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Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development

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A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 44696

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Special Issue Editors

Dr. Alica Pizent

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Institute for Medical Research and Occupational Health, Ksaverska cesta 2, HR-10000 Zagreb, Croatia
Interests: human biomonitoring; metals/metalloids; pesticides; oxidative stress; antioxidants; combined exposure and interactions; health effects; metabolomics; biomarkers; analytical chemistry
Special Issues, Collections and Topics in MDPI journals

Dr. Eva Tvrdá

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The Institute of Biotechnology, Faculty of Biotechnology and Food Sciences, Slovak University of Agriculture in Nitra, Trieda A. Hlinku 2, 949 76 Nitra, Slovakia
Interests: reproductive biology; andrology; toxicology; oxidative stress; antioxidants
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Many environmental and lifestyle factors exert their toxic effects on reproductive health and development through impaired antioxidant defence and oxidative damage. Moreover, the environmental exposure and lifestyle of parents may have an important role in the programming of the future (reproductive) health and disease of offspring, and oxidative stress may be a key mediator in this programming. The identification of risk factors and understanding the complex mechanisms underlying the various reproductive and/or developmental health disorders represent research priorities. This Special Issue of Antioxidants entitled “Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development” focuses on the latest research related but not restricted to

Reproductive and developmental toxicity of metals/metalloids, pesticides, mycotoxins, phtalates, bisphenol A, parabens and flame retardants;
Biomonitoring and risk assessment;
Contribution of smoking, alcohol, drug of abuse, nutrition and obesity to oxidative stress and adverse health effects;
Adverse effects of circadian rhythm disruption (chronodisruption) on reproductive health and development;
Ameliorative/beneficial effects of antioxidants;
Parameters of oxidative stress/antioxidant defence as potential novel biomarkers of reproductive and developmental health disorders;
Proteomic and metabolomic signature of oxidative stress;
Role of oxidative stress in epigenetic modification of reproductive health and development.

Of particular interest are studies on low-level exposure and effects of multiple toxicants/stressors and their interactions. Both observational (human biomonitoring) and experimental (in vivo and in vitro) studies are welcome. We invite authors in the field to submit their original articles, reviews and short communications on this important topic.

Dr. Alica Pizent

Dr. Eva Tvrdá
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

Reproductive toxicology
Human biomonitoring
Fertility
Pregnancy
Offspring
Foetal programming (Developmental Origins of Health and Disease)
Cancers of the reproductive system
Biomarker discovery
“Omics”
Epigenetics
Antioxidants

Published Papers (11 papers)

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Research

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20 pages, 10793 KiB

Open AccessArticle

A Dynamic Model for Estimating the Interaction of ROS–PUFA–Antioxidants in Rabbit

by Simona Mattioli, Corrado Dimauro, Alberto Cesarani, Alessandro Dal Bosco, Desiree Bartolini, Francesco Galli, Anna Migni, Bartolomeo Sebastiani, Cinzia Signorini, Camille Oger, Giulia Collodel and Cesare Castellini

Antioxidants 2022, 11(3), 531; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11030531 - 10 Mar 2022

Cited by 5 | Viewed by 2172

Abstract

Defining optimal nutrition in animals and humans remains a main scientific challenge. The objective of the work was to develop a dynamic model of reactive oxygen species (ROS)–polyunsaturated fatty acid (PUFA)–antioxidant homeostasis using the rabbit as a model. The problem entity was to evaluate the main metabolites generated from interactions between traits included in the conceptual model and identified by three main sub–models: (i) ROS generation, (ii) PUFA oxidation and (iii) antioxidant defence. A mathematical model (VENSIM software) that consisted of molecular stocks (INPUTs, OUTPUTs), exchange flows (intermediate OUTPUTs) and process rates was developed. The calibration was performed by using standard experimental data (Experiment 1), whereas the validation was carried out in Experiments 2 and 3 by using supra–nutritional dietary inputs (VIT E+ and PUFA+). The accuracy of the models was measured using 95% confidence intervals. Analytical OUTPUTs (ROS, PUFA, Vit E, Ascorbic acid, Iso–/NeuroProstanes, Aldehydes) were well described by the standard model. There was also good accuracy for the VIT E+ scenario, whereas some compensatory rates (Kc1–Kc4) were added to assess body compensation when high levels of dietary PUFA were administered (Experiment 3). In conclusion, the model can be very useful for predicting the effects of dietary treatments on the redox homeostasis of rabbits. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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14 pages, 1561 KiB

