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Reviews on Environmental Health Mar 2023Inappropriate processing and disposal of electronic waste (e-waste) expose workers and surrounding populations to hazardous chemicals, including clastogens and aneugens.... (Meta-Analysis)
Meta-Analysis Review
OBJECTIVES
Inappropriate processing and disposal of electronic waste (e-waste) expose workers and surrounding populations to hazardous chemicals, including clastogens and aneugens. Recently, considerable literature has grown around e-waste recycling, associated chemical exposures and intermediate health outcomes, including DNA damage. Micronuclei (MN) frequency has been widely used as a biomarker to investigate DNA damage in human populations exposed to genotoxic agents. We conducted a systematic review of published studies to assess DNA damage in e-waste-exposed populations and performed a meta-analysis to evaluate the association between e-waste exposure and DNA damage.
METHODS
This systematic review with meta-analysis was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement checklist. Articles published in English from January 2000 through December 2020 investigating the associations between e-waste exposure and DNA damage were retrieved from the following three major databases: MEDLINE, ProQuest, and Scopus. Studies that reported the use of MN assay as a biomarker of DNA damage were included for meta-analysis. Studies that also reported other DNA damage biomarkers such as chromosomal aberrations, comet assay biomarkers, 8-hydroxy-2'-deoxyguanosine (8-OHdG), telomere length, apoptosis rate were reported using narrative synthesis.
RESULTS
A total of 20 publications were included in this review, of which seven studies were within the occupational setting, and the remaining 13 studies were ecological studies. The review found six biomarkers of DNA damage (micronuclei, comets assay parameters (tail length, % tail DNA, tail moment, and olive tail moment), 8-OHdG, telomere length, apoptosis rate and chromosomal aberrations) which were assessed using seven different biological matrices (buccal cells, blood, umbilical cord blood, placenta, urine and semen). Most studies showed elevated levels of DNA damage biomarkers among e-waste exposed populations than in control populations. The most commonly used biomarkers were micronuclei frequency (n=9) in peripheral blood lymphocytes or buccal cells and 8-OHdG (n=7) in urine. The results of the meta-analysis showed that electronic waste recycling has contributed to an increased risk of DNA damage measured using MN frequency with a pooled estimate of the standardized mean difference (SMD) of 2.30 (95% CI: 1.36, 3.24, p<0.001) based on 865 participants.
CONCLUSIONS
Taken together, evidence from this systematic review with meta-analysis suggest that occupational and non-occupational exposure to e-waste processing is associated with increased risk of DNA damage measured through MN assay and other types of DNA damage biomarkers. However, more studies from other developing countries in Africa, Latin America, and South Asia are needed to confirm and increase these results' generalizability.
Topics: Humans; Electronic Waste; Mouth Mucosa; DNA Damage; Chromosome Aberrations; Biomarkers
PubMed: 34727591
DOI: 10.1515/reveh-2021-0074 -
Biomedical Papers of the Medical... Mar 2024Oxidative DNA damage markers (8OHdG, comet assay, gammaH2AX) are becoming widely used in clinical cardiology research. To conduct this review of DNA damage in relation... (Meta-Analysis)
Meta-Analysis Review
Oxidative DNA damage markers (8OHdG, comet assay, gammaH2AX) are becoming widely used in clinical cardiology research. To conduct this review of DNA damage in relation to hypertension in humans, we used databases (e.g. PubMed, Web of Science) to search for English-language publications up to June 30, 2022 and the terms: DNA damage, comet assay, gammaH2AX, 8OHdG, strand breaks, and arterial hypertension. Exclusion criteria were: children, absence of relevant controls, extra-arterial hypertensive issues, animal, cell lines. From a total of 79526, 15 human studies were selected. A total of 902 hypertensive patients (pts): (comet: N=418 pts; 8OHdG: N=484 pts) and 587 controls (comet: N=203; 8OHdG: N=384) were included. DNA damage was significantly higher in hypertensive pts than healthy controls (comet 26.6±11.0 vs 11.7±4.07 arbitrary units /A.U./; P<0.05 and="" 8ohdg="" 13="" 1="" 4="" 12="" vs="" 6="" 97="" 2="" 67="" ng="" mg="" creatinine="" i=""> P<0.05) confirmed with meta-analysis for both. Greater DNA damage was observed in more adverse cases (concentric cardiac hypertrophy 43.4±15.4 vs 15.6±5.5; sustained/untreated hypertension 31.4±12.1 vs 14.2±5/35.0±5.0 vs 25.0 ±5.0; non-dippers 39.2±15.5 vs 29.4±11.1 A.U.; elderly 14.9±4.5 vs 9.3±4.1 ng/mg creatinine; without carvedilol 9.1±4.2 vs 5.7±3.9; with coronary heart disease 0.5±0.1 vs 0.2±0.1 ng/mL) (P<0.05) confirmed with meta-analysis. DNA damage correlated strongly positively with serum glycosylated haemoglobin (r=0.670; P<0.05) and negatively with total antioxidant status (r=-0.670 to -0.933; P<0.05). This is the first systematic review with meta-analysis showing that oxidative DNA damage was increased in humans with arterial hypertension compared to controls.
