Deoxyribonucleic Acid Damage Research Articles

Mitigation of Toxic Effects of 2 Naphthalene Sulfonate after its Treatment with Microbial Consortia

Present study aimed to treat 2 Napthalene Sulfonate (2NS), a dye intermediate with microbial consortia and assess its potential toxicological impact before and after treatment on the integrity of Deoxyribo-Nucleic Acid (DNA) in blood cells of Channa punctatus. Symbolic elevation in DNA damage with untreated 2NS administered fishes was observed as revealed by comet assay and micronucleus test. However, 2NS after being degraded using mixed bacterial population showed significant reduction in toxicological effects of 2NS. Thus, this study not only illustrated the adverse impact of such toxic contaminant of industrial waste but also suggested a highly efficient and eco-friendly way to remove the harmful xenobiotics from the environment which may help to reduce the exposure of aquatic fauna and flora to such lethal toxicants.

Histopathological Changes on Liver Architecture Due to Toxic Effect of Chromium with Protective Role of Vitamin E on Albino Rats: A Prospective Study

Abstract Introduction This histopathological study was done with an aim to learn about the biohazardous effects of chromium toxicity with protective role of alpha-tocopherol on liver parenchyma of albino rat when fed orally. Materials and Methods The study was conducted in the Department of Anatomy at Subharti Medical College, Meerut (Uttar Pradesh), India, in collaboration with Department of Pathology and Pharmacology.The experiment was conducted as per the guidelines of the Committee for Purpose of Control and Supervision of Experiments on Animals, with registration number 1204/PO/Re/S/2008/CPSEA, and with permission of the Animal Ethical Committee, on 36 adult male rats of ∼60 days of age; 140 ± 20 g of body weight was used; all the experimental animals were kept in polypropylene cage, and fed with pellet diet and water. Result When exposed to chromium for long, it resulted in toxicity and damaged the cellular components during reduction process of chromium by releasing of free radicals, leading to deoxyribonucleic acid damage, but the chain-breaking antioxidant effects of alpha-tocopherol played an important role by reversing the damage caused by chromium toxicity, hence proved hepatoprotective. Conclusion Vitamin E (alpha-tocopherol) is proved to be hepatoprotective against hepatotoxic effect of chromium metal.

Detection of Sperm DNA Integrity and Some Immunological Aspects in Infertile Males

Immunoinfertility caused by anti-sperm antibodies (ASAs) represents about 10–20% of infertility among couples, which interfere with sperm motility and ability to penetrate cervical mucus, sperm-oocyte binding, fertilization, and embryo development. In addition, deoxyribonucleic acid (DNA) damages are increasingly found with infertile cases affecting male reproduction potency and progeny. This study aims to assess the semen, presence of ASAs, and DNA fragmentation index in normozoospermic patients. A total number of 116 cases with an average age of 20–51 years old, and duration of infertility at 4.70 ± 2.77 are classified into 77 and 39 primary and secondary types of infertility, respectively. Mixed agglutination reaction test was used to estimate the ASAs in semen (direct method) and in seminal plasma and blood serum (indirect method), for both immunoglobulins IgG and IgA. Acridine orange test was used to detect DNA fragmentation index. The results showed a significant difference (P > 0.05) for those with a secondary type of infertility at means 24.37 and 31.48 for IgG, and 14.46 ± 1.76 and 6.86 ± 0.39 for IgA by both direct and indirect methods, respectively. The direct method showed a significant difference only for the sperm tail, while that for indirect method was in sperm mid-piece. The mean of DFI for all cases was 38.25 ± 2.08, at 41.61 ± 2.19 and 31.63 ± 4.29, for both primary and secondary cases, respectively. The percentage of ASAs revealed no significant difference with DFI, except in some parts of sperm.

8- Hydroxy-Deoxyguanosine (8-OhDG) urine as a biomarker of oxidative damage in late elderly diabetes mellitus

Diabetes Mellitus (DM) is a chronic metabolic disease characterized by high blood sugar levels that exceed normal limits. The DM pathomechanism involves oxidative stress, which has the potential to cause damage to cell components, including Deoxyribonucleic Acid (DNA). 8-hydroxy-deoxyguanosine (8-OhDG) is the most frequently detected oxidative DNA lesion. It is water-soluble and excreted in the urine. This study aimed to compare urine 8-OhDG levels in patients with controlled and uncontrolled blood sugar diabetes and healthy controls aged 56-65 years. Analytical descriptive research with a cross-sectional study design involved 80 participants determined with purposive sampling. The levels of 8-OhDG were measured using the Enzyme-Linked Immunosorbent Assay (ELISA) method. The results showed that urine 8-OhDG levels in DM patients (1.426±0.204ng/mL) were higher than in healthy controls (1.372±0.190ng/mL), although not statistically significant. Urine levels of 8-OhDG in DM patients aged 61-65 years (1.468±0.220ng/mL) were higher than in DM patients aged 56-60 years (1.394±0.190ng/mL), although not statistically significant. Urine levels of 8-Ohdg in controlled DM patient were lower (1.282±0.131 ng/mL) than in uncontrolled DM patient (1.569±0.159 ng/mL), were significantly different (p<0.05). 8-OhDG produced by the body is the final product of oxidative DNA damage.

