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Sports Medicine (Auckland, N.Z.) Jan 2020Page 17, Fig. 2.
Page 17, Fig. 2.
PubMed: 31578701
DOI: 10.1007/s40279-019-01197-4 -
The International Journal of... Jun 2017People with schizophrenia and other psychosis show increased proinflammatory and prooxidative status. However, the few studies that have specifically assessed oxidative... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
People with schizophrenia and other psychosis show increased proinflammatory and prooxidative status. However, the few studies that have specifically assessed oxidative and inflammatory markers in early onset psychosis (onset before age 18) have shown contradictory results.
METHODS
Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines for systematic reviews and meta-analyses were used to conduct a systematic literature search to detect studies comparing inflammatory and oxidative markers in early onset psychosis patients and healthy controls.
RESULTS
Seven studies met criteria for the qualitative analysis. Four studies met criteria for meta-analysis, comprising an overall sample of 261 early onset psychosis patients and 246 healthy controls. Six independent meta-analyses were performed for catalase, glutathione, glutathione peroxidase, superoxide dismutase, total antioxidant status, and cell/DNA oxidative damage. No significant differences were found between early onset psychosis patients and controls in any of the parameters assessed. Heterogeneity among studies was high. Qualitative analysis of individual studies showed an association of inflammatory and oxidative markers with clinical, cognitive, and neurobiological outcomes, especially in longitudinal assessments.
CONCLUSIONS
Despite the lack of significant differences between early onset psychosis patients and controls in the oxidative markers assessed in the meta-analyses, results based on individual studies suggest that greater inflammation and oxidative stress might lead to poorer outcomes in patients with first episodes of early onset psychosis.
Topics: Acute Disease; Humans; Inflammation; Oxidative Stress; Psychotic Disorders; Schizophrenia
PubMed: 28575316
DOI: 10.1093/ijnp/pyx015 -
Occupational benzene exposure and the risk of genetic damage: a systematic review and meta-analysis.BMC Public Health Jul 2020Benzene, an important component of organic solvents, is commonly used in industry. Meanwhile, benzene is a human carcinogen leading to leukemia. Although the links... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Benzene, an important component of organic solvents, is commonly used in industry. Meanwhile, benzene is a human carcinogen leading to leukemia. Although the links between benzene and various types of genetic damage indicators have been evaluated in several studies, but their results remain inconsistent. So we conducted a meta-analysis, and to explore the influence of low concentration benzene exposure on workers' genetic damage indicators using 3.25 mg/m as the boundary value, in order to provide a basis for improved prevention and control of the harm from benzene exposure to the occupational population.
METHODS
We conducted a search of five databases, including Pub Med, Web of Science, China National Knowledge Infrastructure (CNKI), Wan Fang Data and Chongqing VIP, to identify relevant articles up to December 25, 2018. Two researchers independently extracted and evaluated the data according to the inclusion and exclusion criteria of the literature. The imported articles were managed by Endnote X7, and the data were extracted and sorted by Excel 2013. We utilized Stata 12.0 software to perform the meta-analysis in the present study.
RESULTS
A total of 68 eligible articles were finally included for the synthetic analyses. The meta-analysis results showed that occupational benzene exposure led to significantly increased Micronucleus (MN) frequency, Sister chromatid exchange (SCE) frequency, Chromosome aberration (CA) frequency, Olive Tail moment (OTM), Tail moment (TM), Tail length (TL), and Tail DNA% (T DNA%) compared to the control group (P < 0.05), and the pooled effect value estimates were 1.36, 0.98, 0.76, 1.06, 0.96, 1.78, and 1.42, respectively. Subsequent analysis of the effect of low concentration benzene exposure on genetic damage found significantly increased MN frequency increased compared with the control group (P < 0.05).
CONCLUSIONS
Occupational benzene exposure can affect multiple genetic damage indicators. Even at an exposure concentration lower than 3.25 mg/m, benzene exposure has genotoxicity. These data provide an important scientific basis for the further revision of occupational disease prevention strategies. At the same time, increased attention should be focused on the health monitoring of the occupational population exposed to benzene, and health management should be strengthened to improve the health of the occupational population.
