Oxidative stress, telomere shortening, and
            DNA
            methylation in relation to low‐to‐moderate occupational exposure to welding fumes

Urinary concentrations of 16 different exposure biomarkers to metals were determined at the beginning and at the end of a working shift on a group of workers in the metal carpentry industry. Five different oxidative stress biomarkers were also measured, such as the oxidation products of RNA and DNA metabolized and excreted in the urine. The results of workers exposed to metals were compared to those of a control group. The metal concentrations found in these workers were well below the occupational exposure limit values and exceeded the mean concentrations of the same metals in the urine of the control group by a factor of four at maximum. Barium (Ba), mercury (Hg), lead (Pb) and strontium (Sr) were correlated with the RNA oxidative stress biomarker, 8-oxo-7, 8-dihydroguanosine (8-oxoGuo), which was found able to discriminate exposed workers from controls with a high level of specificity and sensitivity. The power of this early diagnostic technique was assessed by means of the ROC curve. Ba, rubidium (Rb), Sr, tellurium (Te), and vanadium (V) were correlated with the level of the protein oxidation biomarker 3-Nitrotyrosine (3-NO2Tyr), and Ba, beryllium (Be), copper (Cu), and Rb with 5-methylcytidine (5-MeCyt), an epigenetic marker of RNA damage. These effect biomarkers can help in identifying those workers that can be defined as “occupationally exposed” even at low exposure levels, and they can provide information about the impact that such doses have on their health.

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Oxidative stress status of Turkish welders

Toxicology and Industrial Health ◽

10.1177/0748233720922722 ◽

2020 ◽

Vol 36 (4) ◽

pp. 263-271

Author(s):

Dilek Tokaç ◽

Hatice Gül Anlar ◽

Merve Bacanlı ◽

Sevtap Aydın Dilsiz ◽

Servet İritaş ◽

...

Keyword(s):

Oxidative Stress ◽

Occupational Exposure ◽

Older Workers ◽

Ultrafine Particles ◽

Oxidative Dna Damage ◽

Modern Society ◽

Welding Fumes ◽

Oxidative Stress Status ◽

Important Health ◽

Different Populations

Welding, a fabrication process that joins metals or thermoplastics by causing coalescence, is indispensable in modern society and ubiquitous in industry. Welding generates fumes that contain several metals and gases that comprise fine and ultrafine particles with the potential for adverse effects. Although health risks of welders have been evaluated in different populations, occupational exposure to welding fumes is still considered to be an important health problem, especially in developing countries. The aim of this study was to investigate the effects of welding fume exposure on important oxidative stress parameters such as superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), total glutathione (GSH), glutathione peroxidase (GPx), malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) in Turkish welders ( n = 48). The influence of confounding factors such as age, smoking habits, alcohol consumption, and duration of exposure on the studied parameters was also analyzed. In our study, significant decreases in the levels of GSH and activities of CAT, SOD, and GPx and significant increases of MDA, 8-OHdG levels and GR activity were found in the workers compared to the controls. There was a negative correlation between GSH levels and alcohol usage. Also, older workers (≥35 years) had significantly higher GR levels than younger workers. But smoking and alcohol usage, duration of exposure, and utilization of protective measures had no significant effect on the studied parameters in the workers. These results indicate that occupational exposure to welding fumes appears to induce oxidative stress and oxidative DNA damage.

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Creatine Alleviates Doxorubicin-Induced Liver Damage by Inhibiting Liver Fibrosis, Inflammation, Oxidative Stress, and Cellular Senescence

Nutrients ◽

10.3390/nu13010041 ◽

2020 ◽

Vol 13 (1) ◽

pp. 41

Author(s):

