ZnO Nanoparticles Alter Redox Metabolism of Limnoperna Fortunei

Abstract Nanoparticles incorporated in consumer and industrial products cause concerns about their potential ecological impacts. Zinc oxide nanoparticles (ZnO-NP) have several applications, which increases their potential for release to the environment, causing ecotoxicological problems. Bivalve mollusks are susceptible targets for nanoparticles toxicity, since nanomaterials can enter the cells by endocytosis mechanisms. Limnoperma fortunei (golden mussel) are validated for biomonitoring purposes and have a wide distribution in the South of Brazil, where it can be collected throughout the year. The aim of this study was to evaluate the influence of ZnO-NP on the redox metabolism by enzymatic and non-enzymatic antioxidant defense assessment in addition to DNA damage by DNA fragmentation assay in L. fortunei after exposure to ZnO-NP. Adult bivalves were placed in contact with 1, 10, and 50 µg mL-1 ZnO-NP during three incubation times: 2, 4 and 24 h. Ionic Zn release, enzymatic and non-enzymatic antioxidant activity, oxidative damage to lipids and proteins and DNA damage were evaluated. Oxidative damage to proteins and lipids were observed after 4 h exposure and returned to baseline levels after 24 h. Superoxide dismutase levels decreased after 4 h exposure and increased after 24 h. No significant alteration was observed in catalase activity or even DNA double strand cleavage. The dissociation of ZnO may occur after 24 h, releasing ionic zinc (Zn2+) by hydrolysis, which was confirmed as the ionic Zn concentration increased following 24 h exposure. In conclusion, ZnO-NP were able to induce oxidative stress in exposed golden mussels. The golden mussel is capable to modulate its own antioxidant defences in response to oxidative stress and seems to be able to hydrolyse the nanoparticle and consequently release Zn2+ into the cellular compartment.

Download Full-text

Paternal impacts on development: identification of genomic regions vulnerable to oxidative DNA damage in human spermatozoa

Human Reproduction ◽

10.1093/humrep/dez153 ◽

2019 ◽

Vol 34 (10) ◽

pp. 1876-1890 ◽

Cited By ~ 8

Author(s):

M J Xavier ◽

B Nixon ◽

S D Roman ◽

R J Scott ◽

J R Drevet ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Male Infertility ◽

Oxidative Damage ◽

Oxidative Dna Damage ◽

Human Spermatozoa ◽

Research Centre ◽

Environmental Toxicants ◽

Next Generation ◽

Genomic Regions

Abstract STUDY QUESTION Do all regions of the paternal genome within the gamete display equivalent vulnerability to oxidative DNA damage? SUMMARY ANSWER Oxidative DNA damage is not randomly distributed in mature human spermatozoa but is instead targeted, with particular chromosomes being especially vulnerable to oxidative stress. WHAT IS KNOWN ALREADY Oxidative DNA damage is frequently encountered in the spermatozoa of male infertility patients. Such lesions can influence the incidence of de novo mutations in children, yet it remains to be established whether all regions of the sperm genome display equivalent susceptibility to attack by reactive oxygen species. STUDY DESIGN, SIZE, DURATION Human spermatozoa obtained from normozoospermic males (n = 8) were split into equivalent samples and subjected to either hydrogen peroxide (H2O2) treatment or vehicle controls before extraction of oxidized DNA using a modified DNA immunoprecipitation (MoDIP) protocol. Specific regions of the genome susceptible to oxidative damage were identified by next-generation sequencing and validated in the spermatozoa of normozoospermic males (n = 18) and in patients undergoing infertility evaluation (n = 14). PARTICIPANTS/MATERIALS, SETTING, METHODS Human spermatozoa were obtained from normozoospermic males and divided into two identical samples prior to being incubated with either H2O2 (5 mm, 1 h) to elicit oxidative stress or an equal volume of vehicle (untreated controls). Alternatively, spermatozoa were obtained from fertility patients assessed as having high basal levels of oxidative stress within their spermatozoa. All semen samples were subjected to MoDIP to selectively isolate oxidized DNA, prior to sequencing of the resultant DNA fragments using a next-generation whole-genomic sequencing platform. Bioinformatic analysis was then employed to identify genomic regions vulnerable to oxidative damage, several of which were selected for real-time quantitative PCR (qPCR) validation. MAIN RESULTS AND THE ROLE OF CHANCE Approximately 9000 genomic regions, 150–1000 bp in size, were identified as highly vulnerable to oxidative damage in human spermatozoa. Specific chromosomes showed differential susceptibility to damage, with chromosome 15 being particularly sensitive to oxidative attack while the sex chromosomes were protected. Susceptible regions generally lay outside protamine- and histone-packaged domains. Furthermore, we confirmed that these susceptible genomic sites experienced a dramatic (2–15-fold) increase in their burden of oxidative DNA damage in patients undergoing infertility evaluation compared to normal healthy donors. LIMITATIONS, REASONS FOR CAUTION The limited number of samples analysed in this study warrants external validation, as do the implications of our findings. Selection of male fertility patients was based on high basal levels of oxidative stress within their spermatozoa as opposed to specific sub-classes of male factor infertility. WIDER IMPLICATIONS OF THE FINDINGS The identification of genomic regions susceptible to oxidation in the male germ line will be of value in focusing future analyses into the mutational load carried by children in response to paternal factors such as age, the treatment of male infertility using ART and paternal exposure to environmental toxicants. STUDY FUNDING/COMPETING INTEREST(S) Project support was provided by the University of Newcastle’s (UoN) Priority Research Centre for Reproductive Science. M.J.X. was a recipient of a UoN International Postgraduate Research Scholarship. B.N. is the recipient of a National Health and Medical Research Council of Australia Senior Research Fellowship. Authors declare no conflict of interest.