Open AccessArticle

Prenatal Fine Particulate Matter, Maternal Micronutrient Antioxidant Intake, and Early Childhood Repeated Wheeze: Effect Modification by Race/Ethnicity and Sex

by Yueh-Hsiu Mathilda Chiu, Kecia N. Carroll, Brent A. Coull, Srimathi Kannan, Ander Wilson and Rosalind J. Wright

Antioxidants 2022, 11(2), 366; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020366 - 11 Feb 2022

Cited by 5 | Viewed by 1961

Abstract

Fine particulate matter (PM_2.5) potentiates in utero oxidative stress influencing fetal development while antioxidants have potential protective effects. We examined associations among prenatal PM_2.5, maternal antioxidant intake, and childhood wheeze in an urban pregnancy cohort (n = 530). Daily PM_2.5 exposure over gestation was estimated using a satellite-based spatiotemporally resolved model. Mothers completed the modified Block98 food frequency questionnaire. Average energy-adjusted percentile intake of β-carotene, vitamins (A, C, E), and trace minerals (zinc, magnesium, selenium) constituted an antioxidant index (AI). Maternal-reported child wheeze was ascertained up to 4.1 ± 2.8 years. Bayesian distributed lag interaction models (BDLIMs) were used to examine time-varying associations between prenatal PM_2.5 and repeated wheeze (≥2 episodes) and effect modification by AI, race/ethnicity, and child sex. Covariates included maternal age, education, asthma, and temperature. Women were 39% Black and 33% Hispanic, 36% with ≤high school education; 21% of children had repeated wheeze. Higher AI was associated with decreased wheeze in Blacks (OR = 0.37 (0.19–0.73), per IQR increase). BDLIMs identified a sensitive window for PM_2.5 effects on wheeze among boys born to Black mothers with low AI (at 33–40 weeks gestation; OR = 1.74 (1.19–2.54), per µg/m³ increase in PM_2.5). Relationships among prenatal PM_2.5, antioxidant intake, and child wheeze were modified by race/ethnicity and sex. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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17 pages, 2350 KiB

Open AccessArticle

Effects of Sub-Chronic Exposure to Imidacloprid on Reproductive Organs of Adult Male Rats: Antioxidant State, DNA Damage, and Levels of Essential Elements

by Blanka Tariba Lovaković, Vilena Kašuba, Ankica Sekovanić, Tatjana Orct, Antonija Jančec and Alica Pizent

Antioxidants 2021, 10(12), 1965; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10121965 - 08 Dec 2021

Cited by 10 | Viewed by 2933

Abstract

Although considered a good alternative to organophosphate pesticides, there are reports indicating adverse effects of neonicotinoid insecticides on reproduction. Our aim was to assess the effects of exposure to low doses of imidacloprid on antioxidant state, DNA damage, and concentration of essential elements in the testes and epididymis using a rat model. Adult male Wistar rats were orally treated with doses comparable to currently proposed health-based reference values: 0.06 (ADI), 0.80 (10× AOEL), or 2.25 (1/200 LD₅₀) mg/kg b.w./day for 28 consecutive days. Exposure to 2.25 mg/kg b.w./day of imidacloprid resulted in a significantly lower testis weight (1.30 ± 0.17 g compared to 1.63 ± 0.15 g in controls). Treatment with 0.06 mg/kg b.w./day increased the level of reduced glutathione in the epididymis (73%), while the activities of epididymal glutathione peroxidase and superoxide dismutase significantly increased in all treated rats (74–92% and 26–39%, respectively). Exposure to imidacloprid resulted in a low, but significant, level of DNA damage in testicular sperm cells regardless of the concentration applied (<28% compared to the negative control). Higher concentrations of Mo were measured in the testes of rats treated with 0.80 and 2.25 mg/kg b.w./day (72.9 ± 7.9 and 73.9 ± 9.1 mg/g, respectively) compared to the control animals (60.5 ± 7.8 mg/g). Higher concentrations of Na were measured in the testes of rats treated with 2.25 mg/kg b.w./day (1679 ± 82 mg/g compared to 1562 ± 56 mg/g in controls). The fact that such low doses of imidacloprid were able to produce measurable biological effects calls for the further evaluation of this widely used insecticide. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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20 pages, 8131 KiB

Open AccessArticle

Maternal Particulate Matter Exposure Impairs Lung Health and Is Associated with Mitochondrial Damage

by Baoming Wang, Yik-Lung Chan, Gerard Li, Kin Fai Ho, Ayad G. Anwer, Bradford J. Smith, Hai Guo, Bin Jalaludin, Cristan Herbert, Paul S. Thomas, Jiayan Liao, David G. Chapman, Paul S. Foster, Sonia Saad, Hui Chen and Brian G. Oliver

