•A close relationship exists between obesity and epigenetic dysregulation in obesity-related genes.•Some dietary phytochemicals can modify epigenetic mechanisms.•Tea polyphenols, curcumin, genistein, ...isothiocyanates, and citrus isoflavonoids downregulate genes involved in adipogenesis and upregulate genes involved in fat oxidation, thus exerting an antiobesity effect.•Dietary phytochemicals may have the potential to manage obesity.
Obesity is an important cause of morbidity and mortality due to its close association with metabolic disorders including diabetes, cardiovascular diseases, and certain types of cancer. According to the Developmental Origins of Adult Health and Disease hypothesis, obesity is likely caused by epigenetic changes. Recent studies have shown an association between epigenetic dysregulation of certain genes and obesity. Due to their reversible characteristic, epigenetic dysregulations can be restored. Restoration of epigenetic dysregulation in obesity-related genes by epigenetic modifiers may be a new treatment option for obesity. Certain phytochemicals such as tea polyphenols, curcumin, genistein, isothiocyanates, and citrus isoflavonoids were shown to prevent weight gain. These phytochemicals are known for their antioxidant effects but they also modify epigenetic mechanisms. These phytochemicals may have a therapeutic potential in the management of obesity. The aim of this study was to review the epigenetic effects of certain phytochemicals on the expression of obesity-related genes.
Abstract DNA methylation is an important mechanism in the regulation of gene expression and maintenance of genomic integrity. Aberrant DNA methylation is an early event in carcinogenesis. DNA ...methyltransferase inhibitors are used to restore aberrant DNA methylation and inhibit tumor growth. Evaluation of DNA methylation level is important for an effective anti-cancer therapy. In the present study, the determination of global DNA methylation levels in patients with urinary bladder cancer was proposed. The methylation-sensitive comet assay determined the global DNA methylation level at the level of single cells. McrBC enzyme, a methylation-sensitive restriction endonuclease, was used for enzymatic digestion to generate additional breaks at methylated sites. % DNA methylation level was significantly higher in patients with bladder cancer compared to the control group. The clinical performance of % DNA methylation analysis by methylation-sensitive comet assay was evaluated by ROC curve. Using the cutoff value of 6.5% DNA methylation, 92% sensitivity, and 42% specificity were obtained. In conclusion, global DNA methylation measured by methylation-sensitive comet assay may be a promising noninvasive biomarker that reduces interventional tests required in the diagnosis and follow-up of urinary bladder cancer.
•Oxidative DNA damage occurs in patients with Alzheimer’s disease.•Even increased oxidative DNA damage can be detected in plasma.•DNA repair gene OGG1 Ser326Cys polymorphism influences oxidative DNA ...damage level.•Patients carrying Cys326 variant of OGG1 have a higher oxidative DNA damage.
There is considerable evidence that oxidative DNA damage is increased, DNA repair capacity is decreased in patients with Alzheimer’s disease. Base excision repair is the major pathway in removal of oxidative DNA damage. 8-oxo-deoxyguanosine DNA glycosylase 1 (OGG1) is the enzyme which is involved in the first step of this repair process. Alterations in DNA repair capacity may be related with polymorphisms in DNA repair genes. In order to investigate the effect of OGG1 Ser326Cys polymorphism on oxidative DNA damage level, OGG1 genotyping was performed, basal and oxidative DNA damage in lymphocytes and 8-OHdG level in plasma were examined in patients with Alzheimer’s disease. Basal and oxidative DNA damage and 8-OHdG level were measured by OGG1-modified comet assay and enzyme-linked immunoassay, respectively. OGG1 genotyping was performed by polymerase chain reaction- restriction fragment length polymorphism assay. Basal and oxidative DNA damage and plasma 8-OHdG levels were found to be higher in the Alzheimer’s disease group than those in the control group (P < 0.001). In the Alzheimer’s disease group, the levels of oxidative DNA damage was higher in the patients having OGG1 (Ser326Cys + Cys326Cys) genotype than those in the patients having OGG1 Ser326Ser genotype. It was concluded that oxidative DNA damage is increased in patients with Alzheimer’s disease and OGG1 Ser326Cys polymorphism may be responsible for this increase.
Objective The pecten oculi are an intraocular, vascular, and pigmented structure peculiar to the avian eye. In this study, we investigated the pecten oculi of the common buzzard (Buteo buteo) using ...stereomicroscopy and light and scanning electron microscopy (SEM).
