent antioxidant and anti-inflammatory activities. AGSE is a dark, purple-colored powder with limited solubility, which restricts its use in a broad range of formulations.

Polydopamine-Based Nanocomposite as a Biomimetic Antioxidant with a Variety of Enzymatic Activities for Parkinson's Disease.

Overproduction of reactive oxygen species (ROS) and cumulative oxidative stress induce the degeneration of neuromelanin-containing dopaminergic neurons in the substantia nigra pars compacta (SNpc) of PD patients. Due to its redox property, melanin-like polydopamine (PDA) has been studied for its ability to remove ROS with a series of antioxidant enzyme mimetic activities including superoxide dismutase (SOD) and catalase (CAT). Glutathione peroxidase (GPx) is important for maintaining ROS metabolic homeostasis, but only a few GPx-like nanozymes have been studied for in vivo therapy. As we know, selenocysteine is essential for the antioxidant activity of GPx. Hence, we co-synthesized PDA with selenocystine (SeCys) to prepare a nanocomposite (PDASeCys) with GPx-like activity. The results showed that the PDASeCys nanocomposite has the same CAT and SOD enzymatic activities as PDA but better free radical scavenging efficiency and additional GPx enzymatic activity than PDA. In the 1-methyl-4-phenyl-pyridine ion (MPP+)-induced PD cell model, PDASeCys could increase intracellular GPx levels effectively and protect SH-SY5Y neuronal cells from oxidative stress caused by MPP+. In vivo, the PDASeCys nanocomposite effectively inhibited 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinium (MPTP)-induced Parkinson-related symptoms of mice when it was injected into the substantia nigra (SN). This polydopamine-based nanocomposite containing selenocystine with a variety of enzymatic activities including GPx-like activity synthesized by a one-pot method provides convenience and safety in the neuromelanin-like nanozyme-based therapeutic strategy for oxidative stress-induced PD.

Mixture effects of air pollutants on children’s urinary levels of 8-isoprostane, a biomarker of oxidative stress

BACKGROUND AND AIM: In single-pollutant models, individual air pollutants are reported to be associated with elevated levels of urinary 8-isoprostane, a marker of oxidative stress. Several air pollutants are highly correlated and might have joint effects in inducing oxidative stress, best assessed using mixture methods. METHODS: Urinary total 8-isoprostane was measured in 299 children (ages 6–8) from the Fresno, CA area and adjusted for creatinine levels. Individual-level exposure to seven pollutants: (sum of 4-, 5-, and 6-ring polycyclic aromatic hydrocarbon compounds (PAH456), nitrogen dioxide (NO₂), carbon monoxide (CO), ozone (O₃), elemental carbon (EC), and particulate matter 2.5 μm (PM2.5) and 10 μm in diameter (PM10)) at the primary residential location was modelled with a spatiotemporal model up to a year prior to outcome assessment. To estimate mixture cumulative, potential non-linear and interactions in effects of pollutants on levels of 8-isoprostane, we relied on weighted quantile sum (WQS) regression and Bayesian kernel machine regression (BKMR). RESULTS:WQS regression indicated a 70% (95% CI: 11%, 130%) increase in the urinary levels of the 8-isoprostane associated with a tertile increase in the WQS index of the air pollution mixture averaged over a 6-month period. O₃, EC and PAH456 contributed most to this overall mixture effect (sum of average weights = 79%). Associations were lower in magnitude and CIs included the null for other exposure windows. BKMR did not yield a significant mixture effect, although, similar to WQS, this model highlighted O₃, EC, and PAH456 as important contributors to the overall mixture effect (posterior inclusion probabilities range: 41 to 57%). BKMR was also suggestive of interactions between various pollutants. CONCLUSIONS:Air pollutants may induce cumulative and joint oxidative stress effects in children. Future studies with larger samples may help confirm findings on the magnitude of mixture effects as well as presence of interactions between pollutants. KEYWORDS: Air pollution, Mixtures, Oxidative stress

113 Encapsulated Activated-Grape Seed Extract (ACTIVITIS™) inhibits demethylation of PP2A promoting anti-aging benefits and barrier repair for human skin