Antioxidants 2021, 10(7), 1029; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10071029 - 25 Jun 2021

Cited by 14 | Viewed by 4134

Abstract

Relatively little is known about the transgenerational effects of chronic maternal exposure to low-level traffic-related air pollution (TRAP) on the offspring lung health, nor are the effects of removing such exposure before pregnancy. Female BALB/c mice were exposed to PM_2.5 (PM_2.5, 5 µg/day) for 6 weeks before mating and during gestation and lactation; in a subgroup, PM was removed when mating started to model mothers moving to cleaner areas during pregnancy to protect their unborn child (Pre-exposure). Lung pathology was characterised in both dams and offspring. A subcohort of female offspring was also exposed to ovalbumin to model allergic airways disease. PM_2.5 and Pre-exposure dams exhibited airways hyper-responsiveness (AHR) with mucus hypersecretion, increased mitochondrial reactive oxygen species (ROS) and mitochondrial dysfunction in the lungs. Female offspring from PM_2.5 and Pre-exposure dams displayed AHR with increased lung inflammation and mitochondrial ROS production, while males only displayed increased lung inflammation. After the ovalbumin challenge, AHR was increased in female offspring from PM_2.5 dams compared with those from control dams. Using an in vitro model, the mitochondria-targeted antioxidant MitoQ reversed mitochondrial dysfunction by PM stimulation, suggesting that the lung pathology in offspring is driven by dysfunctional mitochondria. In conclusion, chronic exposure to low doses of PM_2.5 exerted transgenerational impairment on lung health. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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15 pages, 1657 KiB

Open AccessArticle

Maternal Urinary Metal and Metalloid Concentrations in Association with Oxidative Stress Biomarkers

by Pahriya Ashrap, Deborah J. Watkins, Ginger L. Milne, Kelly K. Ferguson, Rita Loch-Caruso, Jennifer Fernandez, Zaira Rosario, Carmen M. Vélez-Vega, Akram Alshawabkeh, José F. Cordero and John D. Meeker

Antioxidants 2021, 10(1), 114; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10010114 - 15 Jan 2021

Cited by 11 | Viewed by 2706

Abstract

Metal exposure has been associated with a wide range of adverse birth outcomes and oxidative stress is a leading hypothesis of the mechanism of action of metal toxicity. We assessed the relationship between maternal exposure to essential and non-essential metals and metalloids in pregnancy and oxidative stress markers, and sought to identify windows of vulnerability and effect modification by fetal sex. In our analysis of 215 women from the PROTECT birth cohort study, we measured 14 essential and non-essential metals in urine samples at three time points during pregnancy. The oxidative stress marker 8-iso-prostaglandin F2α (8-iso-PGF2α) and its metabolite 2,3-dinor-5,6-dihydro-15-15-F2t-IsoP, as well as prostaglandin F2α (PGF2α), were also measured in the same urine samples. Using linear mixed models, we examined the main effects of metals on markers of oxidative stress as well as the visit-specific and fetal sex-specific effects. After adjustment for covariates, we found that a few urinary metal concentrations, most notably cesium (Cs) and copper (Cu), were associated with higher 8-iso-PGF2α with effect estimates ranging from 7.3 to 14.9% for each interquartile range, increase in the metal concentration. The effect estimates were generally in the same direction at the three visits and a few were significant only among women carrying a male fetus. Our data show that higher urinary metal concentrations were associated with elevated biomarkers of oxidative stress. Our results also indicate a potential vulnerability of women carrying a male fetus. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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Review

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21 pages, 851 KiB

Open AccessReview

Male Infertility and Oxidative Stress: A Focus on the Underlying Mechanisms

by Robert John Aitken, Joël R. Drevet, Aron Moazamian and Parviz Gharagozloo

Antioxidants 2022, 11(2), 306; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020306 - 02 Feb 2022