The Function of Autophagy as a Regulator of Melanin Homeostasis.

Melanosomes are melanocyte-specific organelles that protect cells from ultraviolet (UV)-induced deoxyribonucleic acid damage through the production and accumulation of melanin and are transferred from melanocytes to keratinocytes. The relatively well-known process by which melanin is synthesized from melanocytes is known as melanogenesis. The relationship between melanogenesis and autophagy is attracting the attention of researchers because proteins associated with autophagy, such as WD repeat domain phosphoinositide-interacting protein 1, microtubule-associated protein 1 light chain 3, autophagy-related (ATG)7, ATG4, beclin-1, and UV-radiation resistance-associated gene, contribute to the melanogenesis signaling pathway. Additionally, there are reports that some compounds used as whitening cosmetics materials induce skin depigmentation through autophagy. Thus, the possibility that autophagy is involved in the removal of melanin has been suggested. To date, however, there is a lack of data on melanosome autophagy and its underlying mechanism. This review highlights the importance of autophagy in melanin homeostasis by providing an overview of melanogenesis, autophagy, the autophagy machinery involved in melanogenesis, and natural compounds that induce autophagy-mediated depigmentation.

Upregulation of exonuclease 1 caused by homology-dependent repair confers cisplatin resistance to gastric cancer cells.

The homology-dependent repair (HDR) pathway is involved in deoxyribonucleic acid (DNA) damage response (DDR), which is crucial to cancer cell survival after treatment with DNA damage agents, including cisplatin (CDDP). Here, we explored the interactions between exonuclease 1 (EXO1), a core gene in the HDR pathway, and CDDP resistance in gastric cancer (GC). Using bioinformatics analysis, we identified the HDR pathway as the most amplified pathway in DDR in GC. In addition, EXO1 was the core gene in the HDR pathway and showed the most significant amplification in GC. The amplification of EXO1 resulted in higher EXO1 expression in cancerous tissues, with malignant prognostic effects. Moreover, we upregulated or downregulated EXO1 in GC cells to examine its effects on the cell malignant phenotype and CDDP resistance in vitro and in vivo. The depletion of EXO1 inhibited cell proliferatory, migratory, and invasive activities, and provided apoptosis resistance to GC cells. EXO1 expression was elevated in CDDP-resistant cells. Ectopic expression of EXO1 increased the resistance of GC cells to CDDP, while downregulation of EXO1 increased the sensitivity of GC cells. Taken together, our study indicates that the HDR pathway is an important player in CDDP resistance in GC through the regulation of EXO1.

Involvement of DNA Damage Response via the Ccndbp1-Atm-Chk2 Pathway in Mice with Dextran-Sodium-Sulfate-Induced Colitis.

The dextran sodium sulfate (DSS)-induced colitis mouse model has been widely utilized for human colitis research. While its mechanism involves a response to double-strand deoxyribonucleic acid (DNA) damage, ataxia telangiectasia mutated (Atm)–checkpoint kinase 2 (Chk2) pathway activation related to such response remains unreported. Recently, we reported that cyclin D1-binding protein 1 (Ccndbp1) activates the pathway reflecting DNA damage in its knockout mice. Thus, this study aimed to examine the contribution of Ccndbp1 and the Atm–Chk2 pathway in DSS-induced colitis. We assessed the effect of DSS-induced colitis on colon length, disease activity index, and histological score and on the Atm–Chk2 pathway and the subsequent apoptosis in Ccndbp1-knockout mice. DSS-induced colitis showed distal colon-dominant Atm and Chk2 phosphorylation, increase in TdT-mediated dUTP-biotin nick end labeling and cleaved caspase 3-positive cells, and histological score increase, causing disease activity index elevation and colon length shortening. These changes were significantly ameliorated in Ccndbp1-knockout mice. In conclusion, Ccndbp1 contributed to Atm–Chk2 pathway activation in the DSS-induced colitis mouse model, causing inflammation and apoptosis of mucosal cells in the colon.

Phytochemical Analysis, Antimutagenic and Antiviral Activity of Moringa oleifera L. Leaf Infusion: In Vitro and In Silico Studies.