Topics: Adult; Benzene; Carcinogens; Case-Control Studies; Chromosome Aberrations; DNA Damage; Female; Humans; Industry; Male; Occupational Diseases; Occupational Exposure; Recombination, Genetic; Risk Factors
PubMed: 32669091
DOI: 10.1186/s12889-020-09215-1 -
Cellular and Molecular Gastroenterology... 2021Inflammatory bowel disease (IBD) patients have an increased risk of developing colitis-associated colon cancer (CAC); however, the basis for inflammation-induced genetic... (Review)
Review
Inflammatory bowel disease (IBD) patients have an increased risk of developing colitis-associated colon cancer (CAC); however, the basis for inflammation-induced genetic damage requisite for neoplasia is unclear. Several studies have shown that IBD patients have signs of increased oxidative damage, which could be a result of genetic and environmental factors such as an excess in oxidant molecules released during chronic inflammation, mitochondrial dysfunction, a failure in antioxidant capacity, or oxidant promoting diets. It has been suggested that chronic oxidative environment in the intestine leads to the DNA lesions that precipitate colon carcinogenesis in IBD patients. Indeed, several preclinical and clinical studies show that different endogenous and exogenous antioxidant molecules are effective at reducing oxidation in the intestine. However, most clinical studies have focused on the short-term effects of antioxidants in IBD patients but not in CAC. This review article examines the role of oxidative DNA damage as a possible precipitating event in CAC in the context of chronic intestinal inflammation and the potential role of exogenous antioxidants to prevent these cancers.
Topics: Animals; Antioxidants; Colitis; Colitis-Associated Neoplasms; Humans
PubMed: 33418102
DOI: 10.1016/j.jcmgh.2020.12.013 -
Noise & Health 2020Noise-induced hearing loss (NIHL) is one of the leading causes of acquired sensorineural hearing loss. However, molecular mechanisms responsible for its pathogenesis...
BACKGROUND
Noise-induced hearing loss (NIHL) is one of the leading causes of acquired sensorineural hearing loss. However, molecular mechanisms responsible for its pathogenesis remain to be elucidated. Epigenetic changes, i.e. DNA methylation, histone and microRNA expression modifications may function as a link between noise exposure and hearing loss. Therefore, the aim of the present review was to assess whether epigenetic alterations may serve as biomarkers of noise exposure or early effect.
MATERIALS AND METHODS
A systematic review of studies available in Pubmed, Scopus, and ISI Web of Science databases was performed.
RESULTS
Noise exposure was able to induce alterations in DNA methylation levels in workers and animal models, resulting in expression changes of genes related to hearing loss and also to extra-auditory effects. Differently expressed microRNAs were determined in NIHL workers compared to noise-exposed subjects with normal hearing, supporting their possible role as biomarkers of effect. Acoustic trauma affected histon acethylation and methylation levels in animals, suggesting their influence in the pathogenesis of acute noise-induced damage and their role as targets for potential therapeutic treatments.
CONCLUSIONS
Although preliminary data suggest a relationship between noise and epigenetic effects, the limited number of studies, their different methodologies and the lack of adequate characterization of acoustic insults prevent definite conclusions. In this context, further research aimed to define the epigenetic impact of workplace noise exposure and the role of such alterations in predicting hearing loss may be important for the adoption of correct risk assessment and management strategies in occupational settings.