Cited by 67 | Viewed by 6254

Abstract

Reactive oxygen species (ROS) play a critical role in defining the functional competence of human spermatozoa. When generated in moderate amounts, ROS promote sperm capacitation by facilitating cholesterol efflux from the plasma membrane, enhancing cAMP generation, inducing cytoplasmic alkalinization, increasing intracellular calcium levels, and stimulating the protein phosphorylation events that drive the attainment of a capacitated state. However, when ROS generation is excessive and/or the antioxidant defences of the reproductive system are compromised, a state of oxidative stress may be induced that disrupts the fertilizing capacity of the spermatozoa and the structural integrity of their DNA. This article focusses on the sources of ROS within this system and examines the circumstances under which the adequacy of antioxidant protection might become a limiting factor. Seminal leukocyte contamination can contribute to oxidative stress in the ejaculate while, in the germ line, the dysregulation of electron transport in the sperm mitochondria, elevated NADPH oxidase activity, or the excessive stimulation of amino acid oxidase action are all potential contributors to oxidative stress. A knowledge of the mechanisms responsible for creating such stress within the human ejaculate is essential in order to develop better antioxidant strategies that avoid the unintentional creation of its reductive counterpart. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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25 pages, 811 KiB

Open AccessReview

The Pressing Issue of Micro- and Nanoplastic Contamination: Profiling the Reproductive Alterations Mediated by Oxidative Stress

by Maria Carmela Ferrante, Anna Monnolo, Filomena Del Piano, Giuseppina Mattace Raso and Rosaria Meli

Antioxidants 2022, 11(2), 193; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020193 - 19 Jan 2022

Cited by 27 | Viewed by 4535

Abstract

Micro- and nanoplastics (MPs/NPs) are among the most widely distributed pollutants in the environment. It has been suggested that exposure to MPs/NPs can trigger toxicity pathways among which inflammation and oxidative stress (OS) play a pivotal role. Once absorbed, MPs/NPs may act locally or access the bloodstream and, following the translocation process, reach several organs and tissues, including the gonads. Notably, MPs/NPs can bioaccumulate in human and murine placenta, opening new scenarios for toxicological evaluations. We review recent studies on the effects of MPs/NPs on the reproductive health in aquatic and terrestrial organisms of both sexes, focusing on the role of OS and the antioxidant defence system failure as the main underlying mechanisms. Alterations in gametogenesis, embryonic and offspring development, and survival have been shown in most studies and often related to a broken redox balance. All these detrimental effects are inversely related to particle size, whereas they are closely linked to shape, plastic polymer type, superficial functionalization, concentration, and time of exposure. To date, the studies provide insights into the health impacts, but no conclusions can be drawn for reproduction toxicity. The main implication of the few studies on antioxidant substances reveals their potential role in mitigating MP-induced toxic effects. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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21 pages, 1366 KiB

Open AccessReview

The Impact of Oxidative Stress of Environmental Origin on the Onset of Placental Diseases

by Camino San Martin Ruano, Francisco Miralles, Céline Méhats and Daniel Vaiman

Antioxidants 2022, 11(1), 106; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11010106 - 01 Jan 2022

Cited by 12 | Viewed by 2623

Abstract

Oxidative stress (OS) plays a pivotal role in placental development; however, abnormal loads in oxidative stress molecules may overwhelm the placental defense mechanisms and cause pathological situations. The environment in which the mother evolves triggers an exposure of the placental tissue to chemical, physical, and biological agents of OS, with potential pathological consequences. Here we shortly review the physiological and developmental functions of OS in the placenta, and present a series of environmental pollutants inducing placental oxidative stress, for which some insights regarding the underlying mechanisms have been proposed, leading to a recapitulation of the noxious effects of OS of environmental origin upon the human placenta. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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17 pages, 1593 KiB

Open AccessReview

Impact of Environmental and Lifestyle Use of Chromium on Male Fertility: Focus on Antioxidant Activity and Oxidative Stress

by Sara C. Pereira, Pedro F. Oliveira, Sónia Rodrigues Oliveira, Maria de Lourdes Pereira and Marco G. Alves

Antioxidants 2021, 10(9), 1365; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10091365 - 27 Aug 2021