Download Full-text

Nuclear Phospho-SOD1 Protects DNA from Oxidative Stress Damage in Amyotrophic Lateral Sclerosis

Journal of Clinical Medicine ◽

10.3390/jcm8050729 ◽

2019 ◽

Vol 8 (5) ◽

pp. 729 ◽

Cited By ~ 8

Author(s):

Matteo Bordoni ◽

Orietta Pansarasa ◽

Michela Dell’Orco ◽

Valeria Crippa ◽

Stella Gagliardi ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Amyotrophic Lateral Sclerosis ◽

Oxidative Damage ◽

Motor Neurons ◽

Mononuclear Cells ◽

Sporadic Amyotrophic Lateral Sclerosis ◽

Peripheral Blood Mononuclear ◽

High Level ◽

Lateral Sclerosis

We already demonstrated that in peripheral blood mononuclear cells (PBMCs) of sporadic amyotrophic lateral sclerosis (sALS) patients, superoxide dismutase 1 (SOD1) was present in an aggregated form in the cytoplasmic compartment. Here, we investigated the possible effect of soluble SOD1 decrease and its consequent aggregation. We found an increase in DNA damage in patients PBMCs characterized by a high level of aggregated SOD1, while we found no DNA damage in PBMCs with normal soluble SOD1. We found an activation of ataxia-telangiectasia-mutated (ATM)/Chk2 and ATM and Rad3-related (ATR)/Chk1 DNA damage response pathways, which lead to phosphorylation of SOD1. Moreover, data showed that phosphorylation allows SOD1 to shift from the cytoplasm to the nucleus, protecting DNA from oxidative damage. Such pathway was finally confirmed in our cellular model. Our data lead us to suppose that in a sub-group of patients this physiologic pathway is non-functional, leading to an accumulation of DNA damage that causes the death of particularly susceptible cells, like motor neurons. In conclusion, during oxidative stress SOD1 is phosphorylated by Chk2 leading to its translocation in the nuclear compartment, in which SOD1 protects DNA from oxidative damage. This pathway, inefficient in sALS patients, could represent an innovative therapeutic target.

