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Iranian Journal of Public Health Jan 2024Cell aging is associated with changes in telomeres due to DNA damage arising from chronic inflammation in obese patients. The aim of the systematic review and... (Review)
Review
BACKGROUND
Cell aging is associated with changes in telomeres due to DNA damage arising from chronic inflammation in obese patients. The aim of the systematic review and meta-analysis was to find the relationship between obesity and aging or senescence.
METHODS
The systematic review was conducted through PRISMA guideline, beginning with literature search within 2012-2022 in several databases (PubMed, EBSCOHost, Science Direct, Scopus, and Cochrane) followed by screening process using predetermined PICO criteria. Original studies on the topic of obesity and senescence (aging), from preclinical studies to clinical research (cohort or cross-sectional studies) that were published within the last ten years. All studies were appraised using SYRCLE risk of bias tool for preclinical studies and Newcastle-Ottawa Scale (NOS) for cross-sectional and cohort studies. The data extraction on the studies' characteristic and outcome on aging or senescence were followed by quantitative analysis using MetaXL process on prevalence ratio and hazard ratio of obesity to comorbidities and mortality.
RESULTS
Fifteen studies were enrolled. Obesity and white adipose tissue cause increased levels of pro-inflammatory and pro-senescence cytokine and macrophage whilst the aging process lowers metabolism with increased insulin resistance and linked to increased risk of obesity. Obesity occurs in 22% (95% CI 18%-26%) of elderly population with higher prevalence rate in the women population. Obesity is associated with significant increased risk of multimorbidity by 56% (OR = 1.58 [95% CI 1.48-1.96]).
CONCLUSION
The obesity and aging or senescence has reciprocal relationship between each other.
PubMed: 38694856
DOI: 10.18502/ijph.v53i1.14679 -
International Journal of Molecular... Nov 2022Aldehydes, particularly acetaldehyde, are carcinogenic molecules and their concentrations in foodstuffs should be controlled to avoid upper aerodigestive tract (UADT)... (Review)
Review
Aldehydes, particularly acetaldehyde, are carcinogenic molecules and their concentrations in foodstuffs should be controlled to avoid upper aerodigestive tract (UADT) and liver cancers. Highly reactive, acetaldehyde forms DNA and protein adducts, impairing physiological functions and leading to the development of pathological conditions. The consumption of aged beer, outside of the ethanol metabolism, exposes habitual drinkers to this carcinogen, whose concentrations can be over-increased due to post-brewing chemical and biochemical reactions. Storage-related changes are a challenge faced by the brewing industry, impacting volatile compound formation and triggering flavor instability. Aldehydes are among the volatile compounds formed during beer aging, recognized as off-flavor compounds. To track and understand aldehyde formation through multiple pathways during beer storage, consequent changes in flavor but particularly quality losses and harmful compound formation, this systematic review reunited data on volatile compound profiles through gas chromatography analyses from 2011 to 2021. Conditions to avoid flavor instability and successful methods for reducing beer staling, and consequent acetaldehyde accumulation, were raised by exploring the dynamic conversion between free and bound-state aldehydes. Future research should focus on implementing sensory analyses to investigate whether adding aldehyde-binding agents, e.g., cysteine and bisulfite, would contribute to consumer acceptance, restore beer flavor, and minimize acetaldehyde-related health damage.
Topics: Humans; Aged; Acetaldehyde; Aldehydes; Beer; Carcinogens; Carcinogenesis
PubMed: 36430619
DOI: 10.3390/ijms232214147 -
Sultan Qaboos University Medical Journal Feb 2023This systematic review and meta-analysis aimed to assess the cytotoxic and genotoxic impacts of waterpipe smoking on oral health. The databases MEDLINE, Cochrane Library... (Meta-Analysis)
Meta-Analysis Review
This systematic review and meta-analysis aimed to assess the cytotoxic and genotoxic impacts of waterpipe smoking on oral health. The databases MEDLINE, Cochrane Library and Dimensions were searched to find studies evaluating whether waterpipe smokers exhibited any cytotoxic or genotoxic effects on their oral cells compared to non-smokers, with regard to mouth neoplasms. Particularly, changes in DNA methylation and p53 expression were assessed. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were adopted for the systematic review. Review Manager was utilised for statistical analysis with a significance level at <0.05. To assess the grades of the included articles, a risk of bias analysis was summarised. A forest plot, including some of the included articles included, was created regarding the different grades. A total of 20 studies were included in this review. The results showed that waterpipe smoking has cytotoxic and genotoxic effects on oral cells, with a risk difference of 0.16. Although the published articles are few in number, all confirm the devastating effects of waterpipe smoking related to the carcinogenicity. Waterpipe smoking is harmful to oral health. It causes a series of detrimental cellular and genetic modifications such as acanthosis, epithelial dysplasia and hyperparakeratosis. In addition, waterpipe smoke contains several carcinogenic compounds. As it releases many harmful organic compounds, waterpipe smoking increases the incidence of oral cancer.