Topics: Child; Animals; Humans; Aged; 8-Hydroxy-2'-Deoxyguanosine; Creatinine; DNA Damage; Comet Assay; Hypertension
PubMed: 37916467
DOI: 10.5507/bp.2023.044 -
Iranian Journal of Public Health Aug 2023Asbestos is one of the most important environmental and occupational carcinogens. Nevertheless, the mechanisms by which asbestos fiber exposure causes chronic diseases... (Review)
Review
BACKGROUND
Asbestos is one of the most important environmental and occupational carcinogens. Nevertheless, the mechanisms by which asbestos fiber exposure causes chronic diseases are not fully understood. We performed the first systematic review on the epidemiological evidence to examine the association between occupational exposure to asbestos and oxidative stress and DNA damage.
METHODS
In this systematic review study, the PubMed and Scopus databases were searched for English-language publications. Eleven cross-sectional studies were included in the systematic review. A literature search was conducted by the main keywords including "Asbestos", "crocidolite", "chrysotile", "amphibole", "amosite", "Oxidative Stress", "DNA Damage", and "DNA injury". To evaluate the quality of studies, the "Newcastle-Ottawa Quality Assessment Scale" (NOS) was used.
RESULTS
Overall, 1235 articles were achieved by searching in databases. Finally, by considering the inclusion, and exclusion criteria, 11 articles were conducted for this study. These studies were published between 1986 and 2020. Oxidative stress and DNA damage can occur in exposure to asbestos. Among various biomarkers, 8-OHdG is the best. The analysis of 8-oxodG in asbestos workers can help identify subjects with a higher level of genotoxic damage.
CONCLUSION
This systematic review suggests that oxidative stress and DNA damage are two main outputs of asbestos exposure. Therefore, oxidative stress and DNA damage biomarkers can be used for identifying subjects at higher risk of cancer. These findings support policy initiatives aimed at detecting and eliminating asbestos fiber exposure and preventing potential health hazards in occupational settings.
PubMed: 37744536
DOI: 10.18502/ijph.v52i8.13400 -
Frontiers in Physiology 20238-Hydroxy-2'-deoxyguanosine (8-OHdG) is a byproduct of DNA oxidation resulting from free radical attacks. Paradoxically, treatment with 8-OHdG accelerates tissue...
8-Hydroxy-2'-deoxyguanosine (8-OHdG) is a byproduct of DNA oxidation resulting from free radical attacks. Paradoxically, treatment with 8-OHdG accelerates tissue healing. The aim of this study is to quantify the 8-OHdG response after a single session of exercise in both trained and untrained adults. A systematic review and meta-analysis of exercise intervention studies measuring changes in blood 8-OHdG following resistance exercise and aerobic exercise were conducted. The literature search included Web of Science, PubMed, BASE, and Scopus, with publications up to February 2023 included. Subgroup analysis of training status was also conducted. Sixteen studies involving 431 participants met the eligibility criteria. Resistance exercise showed a medium effect on increasing circulating 8-OHdG levels (SMD = 0.66, < 0.001), which was similar for both trained and untrained participants. However, studies on aerobic exercise presented mixed results. For trained participants, a small effect of aerobic exercise on increasing circulating 8-OHdG levels was observed (SMD = 0.42; < 0.001). In contrast, for untrained participants, a large effect of decreasing circulating 8-OHdG levels was observed, mostly after long-duration aerobic exercise (SMD = -1.16; < 0.05). Similar to resistance exercise, high-intensity aerobic exercise (5-45 min, ≥75% VO) significantly increased circulating 8-OHdG levels, primarily in trained participants. Pooled results from the studies confirm an increase in circulating 8-OHdG levels after resistance exercise. However, further studies are needed to fully confirm the circulating 8-OHdG response to aerobic exercise. Increases in 8-OHdG after high-intensity aerobic exercise are observed only in trained individuals, implicating its role in training adaptation. : [https://Systematicreview.gov/], identifier [CRD42022324180].