Download Full-text

Carious Lesion Severity Induces Higher Antioxidant System Activity and Consequently Reduces Oxidative Damage in Children’s Saliva

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/3695683 ◽

2020 ◽

Vol 2020 ◽

pp. 1-9

Author(s):

Heitor Ceolin Araujo ◽

Ana Cláudia Melo Stevanato Nakamune ◽

Wilson Galhego Garcia ◽

Juliano Pelim Pessan ◽

Cristina Antoniali

Keyword(s):

Oxidative Stress ◽

Antioxidant Activity ◽

Oxidative Damage ◽

Antioxidant System ◽

Oxidative Stress Biomarkers ◽

System Activity ◽

Enzymatic Antioxidant ◽

Stress Biomarkers ◽

Salivary Biomarkers ◽

Carious Lesions

Oxidative stress biomarkers can be found at detectable concentrations in saliva. These salivary biomarkers reflect specific oxidation pathways associated with caries and periodontitis. Our study evaluated the influence of dental caries severity (assessed using the ICCMS™ criteria) on the levels of oxidative stress biomarkers in saliva from children. Unstimulated saliva samples were collected from patients (from one to three years old) in a day care center in Birigui, SP, Brazil, two hours after fasting. Children were divided into four groups (n=30/group), according to caries severity: caries free (group A), early carious lesions (group B), moderate carious lesions (group C), and advanced carious lesions (group D). The following salivary biomarkers were determined: total proteins (TP), measured by the Lowry method; oxidative damage, measured by the TBARS method; total antioxidant capacity (TAC); superoxide dismutase (SOD) enzymatic antioxidant activity; and uric acid (UA) non-enzymatic antioxidant activity. Data were analyzed by ANOVA, followed by the Student-Newman-Keuls test, Pearson and Spearman correlation coefficients, and multivariable linear regression (p<0.05). TP, TAC, SOD enzymatic antioxidant activity, and UA non-enzymatic antioxidant activity increased with caries severity, consequently reducing salivary oxidative damage. It was concluded that higher caries severity increases salivary antioxidant system activity, with consequent reduction in salivary oxidative damage.

Download Full-text

Selective Damage to Antioxidant Gene Promoters in FA Cells

Blood ◽

10.1182/blood.v118.21.2413.2413 ◽

2011 ◽

Vol 118 (21) ◽

pp. 2413-2413

Author(s):

Wei Du ◽

Reena Rani ◽

Jared Sipple ◽

Jonathan Schick ◽

Qishen Pang

Keyword(s):

Oxidative Stress ◽

Bone Marrow ◽

Dna Damage ◽

Oxidative Damage ◽

Oxidative Dna Damage ◽

Defense Genes ◽

Atpase Subunit ◽

Promoter Complex ◽

Anti Oxidant ◽

Promoter Dna

Abstract Abstract 2413 Oxidative stress has been implicated in the pathogenesis of many human diseases including Fanconi anemia (FA), a genetic disorder associated with bone marrow failure and progression to leukemia and other cancers. Here we show that several major anti-oxidant defense genes, including Glutathione peroxidase 1, Peroxiredoxin 3, Thioredoxin reductase 1, Superoxide dismutases 1, NAD(P)H:quinone oxireductase and Catalase, are down-regulated in bone marrow cells of FA patients. This gene down-regulation is selectively associated with increased oxidative DNA damage in the promoters of these anti-oxidant defense genes. Further, we show that both increased initial damage and reduced repair rate contribute to augmented oxidative DNA damage in FA cells. Using cell-based assays to assess promoter activity and damage repair kinetics, we demonstrate that FA proteins function to protect the promoter DNA from oxidative damage. Mechanistically, FA proteins appeared to act in concert with Brg1, a chromatin-remodeling ATPase subunit of the BAF complex. Specifically, Brg1 binds to the promoters of the anti-oxidant defense genes in steady state. Upon challenge with oxidative stress, FANCA and FANCD2 proteins are recruited to the promoter DNA, which correlates with significant increase in the binding of Brg1 within the promoter regions. Intriguingly, the formation of the FA-Brg1-promoter complex results in a marked decrease in nuclease hypersensitivity and oxidative damage in the promoter DNA in normal cells compared to FA cells. Finally, disassociation of the FA proteins from the Brg1-promoter complex parallels Pol II loading, suggesting a regulatory role for the FA proteins in transcription. Taken together, the study identifies a role of FA proteins in protecting anti-oxidant genes from oxidative damage. Disclosures: No relevant conflicts of interest to declare.