Procedures Twenty eyes from 10 adult buzzards were studied. Specimens from each buzzard were preserved in 10% buffered formalin and observed stereomicroscopically before being embedded in paraffin, sectioned, and stained with three stains: Mallory’s triple staining technique as modified by Crossman, Hematoxylin‐Eosin (HE), and Safranin O, and for examination by light microscopy. Specimens from two buzzards were also prepared for SEM.
Results Stereomicroscopy and SEM examination showed the pecten oculi in the common buzzard to be pleated—consisting of 17–18 100 μm thick folds. These folds are connected to one another by bands of connective tissue extending vertically between the plications. Blood vessels, approximately 30–40 μm in diameter, were seen on the surface of the each fold. These vessels arise from the base of pecten, becoming thinner toward the apical end of the structure. A network of capillary vessels at the base of the plicated structure resembles contour lines. At high amplification, melanin granule accumulations were observed around the vascular structures of the plica on SEM images. Light microscopy supported the SEM observations.
Conclusions These findings reveal that the pecten oculi in the common buzzard are plicated and are remarkably similar to that of the other diurnal raptors.
Abstract
Post-COVID conditions are defined as the continuation of the symptoms of Coronavirus Disease 2019 (COVID-19) 3 months after the initial Severe Acute Respiratory Syndrome Coronavirus 2 ...(SARS-CoV-2) infection, with no other explanation. Post-COVID conditions are seen among 30%–60% of patients with asymptomatic or mild forms of COVID-19. The underlying pathophysiological mechanisms of post-COVID conditions are not known. In SARS-CoV-2 infection, activation of the immune system leads to increased production of reactive oxygen molecules, depleted antioxidant reserve, and finally occurrence of oxidative stress. In oxidative stress conditions, DNA damage increases and DNA repair systems impair. In this study, glutathione (GSH) level, glutathione peroxidase (GPx) activity, 8-hydroxydeoxyguanosine (8-OHdG) level, basal, induced, and post-repair DNA damage were investigated in individuals suffering from post-COVID conditions. In the red blood cells, GSH levels and GPx activities were measured with a spectrophotometric assay and a commercial kit. Basal, in vitro H2O2 (hydrogen peroxide)-induced, and post-repair DNA damage (DNA damage after a repair incubation following H2O2-treatment, in vitro) were determined in lymphocytes by the comet assay. The urinary 8-OHdG levels were measured by using a commercial ELISA kit. No significant difference was found between the patient and control groups for GSH level, GPx activity, and basal and H2O2-induced DNA damage. Post-repair DNA damage was found to be higher in the patient group than those in the control group. Urinary 8-OHdG level was lower in the patient group compared to the control group. In the control group, GSH level and post-repair DNA damage were higher in the vaccinated individuals. In conclusion, oxidative stress formed due to the immune response against SARS-COV-2 may impair DNA repair mechanisms. Defective DNA repair may be an underlying pathological mechanism of post-COVID conditions.
Ionizing radiation （IR） is a potential carcinogen. Evidence for the carcinogenic effect of IR radiation has been shown after long-term animal investigations and observations on survivors of the atom ...bombs in Hiroshima and Nagasaki. However, IR has been widely used in a controlled manner in the medical imaging for diagnosis and monitoring of various diseases and also in cancer therapy. The collective radiation dose from medical imagings has increased six times in the last two decades, and grow continuously day to day. A large number of evidence has revealed the increased cancer risk in the people who had frequently exposed to x-rays, especially in childhood. It has also been shown that secondary malignancy may develop within the five years in cancer survivors who have received radiotherapv, because of IR-mediated damage to healthy cells. In this article, we review the current knowledge about the role of medical x-ray exposure in cancer development in humans, and recently recognized epigenetic mechanisms in IR-induced carcinogenesis.
Chronic inflammation may contribute to cancer risk through the accumulation of specific products as a result of DNA damage. Endogenous antioxidant enzymes prevent the formation of these harmful ...products. Oxidative DNA damage and endogenous antioxidant defense were determined in patients with inflammatory bowel disease (IBD). Plasma levels of 8-hydroxydeoxyguanosine (8-OHdG) and nitric oxide (NO) and plasma activities of glutathione peroxidase (G-Px) and superoxide dismutase (SOD) were determined in patients with IBD by ELISA and spectrophotometric assay, respectively. Plasma levels of 8-OHdG, SOD, and G-Px activity were found to be increased in the patient group compared to the control group (P < 0.02, P < 0.001, and P < 0.001, respectively), whereas NO was unchanged. 8-OHdG level was found to be weakly correlated with age, NO, and SOD. The results show increased DNA damage in patients with IBD. This may explain the increased risk of developing colon cancer in these patients.
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