Cumulative oxidative stress and chronic inflammation are critical during skin aging. One pathway that regulates both processes involves Protein phosphatase 2A (PP2A), a serine/threonine phosphatase. Reversible methylation of the C-terminal leucine of the PP2A catalytic subunit (PP2Ac) plays a crucial role in regulating PP2A function. Oxidative stress has been previously shown to dramatically decrease methylation of the C-terminal leucine of the PP2A catalytic subunit (PP2Ac) in dermal fibroblasts. Previously, we developed a novel, proprietary grape seed extract called Activated-Grape Seed Extract, or ACTIVITIS™ (INCI name: anthocyanins and hydrolyzed proanthocyanidins) which is enriched for PP2A-activating flavonoids with increased potency in preventing PP2A demethylation when compared to commercial Grape Seed Extract. To enhance skin delivery and other potential benefits of ACTIVITIS™, we developed a chemical encapsulation formulation utilizing a liposome-based approach. Results demonstrate that this novel encapsulated form of ACTIVITIS™ retains PP2A demethylating activity with similar potency as the non-encapsulated form. To explore the potential benefits of encapsulated ACTIVITIS™, we performed in vitro assays utilizing 3D epidermal skin tissue models and UVB irradiation. We found encapsulated ACTIVITIS™ significantly increases both cell proliferation (Ki67) and skin barrier (Filaggrin) marker expression after UVB irradiation. Moreover, encapsulated ACTIVITIS™ formulation decreases DNA damage marker Cyclobutane pyrimidine dimers (CPD), thus enhancing epidermal integrity and barrier repair after UVB-induced effects. Lastly, clinical results in human subjects demonstrates that encapsulated ACTIVITIS™ is well tolerated and provides anti-aging benefits such as improving fine lines and wrinkles when applied topically.

Association between nutrient intake and telomere length in Japanese female university students

Objective Telomere length can be a biomarker of cumulative oxidative stress and inflammation indicating biological aging. Previous studies examined association of nutrient intake with telomere length targeting middle-aged and elderly individuals. This study examined whether dietary macro- and micronutrient intake was associated with telomere length in young females. Methods Seventy-four Japanese young females (median (interquartile range) age was 19 (19 − 20) years) participated. We estimated their intake of nutrients (energy, protein, fat, carbohydrate, essential elements, vitamins, fatty acids, and dietary fibre) using a semi-quantitative food frequency questionnaire and measured telomere length (T/S ratio, the ratio of telomere repeat copy number (T) to single-copy gene number (S)) of DNA extracted from blood by qPCR. The association between telomere length and tertiles of nutrient intake were analysed. Results The median (interquartile range) of telomere length was 0.70 (0.52 − 0.98). Vitamin A intake was positively associated with telomere length (tertile 1 vs. 2, coefficient [95% confidence interval] = 0.42 [0.12, 0.71]; tertile 1 vs. 3, coefficient [95% confidence interval] = 0.33 [0.04, 0.62]) after adjusting for covariates (age, BMI, passive smoking, and drinking). Conclusions Our findings suggest that variation in vitamin A intake might influence telomere attrition in healthy individuals.

MiRNA-146a-5p mitigates stress-induced premature senescence of D-galactose-induced primary thymic stromal cells

Senescent thymic stromal cells (TSCs) producing senescence-associated secretory phenotype (SASP) may play a role at later phases of thymic involution. However, the etiology and mechanisms responsible for TSC senescence remain to be elucidated. In the present study, the effects of oxidative stress on TSCs and role of miRNA-146a-5p in stress-induced premature senescence (SIPS) were identified. D-galactose (D-gal) induced oxidative stress in primary TSCs and a limited cumulative oxidative stress induced premature senescence but not apoptosis of TSCs. miRNA-146a-5p overexpression can mitigate the SIPS by targeting tumor necrosis factor receptor-associated factor 6 (TRAF6) instead of increasing autophagy clearance. Furthermore, exogenous miRNA-146a-5p reversed the upregulation of chemokines including Cxcl5, pro-inflammatory cytokines, and antimicrobial peptides in TSCs with SIPS. In conclusion, the accumulated oxidative stress may be partially responsible for senescence in TSCs and modulation of miRNA-146a-5p may attenuate this process.

Shedding light on human cerebral lipofuscin: An explorative study on identification and quantification.