Download Full-text

Effect of Oxidative Stress on Lymphocytes from Elderly Subjects

Clinical Science ◽

10.1042/cs0940447 ◽

1998 ◽

Vol 94 (4) ◽

pp. 447-452 ◽

Cited By ~ 11

Author(s):

E. García-Arumí ◽

A. L. Andreu ◽

J. López-Hellín ◽

S. Schwartz

Keyword(s):

Oxidative Stress ◽

Enzyme Activity ◽

Oxidative Damage ◽

Antioxidant Enzyme ◽

Antioxidant Enzyme Activity ◽

Elderly Subjects ◽

Antioxidant Enzyme Activities ◽

Antioxidant Defences ◽

Protein Carbonyl Content ◽

Healthy Elderly

1. Oxidative damage has been associated with ageing, but there is no agreement as to whether or not it is produced by a decrease in antioxidant defences with the ageing process. In purified lymphocytes from 47 healthy elderly (75.27 ± 0.91 years) and 47 healthy young (29.87 ± 0.53 years) volunteers, we studied the levels of antioxidant enzyme activity (superoxide dismutase, catalase and glutathione peroxidase), protein oxidative damage (as protein carbonyl content) and lysosomal proteolytic activity (cathepsins B, H and L), with and without exposure to oxidative stress produced by 25 μmol/l H2O2. 2. There were no differences in antioxidant enzyme activities in the stressed and non-stressed samples between the young and elderly subjects, indicating that there was no relationship between age and antioxidant enzyme activity even in oxidative stress. However, a dissimilar response to oxidative stress was observed in protein oxidative damage and cathepsin B and L activities, depending on the age of the donor. 3. With these results we conclude that oxidative stress produces greater protein oxidative damage and increased protein degradation in elderly subjects than in young ones; this effect cannot be attributed to dissimilar antioxidant enzyme responses to oxidative stress, since these did not differ between the two age groups.

Download Full-text

Metals as a cause of oxidative stress in fish: a review

Veterinární Medicína ◽

10.17221/4272-vetmed ◽

2011 ◽

Vol 56 (No. 11) ◽

pp. 537-546 ◽

Cited By ~ 139

Author(s):

M. Sevcikova ◽

H. Modra ◽

A. Slaninova ◽

Z. Svobodova

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Oxidative Damage ◽

Metal Binding ◽

Special Functions ◽

Current Knowledge ◽

Reactive Oxygen ◽

Enzyme Inactivation ◽

Oxygen Species ◽

Antioxidant Defences

This review summarizes the current knowledge on the contribution of metals to the development of oxidative stress in fish. Metals are important inducers of oxidative stress in aquatic organisms, promoting formation of reactive oxygen species through two mechanisms. Redox active metals generate reactive oxygen species through redox cycling, while metals without redox potential impair antioxidant defences, especially that of thiol-containing antioxidants and enzymes. Elevated levels of reactive oxygen species lead to oxidative damage including lipid peroxidation, protein and DNA oxidation, and enzyme inactivation. Antioxidant defences include the enzyme system and low molecular weight antioxidants. Metal-binding proteins, such as ferritin, ceruloplasmin and metallothioneins, have special functions in the detoxification of toxic metals and also play a role in the metabolism and homeostasis of essential metals. Recent studies of metallothioneins as biomarkers indicate that quantitative analysis of mRNA expression of metallothionein genes can be appropriate in cases with elevated levels of metals and no evidence of oxidative damage in fish tissue. Components of the antioxidant defence are used as biochemical markers of oxidative stress. These markers may be manifested differently in the field than in results found in laboratory studies. A complex approach should be taken in field studies of metal contamination of the aquatic environment.  

Download Full-text

Yolk testosterone reduces oxidative damages during postnatal development

Biology Letters ◽

10.1098/rsbl.2010.0421 ◽

2010 ◽

Vol 7 (1) ◽

pp. 93-95 ◽

Cited By ~ 25

Author(s):