Nouf Aljobaily ◽

Michael J. Viereckl ◽

David S. Hydock ◽

Hend Aljobaily ◽

Tsung-Yen Wu ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Methylation ◽

Body Weight ◽

Liver Fibrosis ◽

Liver Damage ◽

Cellular Senescence ◽

Weight Ratio ◽

Mrna Levels ◽

Body Weight Ratio ◽

Chromosomal Stability

Background: Treatment with the chemotherapy drug doxorubicin (DOX) may lead to toxicities that affect non-cancer cells including the liver. Supplementing the diet with creatine (Cr) has been suggested as a potential intervention to minimize DOX-induced side effects, but its effect in alleviating DOX-induced hepatoxicity is currently unknown. Therefore, we aimed to examine the effects of Cr supplementation on DOX-induced liver damage. Methods: Male Sprague-Dawley rats were fed a diet supplemented with 2% Cr for four weeks, 4% Cr for one week followed by 2% Cr for three more weeks, or control diet for four weeks. Animals then received either a bolus i.p. injection of DOX (15 mg/kg) or saline as a placebo. Animals were then sacrificed five days-post injection and markers of hepatoxicity were analyzed using the liver-to-body weight ratio, aspartate transaminase (AST)-to- alanine aminotransferase (ALT) ratio, alkaline phosphatase (ALP), lipemia, and T-Bilirubin. In addition, hematoxylin and eosin (H&E) staining, Picro-Sirius Red staining, and immunofluorescence staining for CD45, 8-OHdG, and β-galactosidase were performed to evaluate liver morphology, fibrosis, inflammation, oxidative stress, and cellular senescence, respectively. The mRNA levels for biomarkers of liver fibrosis, inflammation, oxidative stress, and senescence-related genes were measured in liver tissues. Chromosomal stability was evaluated using global DNA methylation ELISA. Results: The ALT/AST ratio and liver to body weight ratio tended to increase in the DOX group, and Cr supplementation tended to attenuate this increase. Furthermore, elevated levels of liver fibrosis, inflammation, oxidative stress, and senescence were observed with DOX treatment, and Cr supplementation prior to DOX treatment ameliorated this hepatoxicity. Moreover, DOX treatment resulted in chromosomal instability (i.e., altered DNA methylation profile), and Cr supplementation showed a tendency to restore chromosomal stability with DOX treatment. Conclusion: The data suggest that Cr protected against DOX-induced hepatotoxicity by attenuating fibrosis, inflammation, oxidative stress, and senescence.

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Telomere Shortening and Psychiatric Disorders: A Systematic Review

Cells ◽

10.3390/cells10061423 ◽

2021 ◽

Vol 10 (6) ◽

pp. 1423

Author(s):

Pedro A. Pousa ◽

Raquel M. Souza ◽

Paulo Henrique M. Melo ◽

Bernardo H. M. Correa ◽

Tamires S. C. Mendonça ◽

...

Keyword(s):

Oxidative Stress ◽

Psychological Distress ◽

Mental Disorders ◽

Psychiatric Disorders ◽

Telomere Length ◽

Traumatic Stress ◽

Molecular Mechanisms ◽

Cochrane Library ◽

Telomere Shortening ◽

Anxiety Depression

Telomeres are aging biomarkers, as they shorten while cells undergo mitosis. The aim of this study was to evaluate whether psychiatric disorders marked by psychological distress lead to alterations to telomere length (TL), corroborating the hypothesis that mental disorders might have a deeper impact on our physiology and aging than it was previously thought. A systematic search of the literature using MeSH descriptors of psychological distress (“Traumatic Stress Disorder” or “Anxiety Disorder” or “depression”) and telomere length (“cellular senescence”, “oxidative stress” and “telomere”) was conducted on PubMed, Cochrane Library and ScienceDirect databases. A total of 56 studies (113,699 patients) measured the TL from individuals diagnosed with anxiety, depression and posttraumatic disorders and compared them with those from healthy subjects. Overall, TL negatively associates with distress-related mental disorders. The possible underlying molecular mechanisms that underly psychiatric diseases to telomere shortening include oxidative stress, inflammation and mitochondrial dysfunction linking. It is still unclear whether psychological distress is either a cause or a consequence of telomere shortening.