Increased oxidative stress has been associated with several neurodegenerative diseases such as Alzheimer's disease, but also with neurological diseases sharing pathophysiological pathways like epilepsy. Lipofuscin is a nondegradable end-product of oxidative stress; its cerebral presence reflects the cumulative amount of oxidative stress the brain has endured. In this study, we have observed prominent autofluorescent particles in the pial arterial wall and in neocortical parenchyma of young, drug-resistant epilepsy patients (18-28 years old) who underwent resective brain surgery (n = 6), as well as in older control patients (n = 3). With fluorescence spectroscopic imaging, brightfield microscopy, histochemistry and fluorescence lifetime imaging, these autofluorescent particles were identified as the age pigment lipofuscin. An evaluation of these lipofuscin particles using Imaris© software allowed robust quantification, while the 3D properties allowed visualization of the complex configuration. We elaborate on the usefulness of lipofuscin as a marker of cumulative oxidative stress in the brain. Furthermore, we speculate on the observed differences in particle size and density that we found between young patients and older controls, which could imply a role for lipofuscin in the pathophysiology of epilepsy and possibly other neurological diseases.

Association between skin autofluorescence of advanced glycation end products and affective disorders in the lifelines cohort study

BackgroundOxidative stress may be a mechanistic link between affective disorders (depressive and anxiety disorders) and somatic disease. Advanced glycation end products are produced under the influence of oxidative stress and in the skin (measured by skin autofluorescence [SAF]) serve as marker for cumulative oxidative stress. Aim of study was to determine whether SAF is associated with presence of affective disorders. MethodsParticipants in the Lifelines cohort study who had completed the Mini-International Neuropsychiatric Interview for affective disorders and a SAF-measurement were included. Cross-sectional associations between SAF and presence of the following psychiatric disorders were investigated through logistic regression analyses adjusted for sociodemographic factors, cardiometabolic parameters, and somatic morbidities: major depressive disorder, dysthymia, generalised anxiety disorder, panic disorder or social phobia. ResultsOf 81,041 included participants (41.7% male, aged 18–91 years), 6676 (8.2%) were cases with an affective disorder. SAF was associated with presence of affective disorders (OR=1.09 [95%CI 1.07–1.12], P<.001 adjusted for sociodemographic factors). Association with major depressive disorder was strongest and significant after adjustment for all confounders (OR=1.31 [95%CI 1.25–1.36], P<.001 in the crude model; OR=1.12 [95%CI 1.07–1.17], P<.001 in the fully adjusted model). For other disorders, associations lost significance after adjustment for cardiometabolic parameters and somatic morbidities. LimitationsPersons of non-Western descent and severely (mentally or physically) ill individuals were underrepresented. ConclusionsSAF was associated with presence of affective disorders, suggesting a link between these disorders and cumulative oxidative stress. For major depressive disorder, this association was strongest and independent of sociodemographic, cardiometabolic factors, and somatic morbidities.

Protective effects of galangin against UVB irradiation-induced photo-aging in CCD-986sk human skin fibroblasts

Photo-aging is caused by cumulative oxidative stress from ultraviolet B irradiation with up-regulating intracellular reactive oxygen species, 4-hydroxynonenal, and matrix metalloproteinases. MMPs are the enzyme that degrades collagens so that impair the function of the dermis. Galangin was identified by 1H-NMR and 13C-NMR spectroscopy and is a natural flavonol that recently known to have many pharmacological effects such as anti-viral, anti-inflammatory, anti-atopic dermatitis and anti-oxidative activities. In this study, the protective effect of galangin on UVB-induced photo-aging in human skin fibroblasts (CCD-986sk) was conducted by Western blot analysis and enzyme-linked immunosorbent assay. Activator protein 1 and nuclear factor-kappa B are the main transcription factors from activated mitogen-activated protein kinases that up-regulates MMPs. Galangin showed down-regulation of intracellular ROS, 4-HNE, and MMPs through inhibition of phosphorylation of the MAPK pathway and showed a protective effect against skin fibroblasts under oxidative stress caused by UVB irradiation. This lead to up-regulation of fibroblast growth factor 2 and type 1 pro-collagen. These findings suggest that galangin can be developed as a potential agent for functional food and cosmetics of UVB-induced skin photo-aging.

Prenatal Household Air Pollution Alters Cord Blood Mononuclear Cell Mitochondrial DNA Copy Number: Sex-Specific Associations.