José Carlos Noguera ◽

Carlos Alonso-Alvarez ◽

Sin-Yeon Kim ◽

Judith Morales ◽

Alberto Velando

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Postnatal Development ◽

Early Development ◽

Early Life ◽

Antioxidant Defences ◽

Oxidative Damages ◽

Plasma Antioxidant ◽

Yolk Testosterone

Conditions experienced during early life can influence the development of an organism and several physiological traits, even in adulthood. An important factor is the level of oxidative stress experienced during early life. In birds, extra-genomic egg substances, such as the testosterone hormone, may exert a widespread influence over the offspring phenotype. Interestingly, testosterone can also upregulate the bioavailability of certain antioxidants but simultaneously increases the susceptibility to oxidative stress in adulthood. However, little is known about the effects of maternally derived yolk testosterone on oxidative stress in developing birds. Here, we investigated the role of yolk testosterone on oxidative stress of yellow-legged gull chicks during their early development by experimentally increasing yolk testosterone levels. Levels of antioxidants, reactive oxygen species and lipid oxidative damage were determined in plasma during nestlings' growth. Our results revealed that, contrary to control chicks, birds hatched from testosterone-treated eggs did not show an increase in the levels of oxidative damage during postnatal development. Moreover, the same birds showed a transient increase in plasma antioxidant levels. Our results suggest that yolk testosterone may shape the oxidative stress-resistance phenotype of the chicks during early development owing to an increase in antioxidant defences and repair processes.

Download Full-text

Effects of Smoking during Pregnancy on DNA Damage and ROS Level Consequences in Maternal and Newborns’ Blood

Archives of Industrial Hygiene and Toxicology ◽

10.2478/10004-1254-64-2013-2232 ◽

2013 ◽

Vol 64 (1) ◽

pp. 35-46 ◽

Cited By ~ 7

Author(s):

Umit Aydogan ◽

Emre Durmaz ◽

Cihangir Mutlu Ercan ◽

Ayse Eken ◽

Onur Kenan Ulutas ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Oxidative Damage ◽

Cord Blood ◽

Third Trimester ◽

Smoking During Pregnancy ◽

Oxidative Stress Parameters ◽

Carcinogenic Substances ◽

Plasma Nitrite ◽

Stress Parameters

Some of the genotoxic/carcinogenic substances or metabolites in cigarette smoke are capable of passing through the placenta and harming a newborn’s health. Smoking is also known as a factor in the formation of oxidative damage and the main mechanism involved in the carcinogenic process. Predetermining this genotoxic risk can be successfully achieved by measuring certain parameters of oxidative stress. The comet assay is considered an important biomarker for the evaluation of genotoxic substances and is effective for detecting DNA damage caused by smoking. This study examined third trimester bloods and the cord blood of 28 actively smoking and 22 non-smoking mothers in terms of DNA damage and oxidative stress parameters. Cu/Zn superoxide dismutase (CuZn-SOD), malondialdehyde (MDA), catalase (CAT), plasma nitrite/nitrates (NO2 -/NO3 -), selenium-dependent glutathione peroxidase (Se-GPx), Cu, and Zn levels were measured as indicators of oxidative damage. There were no significant increases in DNA damage of the actively smoking pregnant group in comparison with the non-smoking pregnant group, either in the third trimester or cord blood. Oxidative stress parameters of smoker and non-smoker groups were statistically different for MDA (p<0.05), CuZn-SOD (p<0.01), Se-GPx (p<0.05) values while the difference was not significant for NO2 -/NO3 -, CAT, Zn, and Cu values. The same values were also investigated in cord blood, and only NO2/NO3 -(p<0.01), Se-GPx (p<0.01 and CAT (p<0.001) values were found statistically different. Smoking mothers may have been exposed to more oxidative stress than non-smoking mothers.

Download Full-text

Mixture Analysis of Associations between Occupational Exposure to Polycyclic Aromatic Hydrocarbons and Sperm Oxidative DNA Damage

Annals of Work Exposures and Health ◽

10.1093/annweh/wxab072 ◽

2021 ◽

Author(s):