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Occupational exposure characterization in professional sprayers: Clinical utility of oxidative stress biomarkers

Environmental Toxicology and Pharmacology ◽

10.1016/j.etap.2011.05.010 ◽

2011 ◽

Vol 32 (2) ◽

pp. 249-258 ◽

Cited By ~ 16

Author(s):

Mariana Astiz ◽

Nathalie Arnal ◽

María J.T. de Alaniz ◽

Carlos Alberto Marra

Keyword(s):

Oxidative Stress ◽

Occupational Exposure ◽

Clinical Utility ◽

Oxidative Stress Biomarkers ◽

Stress Biomarkers

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Assessment of Occupational Exposure to Manganese and Other Metals in Welding Fumes by Portable X-ray Fluorescence Spectrometer

Journal of Occupational and Environmental Hygiene ◽

10.1080/15459624.2010.485262 ◽

2010 ◽

Vol 7 (8) ◽

pp. 456-465 ◽

Cited By ~ 13

Author(s):

Wisanti Laohaudomchok ◽

Jennifer M. Cavallari ◽

Shona C. Fang ◽

Xihong Lin ◽

Robert F. Herrick ◽

...

Keyword(s):

Occupational Exposure ◽

Welding Fumes ◽

X Ray ◽

Fluorescence Spectrometer

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Effects of occupational exposure to aluminium on some oxidative stress and DNA damage parameters

Human & Experimental Toxicology ◽

10.1177/0960327117747024 ◽

2017 ◽

Vol 37 (9) ◽

pp. 901-908 ◽

Cited By ~ 7

Author(s):

AM Samir ◽

LA Rashed

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Occupational Exposure ◽

Tail Length ◽

Significant Negative Correlation ◽

Exposed Workers ◽

Occupationally Exposed ◽

Aluminium Level ◽

Total Antioxidant ◽

Serum Aluminium

Aim: The aim of this work was to investigate the relationships between aluminium levels, oxidative status and DNA damage in workers occupationally exposed to aluminium. Subjects and methods: This study was conducted in a secondary aluminium smelter. It included 96 male workers occupationally exposed to aluminium fume and dust compared to 96 male nonexposed individuals. Full history and clinical examination were done for all participants. Laboratory investigations in the form of serum aluminium, total antioxidant capacity (TAC), urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) and comet assay test were performed. Results: Serum aluminium level ranged from 4 to 30 µg/L of median: 10 µg/L; urinary 8-OHdG ranged from 2.7 to 17.2 ng/mg creatinine of median: 7.6 ng/mg creatinine; comet tail length (CTL) ranged from 19.7 to 50.5 µm of median: 45 µm, were statistically significantly increased in the exposed group compared to nonexposed group. In exposed workers, a statistically significant positive correlations were found between serum aluminium level and urinary 8-OHdG ( r = 0.75, p < 0.001); aluminium level and CTL ( r = 0.71, p < 0.001); and urinary 8-OHdG and CTL ( r = 0.71, p < 0.001). There was a statistically significant negative correlation between serum aluminium and TAC ( r = −0.76, p < 0.001). Conclusion: Occupational exposure to aluminium in secondary aluminium smelters was related to the induction of oxidative stress and DNA damage. This may promote the development of adverse health hazards in the exposed workers

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Oxidative Stress, Telomere Shortening, and Apoptosis Associated to Sarcopenia and Frailty in Patients with Multimorbidity

Journal of Clinical Medicine ◽

10.3390/jcm9082669 ◽

2020 ◽

Vol 9 (8) ◽

pp. 2669 ◽

Cited By ~ 2

Author(s):

Máximo Bernabeu-Wittel ◽

Raquel Gómez-Díaz ◽

Álvaro González-Molina ◽

Sofía Vidal-Serrano ◽

Jesús Díez-Manglano ◽

...

Keyword(s):