PubMed: 38028771
DOI: 10.3389/fphys.2023.1275867 -
Advances in Nutrition (Bethesda, Md.) Nov 2023Accumulation of deoxyribonucleic acid (DNA) damage diminishes cellular health, increases risk of developmental and degenerative diseases, and accelerates aging.... (Review)
Review
Protective Effects of Micronutrient Supplements, Phytochemicals and Phytochemical-Rich Beverages and Foods Against DNA Damage in Humans: A Systematic Review of Randomized Controlled Trials and Prospective Studies.
Accumulation of deoxyribonucleic acid (DNA) damage diminishes cellular health, increases risk of developmental and degenerative diseases, and accelerates aging. Optimizing nutrient intake can minimize accrual of DNA damage. The objectives of this review are to: 1) assemble and systematically analyze high-level evidence for the effect of supplementation with micronutrients and phytochemicals on baseline levels of DNA damage in humans, and 2) use this knowledge to identify which of these essential micronutrients or nonessential phytochemicals promote DNA integrity in vivo in humans. We conducted systematic literature searches of the PubMed database to identify interventional, prospective, cross-sectional, or in vitro studies that explored the association between nutrients and established biomarkers of DNA damage associated with developmental and degenerative disease risk. Biomarkers included lymphocyte chromosome aberrations, lymphocyte and buccal cell micronuclei, DNA methylation, lymphocyte/leukocyte DNA strand breaks, DNA oxidation, telomere length, telomerase activity, and mitochondrial DNA mutations. Only randomized, controlled interventions and uncontrolled longitudinal intervention studies conducted in humans were selected for evaluation and data extraction. These studies were ranked for the quality of their study design. In all, 96 of the 124 articles identified reported studies that achieved a quality assessment score ≥ 5 (from a maximum score of 7) and were included in the final review. Based on these studies, nutrients associated with protective effects included vitamin A and its precursor β-carotene, vitamins C, E, B1, B12, folate, minerals selenium and zinc, and phytochemicals such as curcumin (with piperine), lycopene, and proanthocyanidins. These findings highlight the importance of nutrients involved in (i) DNA metabolism and repair (folate, vitamin B, and zinc) and (ii) prevention of oxidative stress and inflammation (vitamins A, C, E, lycopene, curcumin, proanthocyanidins, selenium, and zinc). Supplementation with certain micronutrients and their combinations may reduce DNA damage and promote cellular health by improving the maintenance of genome integrity.
Topics: Humans; Prospective Studies; Selenium; Lycopene; Cross-Sectional Studies; Curcumin; Proanthocyanidins; Randomized Controlled Trials as Topic; Vitamins; Vitamin A; Micronutrients; Folic Acid; Zinc; Beverages; Phytochemicals; DNA; DNA Damage; Biomarkers; Dietary Supplements
PubMed: 37573943
DOI: 10.1016/j.advnut.2023.08.004 -
Open Medicine (Warsaw, Poland) 2023Today, in the modern world, people are often exposed to electromagnetic waves, which can have undesirable effects on cell components that lead to differentiation and... (Review)
Review
Today, in the modern world, people are often exposed to electromagnetic waves, which can have undesirable effects on cell components that lead to differentiation and abnormalities in cell proliferation, deoxyribonucleic acid (DNA) damage, chromosomal abnormalities, cancers, and birth defects. This study aimed to investigate the effect of electromagnetic waves on fetal and childhood abnormalities. PubMed, Scopus, Web of Science, ProQuest, Cochrane Library, and Google Scholar were searched on 1 January 2023. The Cochran's -test and statistics were applied to assess heterogeneity, a random-effects model was used to estimate the pooled odds ratio (OR), standardized mean difference (SMD), and mean difference for different outcomes, and a meta-regression method was utilized to investigate the factors affecting heterogeneity between studies. A total of 14 studies were included in the analysis, and the outcomes investigated were: change in gene expression, oxidant parameters, antioxidant parameters, and DNA damage parameters in the umbilical cord blood of the fetus and fetal developmental disorders, cancers, and childhood development disorders. Totally, the events of fetal and childhood abnormalities were more common in parents who have been exposed to EMFs compared to those who have not (SMD and 95% confidence interval [CI], 0.25 [0.15-0.35]; , 91%). Moreover, fetal developmental disorders (OR, 1.34; CI, 1.17-1.52; , 0%); cancer (OR, 1.14; CI, 1.05-1.23; , 60.1%); childhood development disorders (OR, 2.10; CI, 1.00-3.21; , 0%); changes in gene expression (mean difference [MD], 1.02; CI, 0.67-1.37; , 93%); oxidant parameters (MD, 0.94; CI, 0.70-1.18; , 61.3%); and DNA damage parameters (MD, 1.01; CI, 0.17-1.86; , 91.6%) in parents who have been exposed to EMFs were more than those in parents who have not. According to meta-regression, publication year has a significant effect on heterogeneity (coefficient: 0.033; 0.009-0.057). Maternal exposure to electromagnetic fields, especially in the first trimester of pregnancy, due to the high level of stem cells and their high sensitivity to this radiation, the biochemical parameters of the umbilical cord blood examined was shown increased oxidative stress reactions, changes in protein gene expression, DNA damage, and increased embryonic abnormalities. In addition, parental exposure to ionizing and non-ionizing radiation can lead to the enhancement of different cell-based cancers and developmental disorders such as speech problems in childhood.