Hueiwang Anna Jeng ◽

Sinjini Sikdar ◽

Chih-Hong Pan ◽

Guo-Ping Chang-Chien

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Oxidative Damage ◽

Oxidative Dna Damage ◽

Selection Process ◽

Coke Oven ◽

Breathing Zone ◽

Suggestive Association ◽

Polycyclic Aromatic ◽

Coke Oven Workers

Abstract Objective This study aimed to determine (i) associations between levels of the polycyclic aromatic hydrocarbon (PAH) mixture with 16 targeted PAH compounds in the personal breathing zone area and sperm oxidative DNA damage, (ii) associations between levels of individual PAH compounds and sperm oxidative DNA damage, (iii) oxidative stress as the mode of action for the genotoxic effects on sperm, and (iv) any dose–response relationship between exposure to the PAH mixture and/or individual PAH compounds and sperm oxidative DNA damage. Methods Sixteen targeted PAH compounds in the personal breathing zone area of 38 coke-oven workers and 24 control subjects were quantified using gas chromatography–mass spectrometry. Sperm oxidative damage and status were evaluated by measuring levels of sperm 7,8-dihydro-8-oxoguanie (8-oxodGuo), seminal malondialdehyde (MDA) and seminal reactive oxygen species (ROS). Bayesian kernel machine regression with hierarchical variable selection process was employed to determine associations of the PAH mixture and the biomarkers of sperm oxidative damage. A novel grouping approach needed for the hierarchical variable selection process was developed based on PAH bay region and molecular weight. Results The PAH mixture exhibited a positive trend with increased sperm 8-oxodGuo levels at their lower percentiles (25th–50th). The exposure of the PAH mixture was associated with increased MDA levels in sperm. Bay and bay-like regions of the PAH mixture were the most important group for estimating the associations between the PAH mixture and sperm oxidative stress status. Benzo[a]anthracene was the main individual PAH compound that was associated with increased MDA levels. Conclusion Sperm oxidative DNA damage induced by occupational exposure to the PAH mixture had a suggestive association with increased MDA levels in coke-oven workers. Finally, the study identified that the individual PAH compound, benzo[a]anthracene, was the primary driver for the suggestive association between the PAH mixture and sperm oxidative damage.

Download Full-text

Oxidative DNA damage and oxidative stress in lead-exposed workers

Human & Experimental Toxicology ◽

10.1177/0960327116665674 ◽

2016 ◽

Vol 36 (7) ◽

pp. 744-754 ◽

Cited By ~ 33

Author(s):

M Dobrakowski ◽

N Pawlas ◽

A Kasperczyk ◽

A Kozłowska ◽

E Olewińska ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Oxidative Damage ◽

Oxidative Dna Damage ◽

Blood Lead ◽

Antioxidant Defense System ◽

Control Group ◽

High Exposure ◽

Human Leukocytes ◽

Low Exposure

There are many discrepancies among the results of studies on the genotoxicity of lead. The aim of the study was to explore lead-induced DNA damage, including oxidative damage, in relation to oxidative stress intensity parameters and the antioxidant defense system in human leukocytes. The study population consisted of 100 male workers exposed to lead. According to the blood lead (PbB) levels, they were divided into the following three subgroups: a group with PbB of 20–35 μg/dL (low exposure to lead (LE) group), a group with a PbB of 35–50 µg/dL (medium exposure to lead (ME) group), and a group with a PbB of >50 μg/dL (high exposure to lead (HE) group). The control group consisted of 42 healthy males environmentally exposed to lead (PbB < 10 μg/dL). A comet assay was used to measure the DNA damage in leukocytes. We measured the activity of superoxide dismutase (SOD), catalase, glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-S-transferase (GST) as well as the concentration of malondialdehyde (MDA), and the value of the total antioxidant capacity. The level of PbB was significantly higher in the examined subgroups than in the control group. The percentage of DNA in the tail was significantly higher in the LE, ME, and HE subgroups than in the control group by 10% ( p = 0.001), 15% ( p < 0.001), and 20% ( p < 0.001), respectively. The activity of GR was significantly lower in the LE and ME subgroups than in the control group by 25% ( p = 0.007) and 17% ( p = 0.028), respectively. The activity of G6PD was significantly lower in the ME subgroup by 25% ( p = 0.022), whereas the activity of GST was significantly higher in the HE subgroup by 101% ( p = 0.001) than in the control group. Similarly, the activity of SOD was significantly higher in the LE and ME subgroups by 48% ( p = 0.026) and 34% ( p = 0.002), respectively. The concentration of MDA was significantly higher in the LE, ME, and HE subgroups than in the control group by 43% ( p = 0.016), 57% ( p < 0.001), and 108% ( p < 0.001), respectively. Occupational lead exposure induces DNA damage, including oxidative damage, in human leukocytes. The increase in DNA damage was accompanied by an elevated intensity of oxidative stress.

Download Full-text