Topics: Animals; DNA Methylation; Environmental Exposure; Epigenesis, Genetic; Genetic Markers; Hearing Loss, Noise-Induced; Histones; Humans; MicroRNAs; Noise; Occupational Diseases; Risk Assessment
PubMed: 33402608
DOI: 10.4103/nah.NAH_17_20 -
Journal of Oral and Maxillofacial... 2016Oral lichen planus (OLP) is a chronic inflammatory mucosal disease that is usually detected in 0.5-2.2% of the human population. Among these, only 0.5-2.9% of the... (Review)
Review
Oral lichen planus (OLP) is a chronic inflammatory mucosal disease that is usually detected in 0.5-2.2% of the human population. Among these, only 0.5-2.9% of the lesions progress to carcinoma. However, there are no prognostic markers available presently to recognize the increased risk in malignant transformation of the lesions. Selected markers for cell proliferation, adhesion, apoptosis and lymphocytic infiltration were analyzed by immunohistochemistry in addition to static cytometry for DNA content. The concept linking OLP and oral squamous cell carcinoma states that chronic inflammation results in crucial DNA damage, which further progresses to development of carcinoma. Even though in the past decade, enormous information has been accumulated on malignant potential of OLP, its transformation still remains unclear. Hence, the purpose of this article was to review cellular and molecular markers to understand the pathogenesis of OLP and its progression toward malignancy.
PubMed: 27194873
DOI: 10.4103/0973-029X.180964 -
Integrative Cancer Therapies Jan 2013Green tea is a beverage widely used by lung cancer patients and the public for its purported anticancer properties. The authors conducted a systematic review of green... (Review)
Review
BACKGROUND
Green tea is a beverage widely used by lung cancer patients and the public for its purported anticancer properties. The authors conducted a systematic review of green tea for the treatment and prevention of lung cancer.
METHODOLOGY
Six electronic databases were searched from inception until November 2011 for human interventional and preclinical evidence pertaining to the safety and efficacy of green tea for lung cancer.
RESULTS
A total of 84 articles met inclusion criteria: two Phase I trials, three reports of one surrogate study, and 79 preclinical studies. There is a lack of controlled trials investigating green tea for lung cancer. Two Phase I studies showed no objective tumor responses at the maximum tolerated dose, ranging from 3 to 4.2 g/m(2) green tea extract (GTE) per day. Four cups of green tea daily decreased DNA damage (8OH-dG) in smokers. Human studies indicate that 800mg of green tea catechins daily does not alter activity of the CYP2D6, CYP1A2, CYP3A4 and CYP2C9 enzymes, however in vitro evidence suggests that green tea may bind to and reduce the effectiveness of bortezomib. Green tea applied topically may improve the healing time of radiation burns.
CONCLUSIONS
Although some evidence suggests that chemopreventative benefits can be accrued from green tea, there is currently insufficient evidence to support green tea as a treatment or preventative agent for lung cancer. Green tea should not be used by patients on bortezomib therapy. Further research is warranted to explore this natural agent for lung cancer treatment and prevention.
Topics: Animals; Antineoplastic Agents; Boronic Acids; Bortezomib; DNA Damage; Herb-Drug Interactions; Humans; Lung Neoplasms; Maximum Tolerated Dose; Phytotherapy; Plant Extracts; Pyrazines; Tea
PubMed: 22532034
DOI: 10.1177/1534735412442378 -
Occupational Medicine (Oxford, England) Dec 2017The waste and recycling sector is a growing part of industry. Whether health surveillance is indicated and how it should be undertaken is unclear. (Review)
Review
BACKGROUND
The waste and recycling sector is a growing part of industry. Whether health surveillance is indicated and how it should be undertaken is unclear.
AIMS
To undertake a review of the literature to identify hazards to health, biological effects and occupational illnesses for workers in the sector.
METHODS
A systematic review of the published literature and two UK databases.
RESULTS
Rates of fatal, non-fatal injuries and self-reported work-related illness were found to be higher in the waste and recycling sector than in UK industry as a whole. There was an increased prevalence of respiratory, gastro-intestinal and skin complaints in workers exposed to compost relative to controls. They may also be at increased risk of extrinsic allergic alveolitis, allergic bronchopulmonary aspergillosis, occupational asthma and abnormalities of lung function. Workers involved with the recycling of batteries and cables may be at risk of lead poisoning and exposure to other heavy metals. There were case reports of mercury poisoning from the recycling of fluorescent lights. Cases of occupational asthma have been reported in association with wood and paper recycling. The recycling of e-waste may cause exposure to heavy metals and organic pollutants, such as polybrominated diphenyl ethers, dioxins and polyaromatic hydrocarbons, which have been associated with damage to DNA and adverse neonatal outcomes.