Topics: Humans; Oral Health; Water Pipe Smoking; Antineoplastic Agents; Mouth Neoplasms; DNA Damage
PubMed: 36865434
DOI: 10.18295/squmj.6.2022.043 -
Acta Obstetricia Et Gynecologica... Sep 2021Immunosuppressant drugs are increasingly being used in the reproductive years. Theoretically, such medications could affect fetal health either through changes in the...
INTRODUCTION
Immunosuppressant drugs are increasingly being used in the reproductive years. Theoretically, such medications could affect fetal health either through changes in the sperm DNA or through fetal exposure caused by a presence in the seminal fluid. This systematic overview summarizes existing literature on the spermatotoxic and genotoxic potentials of methotrexate (MTX), a drug widely used to treat rheumatic and dermatologic diseases, and mycophenolate mofetil (MMF), which alone or supplemented with ganciclovir (GCV) may be crucial for the survival of organ transplants.
MATERIAL AND METHODS
The systematic overview was performed in accordance with the PRISMA guidelines: A systematic literature search of the MEDLINE and Embase databases was done using a combination of relevant terms to search for studies on spermatotoxic or genotoxic changes related to treatment with MTX, GCV or MMF. The search was restricted to English language literature, and to in vivo animal studies (mammalian species) and clinical human studies.
RESULTS
A total of 102 studies were identified, hereof 25 human and 77 animal studies. For MTX, human studies of immunosuppressive dosages show transient effect on sperm quality parameters, which return to reference values within 3 months. No human studies have investigated the sperm DNA damaging effect of MTX, but in other organs the genotoxic effects of immunosuppressive doses of MTX are fluctuating. In animals, immunosuppressive and cytotoxic doses of MTX adversely affect sperm quality parameters and show widespread genotoxic damages in various organs. Cytotoxic doses transiently change the DNA material in all cell stages of spermatogenesis in rodents. For GCV and MMF, data are limited and the results are indeterminate, for which reason spermatotoxic and genotoxic potentials cannot be excluded.
CONCLUSIONS
Data from human and animal studies indicate transient spermatotoxic and genotoxic potentials of immunosuppressive and cytotoxic doses of MTX. There are a limited number of studies investigating GCV and MMF.
Topics: DNA Damage; Ganciclovir; Humans; Immunosuppressive Agents; Male; Methotrexate; Mycophenolic Acid; Spermatozoa
PubMed: 33755191
DOI: 10.1111/aogs.14151 -
Photodermatology, Photoimmunology &... Nov 2020DNA damage is one of the main factors responsible for photoageing and is predominantly attributed to ultraviolet irradiation (UV-R). Photoprotection by conventional...
BACKGROUND
DNA damage is one of the main factors responsible for photoageing and is predominantly attributed to ultraviolet irradiation (UV-R). Photoprotection by conventional sunscreens is exclusively prophylactic, and of no value, once DNA damage has occurred. As a result, the demand for DNA repair mechanisms inhibiting, reversing or delaying the pathologic events in UV-exposed skin has sparked research on anti-photoageing and strategies to improve the effect of conventional sunscreens. This review provides an overview of recent developments in DNA repair enzymes used in sunscreens and their impact on photoageing.
METHODS
A systematic review of the literature, up to March 2019, was conducted using the electronic databases, PubMed and Web of Science. Quality assessment was carried out using the Newcastle-Ottawa scale (NOS) to ensure inclusion of adequate quality studies only (NOS > 5).
RESULTS
Out of the 352 publications, 52 were considered relevant to the key question and included in the present review. Two major enzymes were found to play a major role in DNA damage repair in sunscreens: photolyase and T4 endonuclease V. These enzymes are capable of identifying and removing UV-R-induced dimeric photoproducts. Clinical studies revealed that sunscreens with liposome-encapsulated types of photolyase and/or T4 endonuclease V can enhance these repair mechanisms.
CONCLUSION
There is a lack of randomized controlled trials demonstrating the efficacy of DNA repair enzymes on photoageing, or a superiority of sunscreens with DNA repair enzymes compared to conventional sunscreens. Further studies are mandatory to further reveal pathogenic factors of photoageing and possible therapeutic strategies against it.