PubMed: 37197358
DOI: 10.1515/med-2023-0697 -
Mutation Research. Reviews in Mutation... 2022Carbon black exposure causes oxidative stress, inflammation and genotoxicity. The objective of this systematic review was to assess the contributions of primary (i.e.... (Meta-Analysis)
Meta-Analysis Review
Carbon black exposure causes oxidative stress, inflammation and genotoxicity. The objective of this systematic review was to assess the contributions of primary (i.e. direct formation of DNA damage) and secondary genotoxicity (i.e., DNA lesions produced indirectly by inflammation) to the overall level of DNA damage by carbon black. The database is dominated by studies that have measured DNA damage by the comet assay. Cell culture studies indicate a genotoxic action of carbon black, which might be mediated by oxidative stress. Many in vivo studies originate from one laboratory that has investigated the genotoxic effects of Printex 90 in mice by intra-tracheal instillation. Meta-analysis and pooled analysis of these results demonstrate that Printex 90 exposure is associated with a slightly increased level of DNA strand breaks in bronchoalveolar lavage cells and lung tissue. Other types of genotoxic damage have not been investigated as thoroughly as DNA strand breaks, although there is evidence to suggest that carbon black exposure might increase the mutation frequency and cytogenetic endpoints. Stratification of studies according to concurrent inflammation and DNA damage does not indicate that carbon black exposure gives rise to secondary genotoxicity. Even substantial pulmonary inflammation is at best only associated with a weak genotoxic response in lung tissue. In conclusion, the review indicates that nanosized carbon black is a weak genotoxic agent and this effect is more likely to originate from a primary genotoxic mechanism of action, mediated by e.g., oxidative stress, than inflammation-driven (secondary) genotoxicity.
Topics: Mice; Animals; Soot; Comet Assay; DNA Damage; Nanoparticles; Inflammation; Mammals
PubMed: 36007825
DOI: 10.1016/j.mrrev.2022.108441 -
Biology Apr 2023Senescence is a cellular aging process in all multicellular organisms. It is characterized by a decline in cellular functions and proliferation, resulting in increased... (Review)
Review
BACKGROUND
Senescence is a cellular aging process in all multicellular organisms. It is characterized by a decline in cellular functions and proliferation, resulting in increased cellular damage and death. These conditions play an essential role in aging and significantly contribute to the development of age-related complications. Humanin is a mitochondrial-derived peptide (MDP), encoded by mitochondrial DNA, playing a cytoprotective role to preserve mitochondrial function and cell viability under stressful and senescence conditions. For these reasons, humanin can be exploited in strategies aiming to counteract several processes involved in aging, including cardiovascular disease, neurodegeneration, and cancer. Relevance of these conditions to aging and disease: Senescence appears to be involved in the decay in organ and tissue function, it has also been related to the development of age-related diseases, such as cardiovascular conditions, cancer, and diabetes. In particular, senescent cells produce inflammatory cytokines and other pro-inflammatory molecules that can participate to the development of such diseases. Humanin, on the other hand, seems to contrast the development of such conditions, and it is also known to play a role in these diseases by promoting the death of damaged or malfunctioning cells and contributing to the inflammation often associated with them. Both senescence and humanin-related mechanisms are complex processes that have not been fully clarified yet. Further research is needed to thoroughly understand the role of such processes in aging and disease and identify potential interventions to target them in order to prevent or treat age-related conditions.
OBJECTIVES
This systematic review aims to assess the potential mechanisms underlying the link connecting senescence, humanin, aging, and disease.
PubMed: 37106758
DOI: 10.3390/biology12040558 -
Sports Medicine (Auckland, N.Z.) Jan 2020Exercise is widely recognised for its health enhancing benefits. Despite this, an overproduction of reactive oxygen and nitrogen species (RONS), outstripping antioxidant... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Exercise is widely recognised for its health enhancing benefits. Despite this, an overproduction of reactive oxygen and nitrogen species (RONS), outstripping antioxidant defence mechanisms, can lead to a state of (chronic) oxidative stress. DNA is a vulnerable target of RONS attack and, if left unrepaired, DNA damage may cause genetic instability.