CONCLUSIONS
Ill-health and adverse biological effects have been described in waste and recycling workers, but their true prevalence has probably not been captured. Targeted health surveillance may be required to assess exposure and to identify occupational illness.
Topics: Humans; Manufacturing Industry; Occupational Diseases; Prevalence; Recycling; Waste Disposal Facilities; Workforce
PubMed: 29165683
DOI: 10.1093/occmed/kqx153 -
The Saudi Dental Journal Feb 2024This systematic review aimed to help further elucidate the following question: are endodontics sealers able to induce DNA damage in vitro or in vivo? (Review)
Review
INTRODUCTION
This systematic review aimed to help further elucidate the following question: are endodontics sealers able to induce DNA damage in vitro or in vivo?
METHODS
This study was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement 2020 criteria. A total of 23 studies were carefully selected by the authors.
RESULTS
Regarding the general characteristics, most studies evaluated, on average, 3-5 types of sealers (resin epoxy, salicylate, salicylate + MTA, zinc oxide-eugenol, bioceramic products, calcium hydroxide), performing comparisons between them. Our results demonstrate that endodontic sealers may be a genotoxic agent since most studies demonstrated positive findings, with the resin-based ones being the most potentially genotoxic.
CONCLUSION
The type of genotoxicity assay, material evaluated, and dilution concentration levels influenced the outcome. This study clarifies whether and to what extent endodontic sealers are capable of inducing DNA injury in oral tissues.
PubMed: 38420001
DOI: 10.1016/j.sdentj.2023.11.019 -
Mutation Research 2011Formaldehyde, the recently classified carcinogen and ubiquitous environmental contaminant, has long been suspected of causing adverse reproductive and developmental... (Review)
Review
Formaldehyde, the recently classified carcinogen and ubiquitous environmental contaminant, has long been suspected of causing adverse reproductive and developmental effects, but previous reviews were inconclusive, due in part, to limitations in the design of many of the human population studies. In the current review, we systematically evaluated evidence of an association between formaldehyde exposure and adverse reproductive and developmental effects, in human populations and in vivo animal studies, in the peer-reviewed literature. The mostly retrospective human studies provided evidence of an association of maternal exposure with adverse reproductive and developmental effects. Further assessment of this association by meta-analysis revealed an increased risk of spontaneous abortion (1.76, 95% CI 1.20-2.59, p=0.002) and of all adverse pregnancy outcomes combined (1.54, 95% CI 1.27-1.88, p<0.001), in formaldehyde-exposed women, although differential recall, selection bias, or confounding cannot be ruled out. Evaluation of the animal studies including all routes of exposure, doses and dosing regimens studied, suggested positive associations between formaldehyde exposure and reproductive toxicity, mostly in males. Potential mechanisms underlying formaldehyde-induced reproductive and developmental toxicities, including chromosome and DNA damage (genotoxicity), oxidative stress, altered level and/or function of enzymes, hormones and proteins, apoptosis, toxicogenomic and epigenomic effects (such as DNA methylation), were identified. To clarify these associations, well-designed molecular epidemiologic studies, that include quantitative exposure assessment and diminish confounding factors, should examine both reproductive and developmental outcomes associated with exposure in males and females. Together with mechanistic and animal studies, this will allow us to better understand the systemic effect of formaldehyde exposure.
Topics: Abnormalities, Drug-Induced; Animals; DNA Damage; Female; Formaldehyde; Humans; Infant, Low Birth Weight; Infant, Newborn; Male; Maternal Exposure; Meta-Analysis as Topic; Mice; Oxidative Stress; Paternal Exposure; Pregnancy; Pregnancy Outcome; Rats; Reproduction
PubMed: 21787879
DOI: 10.1016/j.mrrev.2011.07.003