Oxidative Stress ◽

Telomere Length ◽

Prospective Observational Study ◽

Oxygen Species ◽

Oxidative Stress Markers ◽

Blood Leukocytes ◽

Telomere Shortening ◽

Blood Samples ◽

Stress Markers ◽

Total Antioxidant

Background: The presence of oxidative stress, telomere shortening, and apoptosis in polypathological patients (PP) with sarcopenia and frailty remains unknown. Methods: Multicentric prospective observational study in order to assess oxidative stress markers (catalase, glutathione reductase (GR), total antioxidant capacity to reactive oxygen species (TAC-ROS), and superoxide dismutase (SOD)), absolute telomere length (aTL), and apoptosis (DNA fragmentation) in peripheral blood samples of a hospital-based population of PP. Associations of these biomarkers to sarcopenia, frailty, functional status, and 12-month mortality were analyzed. Results: Of the 444 recruited patients, 97 (21.8%), 278 (62.6%), and 80 (18%) were sarcopenic, frail, or both, respectively. Oxidative stress markers (lower TAC-ROS and higher SOD) were significantly enhanced and aTL significantly shortened in patients with sarcopenia, frailty or both syndromes. No evidence of apoptosis was detected in blood leukocytes of any of the patients. Both oxidative stress markers (GR, p = 0.04) and telomere shortening (p = 0.001) were associated to death risk and to less survival days. Conclusions: Oxidative stress markers and telomere length were enhanced and shortened, respectively, in blood samples of polypathological patients with sarcopenia and/or frailty. Both were associated to decreased survival. They could be useful in the clinical practice to assess vulnerable populations with multimorbidity and of potential interest as therapeutic targets.

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Oxidative stress underlies heritable impacts of paternal cigarette smoke exposure

10.1101/750638 ◽

2019 ◽

Author(s):

Patrick J Murphy ◽

Jingtao Guo ◽

Timothy G Jenkins ◽

Emma R James ◽

John R Hoidal ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Dna Methylation ◽

Cigarette Smoke ◽

Cigarette Smoke Exposure ◽

Epigenetic Changes ◽

Sperm Dna ◽

Increased Risk ◽

Paternal Smoking ◽

Sperm Dna Methylation

SUMMARYPaternal cigarette smoke (CS) exposure is associated with increased risk of behavioral disorders and cancer in offspring, but the mechanism has not been identified. This study used mouse models to evaluate: 1) what impact paternal CS exposure has on sperm DNA methylation (DNAme), 2) whether sperm DNAme changes persist after CS exposure ends, 3) the degree to which DNAme and gene expression changes occur in offspring and 4) the mechanism underlying impacts of CS exposure. We demonstrate that CS exposure induces sperm DNAme changes that are partially corrected within 28 days of removal from CS exposure. Additionally, paternal smoking causes changes in neural DNAme and gene expression in offspring. Remarkably, the effects of CS exposure are largely recapitulated in oxidative stress-compromised Nrf2-/- mice and their offspring, independent of paternal smoking. These results demonstrate that paternal CS exposure impacts offspring phenotype and that oxidative stress underlies CS induced heritable epigenetic changes.

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Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening

International Journal of Molecular Sciences ◽

10.3390/ijms222212536 ◽

2021 ◽

Vol 22 (22) ◽

pp. 12536

Author(s):

Szymon Turkiewicz ◽

Marta Ditmer ◽

Marcin Sochal ◽

Piotr Białasiewicz ◽

Dominik Strzelecki ◽

...

Keyword(s):

Oxidative Stress ◽

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Circadian Clock ◽

Chronic Inflammation ◽

Cellular Senescence ◽

Molecular Mechanisms ◽

Telomere Shortening ◽

Age Related ◽

Obstructive Sleep

Obstructive sleep apnea (OSA) is chronic disorder which is characterized by recurrent pauses of breathing during sleep which leads to hypoxia and its two main pathological sequelae: oxidative stress and chronic inflammation. Both are also associated with cellular senescence. As OSA patients present with higher prevalence of age-related disorders, such as atrial hypertension or diabetes mellitus type 2, a relationship between OSA and accelerated aging is observable. Furthermore, it has been established that these OSA are associated with telomere shortening. This process in OSA is likely caused by increased oxidative DNA damage due to increased reactive oxygen species levels, DNA repair disruptions, hypoxia, chronic inflammation, and circadian clock disturbances. The aim of the review is to summarize study outcomes on changes in leukocyte telomere length (LTL) in OSA patients and describe possible molecular mechanisms which connect cellular senescence and the pathophysiology of OSA. The majority of OSA patients are characterized by LTL attrition due to oxidative stress, hypoxia and inflammation, which make a kind of positive feedback loop, and circadian clock disturbance.

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