Background: Associations between prenatal household air pollution (HAP) exposure or cookstove intervention to reduce HAP and cord blood mononuclear cell (CBMC) mitochondrial deoxyribonucleic acid copy number (mtDNAcn), an oxidative stress biomarker, are unknown. Materials and Methods: Pregnant women were recruited and randomized to one of two cookstove interventions, including a clean-burning liquefied petroleum gas (LPG) stove, or control. Prenatal HAP exposure was determined by serial, personal carbon monoxide (CO) measurements. CBMC mtDNAcn was measured by quantitative polymerase chain reaction. Multivariable linear regression determined associations between prenatal CO and cookstove arm on mtDNAcn. Associations between mtDNAcn and birth outcomes and effect modification by infant sex were explored. Results: LPG users had the lowest CO exposures (p = 0.02 by ANOVA). In boys only, average prenatal CO was inversely associated with mtDNAcn (β = -14.84, SE = 6.41, p = 0.03, per 1ppm increase in CO). When examined by study arm, LPG cookstove had the opposite effect in all children (LPG β = 19.34, SE = 9.72, p = 0.049), but especially boys (β = 30.65, SE = 14.46, p = 0.04), as compared to Control. Increased mtDNAcn was associated with improved birth outcomes. Conclusions: Increased prenatal HAP exposure reduces CBMC mtDNAcn, suggesting cumulative prenatal oxidative stress injury. An LPG stove intervention may reverse this effect. Boys appear most susceptible.

Liver Injury in Uncomplicated Malaria is an Overlooked Phenomenon: An Observational Study.

Abstract Background Liver injury is a known feature of severe malaria, but is only incidentally investigated in uncomplicated disease. In such cases, drug-induced hepatotoxicity is often thought to be the primary cause of the observed liver injury, and this can be a major concern in antimalaria drug development. We investigated liver function test (LFT) abnormalities in patients with imported uncomplicated malaria, and in Controlled Human Malaria Infection (CHMI) studies. Methods Clinical and laboratory data from 484 imported malaria cases and 254 CHMI participants were obtained from the Rotterdam Malaria Cohort database, and the Radboud University Medical Center database (between 2001 and 2017), respectively. Routine clinical LFTs, clinical profiles, parasite densities, hematological, and inflammation parameters were assessed in 217 patients with imported falciparum malaria upon admission, and from longitudinal data of 187 CHMI participants. Findings Upon admission, the proportion of patients with imported uncomplicated malaria and elevated liver enzymes was 128/186 (69%). In CHMI, 97/187 (52%) participants showed LFT abnormalities, including mild (64%, >1.0 ≤ 2.5× upper limit of normal (ULN)), moderate (20%, >2.5 ≤ 5.0xULN) or severe (16%, >5.0xULN). LFT abnormalities were primarily ALT/AST elevations and to a lesser extent γGT and ALP. LFT abnormalities peaked shortly after initiation of treatment, regardless of drug regimen, and returned to normal within three to six weeks. Positive associations were found with parasite burden and inflammatory parameters, including cumulative inflammatory cytokine responses and oxidative stress markers (r = 0·65, p = 0·008, and r = −0·63, p = 0·001, respectively). Interpretation This study shows that reversible liver injury is a common feature of uncomplicated falciparum malaria, most likely caused by an enduring pro-inflammatory response post treatment. The recognition of this phenomenon is of clinical relevance for individual patient care as well as clinical development of (new) antimalarial drugs. Fund PATH Malaria Vaccine Initiative (MVI)

Skin Autofluorescence, a Measure of Cumulative Metabolic Stress and Advanced Glycation End Products, Decreases During the Summer in Dialysis Patients.

Tissue advanced glycation end products (AGEs) are a measure of cumulative metabolic and oxidative stress and cytokine-driven inflammatory reactions. AGEs are thought to contribute to the cardiovascular complications of hemodialysis (HD) patients. Skin autofluorescence (SAF) is related to the tissue accumulation of AGEs and rises with age. SAF is one of the strongest prognostic markers of mortality in these patients. The content of AGEs is high in barbecue food. Due to the location in northern Sweden, there is a short intense barbecue season between June and August. The aim of this study was to investigate if seasonal variations in SAF exist in HD patients, especially during the barbecue season. SAF was measured noninvasively with an AGE Reader in 34 HD-patients (15 of those with diabetes mellitus, DM). Each time the median of three measures were used. Skin-AF was measured before and after each one HD at the end of February and May in 31 patients (22 men/9 women); the end of May and August in 28 (20 m/8 w); the end of August and March in 25 (19 m/6 w). Paired statistical analyses were performed during all four periods (n = 23, 17 m/6 w); as was HbA1c of those with DM. There was at a median 5.6% increase in skin-AF during the winter period (February-May, P = 0.004) and a 10.6% decrease in the skin-AF during the summer (May-August, P < 0.001). HbA1c in the DM rose during the summer (P = 0.013). In conclusion, skin-AF decreased significantly during the summer. Future studies should look for favorable factors that prevent skin-AF and subsequently cardiovascular diseases.