Cited by 26 | Viewed by 4964

Abstract

Male reproductive tissues are strongly susceptible to several environmental and lifestyle stressors. In general, male reproductive health is highly sensitive to oxidative stress, which results in reversible and/or irreversible changes in testosterone-producing cells, spermatogenesis, and sperm quality. Chromium compounds are widely used in the +3 and +6 valence states, as food supplements, and in the industrial field, respectively. Chromium (III) compounds, i.e., Cr(III)-tris-picolinate, [Cr(pic)₃], known as chromium picolinate, are used as nutritional supplements for the control of diabetes, body weight, and muscular growth. However, previous studies showed that animal models exposed to chromium picolinate experienced degenerative changes in spermatogenesis. Contradictory results are documented in the literature and deserve discussion. Furthermore, the long-term effects of chromium picolinate on the antioxidant system of treated subjects have not been properly studied. Comprehensive studies on the role of this compound will help to establish the safe and useful use of chromium supplementation. On the other hand, chromium (VI) compounds are widely used in several industries, despite being well-known environmental pollutants (i.e., welding fumes). Chromium (VI) is known for its deleterious effects on male reproductive health as toxic, carcinogenic, and mutagenic. Previous studies have demonstrated severe lesions to mouse spermatogenesis after exposure to chromium (VI). However, workers worldwide are still exposed to hexavalent chromium, particularly in electronics and military industries. Data from the literature pinpoints mechanisms of oxidative stress induced by chromium compounds in somatic and germ cells that lead to apoptosis, thus underlining the impairment of fertility potential. In this review, we analyze the benefits and risks of chromium compounds on male fertility, as well as the mechanisms underlying (in)fertility outcomes. Although supplements with antioxidant properties may maximize male fertility, adverse effects need to be investigated and discussed. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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39 pages, 2925 KiB

Open AccessReview

Environmental Factors-Induced Oxidative Stress: Hormonal and Molecular Pathway Disruptions in Hypogonadism and Erectile Dysfunction

by Shubhadeep Roychoudhury, Saptaparna Chakraborty, Arun Paul Choudhury, Anandan Das, Niraj Kumar Jha, Petr Slama, Monika Nath, Peter Massanyi, Janne Ruokolainen and Kavindra Kumar Kesari

Antioxidants 2021, 10(6), 837; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10060837 - 24 May 2021

Cited by 37 | Viewed by 8041

Abstract

Hypogonadism is an endocrine disorder characterized by inadequate serum testosterone production by the Leydig cells of the testis. It is triggered by alterations in the hypothalamic–pituitary–gonadal axis. Erectile dysfunction (ED) is another common disorder in men that involves an alteration in erectile response–organic, relational, or psychological. The incidence of hypogonadism and ED is common in men aged over 40 years. Hypogonadism (including late-onset hypogonadism) and ED may be linked to several environmental factors-induced oxidative stresses. The factors mainly include exposure to pesticides, radiation, air pollution, heavy metals and other endocrine-disrupting chemicals. These environmental risk factors may induce oxidative stress and lead to hormonal dysfunctions. To better understand the subject, the study used many keywords, including “hypogonadism”, “late-onset hypogonadism”, “testosterone”, “erectile dysfunction”, “reactive oxygen species”, “oxidative stress”, and “environmental pollution” in major online databases, such as SCOPUS and PUBMED to extract relevant scientific information. Based on these parameters, this review summarizes a comprehensive insight into the important environmental issues that may have a direct or indirect association with hypogonadism and ED in men. The study concludes that environmental factors-induced oxidative stress may cause infertility in men. The hypothesis and outcomes were reviewed critically, and the mechanistic approaches are applied through oxidant-sensitive pathways. This study also provides reccomendations on future therapeutic interventions and protective measures against such adverse environmental factors-induced hypogonadism and ED. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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11 pages, 682 KiB

Open AccessPerspective

Particulate Matter, an Intrauterine Toxin Affecting Foetal Development and Beyond

by Hui Chen, Brian G. Oliver, Anushriya Pant, Annabel Olivera, Philip Poronnik, Carol A. Pollock and Sonia Saad

Antioxidants 2021, 10(5), 732; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10050732 - 06 May 2021

Cited by 24 | Viewed by 2686

Abstract

Air pollution is the 9th cause of the overall disease burden globally. The solid component in the polluted air, particulate matters (PMs) with a diameter of 2.5 μm or smaller (PM_2.5) possess a significant health risk to several organ systems. PM_2.5 has also been shown to cross the blood–placental barrier and circulate in foetal blood. Therefore, it is considered an intrauterine environmental toxin. Exposure to PM_2.5 during the perinatal period, when the foetus is particularly susceptible to developmental defects, has been shown to reduce birth weight and cause preterm birth, with an increase in adult disease susceptibility in the offspring. However, few studies have thoroughly studied the health outcome of foetuses due to intrauterine exposure and the underlying mechanisms. This perspective summarises currently available evidence, which suggests that intrauterine exposure to PM_2.5 promotes oxidative stress and inflammation in a similar manner as occurs in response to direct PM exposure. Oxidative stress and inflammation are likely to be the common mechanisms underlying the dysfunction of multiple systems, offering potential targets for preventative strategies in pregnant mothers for an optimal foetal outcome. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Environmental and Lifestyle Stressors: Impact on Reproductive Health and Development)

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