Topics: Animals; DNA Damage; DNA Repair; Deoxyribodipyrimidine Photo-Lyase; Deoxyribonuclease (Pyrimidine Dimer); Humans; Skin Aging; Sunscreening Agents; Ultraviolet Rays; Viral Proteins
PubMed: 32772409
DOI: 10.1111/phpp.12597 -
Journal of Diabetes and Metabolic... Dec 2019There is controversial data regarding the effects of dietary antioxidative supplements on diabetic retinopathy (DR). We conducted a systematic review of both... (Review)
Review
PURPOSE
There is controversial data regarding the effects of dietary antioxidative supplements on diabetic retinopathy (DR). We conducted a systematic review of both observational and randomized controlled clinical trials (RCTs) to clarify whether they are effective or not.
METHODS
All observational and RCTs conducted by antioxidative supplements on DR published up to 1 January 2018 in PubMed, Web of Sciences, Scopus and Cochrane Library databases were included. Exclusion criteria were animal studies, and studies conducted in Type 1 diabetes mellitus (T1DM), children or pregnant women. Main outcome measures were reporting the incidence or progression of DR in T2DM by assessment of visual fields, and measurements of oxidative and antioxidative biomarkers. The quality of reporting of included articles and risk of bias were assessed.
RESULTS
Finally, we reached 14 observational studies and 7 RCTs that conducted on 256,259 subjects. Due to severe methodological heterogeneity, only qualitative synthesis was carried. All studies were reported a significantly lower level of antioxidants and higher level of oxidative stress biomarkers in DR compared with others. There was an inverse significant correlation between vitamin C and malondialdehyde (MDA) (r = -0.81) or DNA damage (r = -0.41). These figures were statistically significant between vitamin E and MDA (r = 0.77) or superoxide dismutase (r = 0.44). Coefficient of correlation between MDA and zinc (-0.82), coenzyme Q10 (0.56), and magnesium (-0.73) was significant. Multi-oxidants trials were shown non-significant beneficial effects on DR.
CONCLUSIONS
Although our study supports the positive effects of antioxidative supplements on DR, more high quality studies are needed to confirm.
PubMed: 31890694
DOI: 10.1007/s40200-019-00434-x -
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 -
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 -
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 -
Cancer Control : Journal of the Moffitt... 2022Evidence shows that gene mutation is a significant proportion of genetic factors associated with prostate cancer. The DNA damage response (DDR) is a signal cascade...
OBJECTIVE
Evidence shows that gene mutation is a significant proportion of genetic factors associated with prostate cancer. The DNA damage response (DDR) is a signal cascade network that aims to maintain genomic integrity in cells. This comprehensive study was performed to determine the link between different DNA damage response gene mutations and prostate cancer.
MATERIALS AND METHODS
A systematic literature search was performed using PubMed, Web of Science, and Embase. Papers published up to February 1, 2022 were retrieved. The DDR gene mutations associated with prostate cancer were identified by referring to relevant research and review articles. Data of prostate cancer patients from multiple PCa cohorts were obtained from cBioPortal. The OR or HR and 95% CIs were calculated using both fixed-effects models (FEMs) and random-effects models (REMs).
RESULTS
Seventy-four studies were included in this research, and the frequency of 13 DDR genes was examined. Through the analysis of 33 articles that focused on the risk estimates of DDR genes between normal people and PCa patients, DDR genes were found to be more common in prostate cancer patients (OR = 3.6293 95% CI [2.4992; 5.2705]). Also, patients in the mutated group had a worse OS and DFS outcome than those in the unmutated group ( < .05). Of the 13 DDR genes, the frequency of 9 DDR genes in prostate cancer was less than 1%, and despite differences in race, was the potential gene with the highest frequency (REM Frequency = .0400, 95% CI .0324 - .0541). The findings suggest that mutations in genes such as and in PCa patients may increase the sensitivity of Olaparib, a PARP inhibitor.
CONCLUSION
These results demonstrate that mutation in any DDR pathway results in a poor prognosis for PCa patients. Furthermore, mutations in and or the expression of and other genes significantly influence Olaparib sensitivity, which may be underlying therapeutic targets in the future.
Topics: Humans; Male; DNA Damage; DNA Repair; Mutation; Poly(ADP-ribose) Polymerase Inhibitors; Prognosis; Prostatic Neoplasms
PubMed: 36283420
DOI: 10.1177/10732748221129451