Ageing at the level of telomeres in association to residential landscape and air pollution at home and work: a review of the current evidence

Studies suggest that leukocyte telomere length is an index of systemic ageing. Here, we discuss telomere length as a marker of biological ageing in relation to residential landscape (greenness), residential air pollution and work-related exposures. Telomere lengths are memories of cumulative oxidative and inflammatory stress, and show to have inverse associations with the risk of non-communicable diseases. For this reason, telomeres are considered as markers of biological ageing. Studies at birth, in children, young adulthood, and elderly show that residential green space, lower traffic exposure and long-term lower exposure to particulate air pollution are associated with longer telomeres. Work-related exposures including exposure to toxic metals, polycyclic aromatic hydrocarbons and particulate matter are associated with shorter telomeres for a given age. In contrast to chronic exposures, evidence is present of the observation that recent exposure is associated with longer telomeres. Our overview shows that the magnitude of residential and work-related environmental factors on telomere length are often as important as many classical lifestyle factors.

Increased levels of the oxidative stress biomarker 8-iso-prostaglandin F2α in wastewater associated with tobacco use.

Wastewater analysis has been demonstrated to be a complementary approach for assessing the overall patterns of drug use by a population while the full potential of wastewater-based epidemiology has yet to be explored. F2-isoprostanes are a prototype wastewater biomarker to study the cumulative oxidative stress at a community level. In this work, 8-iso-prostaglandin F2α (8-iso-PGF2α) was analysed in raw 24 h-composite wastewater samples collected from 4 Norwegian and 7 other European cities in 2014 and 2015. Using the same samples, biomarkers of alcohol (ethyl sulfate) and tobacco (trans-3′-hydroxycotinine) use were also analysed to investigate any possible correlation between 8-iso-PGF2α and the consumption of the two drugs. The estimated per capita daily loads of 8-iso-PGF2α in the 11 cities ranged between 2.5 and 9.9 mg/day/1000 inhabitants with a population-weighted mean of 4.8 mg/day/1000 inhabitants. There were no temporal trends observed in the levels of 8-iso-PGF2α, however, spatial differences were found at the inter-city level correlating to the degree of urbanisation. The 8-iso-PGF2α mass load was found to be strongly associated with that of trans-3′-hydroxycotinine while it showed no correlation with ethyl sulfate. The present study shows the potential for 8-iso-PGF2α as a wastewater biomarker for the assessment of community public health.

Identifying sensitive windows for prenatal particulate air pollution exposure and mitochondrial DNA content in cord blood

IntroductionChanges in mitochondrial DNA (mtDNA) can serve as a marker of cumulative oxidative stress (OS) due to the mitochondria's unique genome and relative lack of repair systems. In utero particulate matter ≤2.5μm (PM2.5) exposure can enhance oxidative stress. Our objective was to identify sensitive windows to predict mtDNA damage experienced in the prenatal period due to PM2.5 exposure using mtDNA content measured in cord blood. Material and methodsWomen affiliated with the Mexican social security system were recruited during pregnancy in the Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS) study. Mothers with cord blood collected at delivery and complete covariate data were included (n=456). Mothers' prenatal daily exposure to PM2.5 was estimated using a satellite-based spatio-temporally resolved prediction model and place of residence during pregnancy. DNA was extracted from umbilical cord leukocytes. Quantitative real-time polymerase chain reaction (qPCR) was used to determine mtDNA content. A distributive lag regression model (DLM) incorporating weekly averages of daily PM2.5 predictions was constructed to plot the association between exposure and OS over the length of pregnancy. ResultsIn models that included child's sex, mother's age at delivery, prenatal environmental tobacco smoke exposure, birth year, maternal education, and assay batch, we found significant associations between higher PM2.5 exposure during late pregnancy (35–40weeks) and lower mtDNA content in cord blood. ConclusionsIncreased PM2.5 during a specific prenatal window in the third trimester was associated with decreased mtDNA content suggesting heightened sensitivity to PM-induced OS during this life stage.