OBJECTIVE
This meta-analysis aimed to systematically investigate and assess the overall effect of studies reporting DNA damage following acute aerobic exercise.
METHODS
Web of Science, PubMed, MEDLINE, EMBASE, and Scopus were searched until April 2019. Outcomes included (1) multiple time-points (TPs) of measuring DNA damage post-exercise, (2) two different quantification methods (comet assay and 8-oxo-2'-deoxyguanosine; 8-OHdG), and (3) protocols of high intensity (≥ 75% of maximum rate of oxygen consumption; VO) and long distance (≥ 42 km).
RESULTS
Literature search identified 4316 non-duplicate records of which 35 studies were included in the meta-analysis. The evidence was strong, showcasing an increase in DNA damage immediately following acute aerobic exercise with a large-effect size at TP 0 (0 h) (SMD = 0.875; 95% CI 0.5, 1.25; p < 0.05). When comparing between comet assay and 8-OHdG at TP 0, a significant difference was observed only when using the comet assay. Finally, when isolating protocols of long-distance and high-intensity exercise, increased DNA damage was only observed in the latter. (SMD = 0.48; 95% CI - 0.16, 1.03; p = 0.15 and SMD = 1.18; 95% CI 0.71, 1.65; p < 0.05 respectively).
CONCLUSIONS
A substantial increase in DNA damage occurs immediately following acute aerobic exercise. This increase remains significant between 2 h and 1 day, but not within 5-28 days post-exercise. Such an increase was not observed in protocols of a long-distance. The relationship between exercise and DNA damage may be explained through the hormesis theory, which is somewhat one-dimensional, and thus limited. The hormesis theory describes how exercise modulates any advantageous or harmful effects mediated through RONS, by increasing DNA oxidation between the two end-points of the curve: physical inactivity and overtraining. We propose a more intricate approach to explain this relationship: a multi-dimensional model, to develop a better understanding of the complexity of the relationship between DNA integrity and exercise.
Topics: DNA Damage; Exercise; Humans
PubMed: 31529301
DOI: 10.1007/s40279-019-01181-y -
Cancer Treatment Reviews Nov 2023PARP inhibitors (PARPi) are a standard-of-care (SoC) treatment option for patients with metastatic castration-resistant prostate cancer (mCRPC). Several clinical trials... (Meta-Analysis)
Meta-Analysis Review
INTRODUCTION
PARP inhibitors (PARPi) are a standard-of-care (SoC) treatment option for patients with metastatic castration-resistant prostate cancer (mCRPC). Several clinical trials have shown the potential of combining PARPi with other anticancer agents. Therefore, we conducted a systematic review and meta-analysis to comprehensively evaluate the efficacy and safety of PARPi in patients with metastatic prostate cancer.
METHODS
MEDLINE, Cochrane CENTRAL, EMBASE, CINAHL, and Web of Science were searched on March 22nd, 2023, for phase 2 or 3 clinical trials. Efficacy (progression-free survival [PFS], overall survival [OS], PSA decline >50% [PSA50], and objective response rate [ORR]) and safety outcomes were assessed in the included studies.
RESULTS
Seventeen clinical trials (PARPi monotherapy [n = 7], PARPi + androgen-receptor signaling inhibitors [ARSI] [n = 6], and PARPi + immune checkpoint inhibitors [ICI] [n = 4]) were included in the quantitative analyses. PARPi monotherapy improved radiographic PFS and OS over SoC in mCRPC patients with alterations in BRCA1 or BRCA2 genes but not in those with alterations in the ATM gene. Higher rates of PSA50 and ORR were reported in participants treated with PARPi + ARSI than in single-agent PARPi or PARPi + ICI. Although the rate of high-grade adverse events was similar across all groups, treatment discontinuation was higher in patients treated with PARPi-based combinations than PARPi monotherapy.
CONCLUSION
The efficacy of PARPi is not uniform across mCRPC patients with alterations in DNA damage repair genes, and optimal patient selection remains a clinical challenge. No unexpected safety signals for this class of agents emerged from this analysis.
Topics: Male; Humans; Poly(ADP-ribose) Polymerase Inhibitors; Prostatic Neoplasms, Castration-Resistant; Immune Checkpoint Inhibitors; Patient Selection; Progression-Free Survival
PubMed: 37716332
DOI: 10.1016/j.ctrv.2023.102623