Moringa oleifera (M. oleifera) leaves are rich in nutrients and antioxidant compounds that can be consumed to prevent and overcome malnutrition. The water infusion of its leaf is the easiest way to prepare the herbal drink. So far, no information is available on the antioxidant, antimutagenic, and antivirus capacities of this infusion. This study aimed to determine the composition of the bioactive compounds in M. oleifera leaf infusion, measuring for antioxidant and antimutagenic activity, and evaluating any ability to inhibit the SARS-CoV-2 main protease (Mpro). The first two objectives were carried out in vitro. The third objective was carried out in silico. The phytochemical analysis of M. oleifera leaf infusion was carried out using liquid chromatography-mass spectrometry (LC-MS). Antioxidant activity was measured as a factor of the presence of the free radical 2,2-diphenyl-1-picrylhydrazyl (DPPH). The antimutagenicity of M. oleifera leaf powder infusion was measured using the plasmid pBR322 (treated free radical). The interaction between bioactive compounds and Mpro of SARS-CoV-2 was analyzed via molecular docking. The totals of phenolic compound and flavonoid compound from M. oleifera leaf infusion were 1.780 ± 5.00 µg gallic acid equivalent/g (µg GAE/g) and 322.91 ± 0.98 µg quercetin equivalent/g (µg QE/g), respectively. The five main bioactive compounds involved in the infusion were detected by LC-MS. Three of these were flavonoid glucosides, namely quercetin 3-O-glucoside, kaempferol 3-O-neohesperidoside, and kaempferol 3-α-L-dirhamnosyl-(1→4)-β-D-glucopyranoside. The other two compounds were undulatoside A, which belongs to chromone-derived flavonoids, and gentiatibetine, which belongs to alkaloids. The antioxidant activity of M. oleifera leaf infusion was IC50 8.19 ± 0.005 µg/mL, which is stronger than the standard butylated hydroxytoluene (BHT) IC50 11.60 ± 0.30 µg/mL. The infusion has an antimutagenic effect and therefore protects against deoxyribonucleic acid (DNA) damage. In silico studies showed that the five main bioactive compounds have an antiviral capacity. There were strong energy bonds between Mpro molecules and gentiatibetine, quercetin, undulatoside A, kaempferol 3-o-neohesperidoside, and quercetin 3-O-glucoside. Their binding energy values are −5.1, −7.5, −7.7, −5.7, and −8.2 kcal/mol, respectively. Their antioxidant activity, ability to maintain DNA integrity, and antimutagenic properties were more potent than the positive controls. It can be concluded that leaf infusion of M. oleifera does provide a promising herbal drink with good antioxidant, antimutagenic, and antivirus capacities.

Exposure to Polybrominated Diphenyl Ether Flame Retardants Causes Deoxyribonucleic Acid Damage in Human Thyroid Cells In Vitro

IntroductionThe incidence of papillary thyroid cancer (PTC) in the United States has tripled in the past 30 y. Polybrominated diphenyl ethers (PBDEs) are flame retardants that were ubiquitously used over that time period, and exposure to PBDEs has been associated with PTC prevalence. They are potential carcinogens via their induction of reactive oxygen species (ROS) formation and resultant deoxyribonucleic acid (DNA) damage. We sought to determine the effects of PBDE and tris(2-chloroethyl) phosphate (TCEP), another flame retardant implicated in PTC incidence, on thyrocytes in vitro and measure PBDE levels in human thyroid tissue to determine their carcinogenic potential. MethodsNthy-Ori, an immortalized benign human thyroid follicular cell line was used as a model of normal human thyroid. MTT assays were used to measure cell viability after exposure to PBDEs and TCEP. ROS levels and double-stranded and single-stranded DNA breaks were measured to determine genotoxicity. DNA damage response protein levels were measured with immunoblotting. ResultsExposure to 20μM PBDE or TCEP for 48 h had minimal effects on thyrocyte viability. There was no significant increase in intracellular ROS up to 6 h following PBDE or TCEP exposure in thyrocytes; however, cells exposed to PBDE 47 showed evidence of DNA single-stranded and double-stranded breaks. There was a dose-dependent increase in γH2AX levels following exposure to PBDEs 47 and 209 in Nthy-Ori cells but not with TCEP treatment. ConclusionsPBDE 47 and 209 demonstrated genotoxicity but not cytotoxicity in follicular thyrocytes in vitro. Therefore, PBDE 47 and 209 may be carcinogenic in human thyroid cells.

Antigenotoxicity and antioxidant activities of bitter leaf (Vernonia amygdalina del.) accessions from different parts of Nigeria

Bitter leaf (Vernonia amygdalina Del.) plant is a tree species that is highly cultivated in Nigeria for its nutritive and therapeutic values. This study aimed to determine the antioxidant and antigenotoxicity effects (in vitro) of 52 accessions of V. amygdalina collected from six geopolitical zones of Nigeria (North East, North West, North Central, South South, East and West) by evaluating the 2,2-diphenyl-1-picrylhydrazyl (DPPH) and nitric oxide (NO-) scavenging antioxidant activities, flavonoid and phenolic contents as well as ethidium bromide-induced DNA (deoxyribonucleic acid) damage of bitter leaf. The results showed that accessions MN628016 (Oshimili South, Delta State) and MN628010 (Akoko Edo, Edo State), respectively had higher amounts of flavonoid (287.19 mg/g/FW) and phenolic (307.90 mg/g/FW) contents. The accessions MN627984 (Ikpoba Okha, Edo State) and MN627975 (Owerri, Imo State) had the highest nitric oxide (85.73%) and DPPH radical scavenging inhibitory effect (98.92%). The highest percentage fragmented DNA (45.05%), was observed in Allium cepa roots homogenised and mixed with ethidium bromide followed by the A. cepa roots homogenised and mixed with the leaf extract of V. amygdalina accession MN627977 (36.12%). However, V. amygdalina accessions MN628008 (457.62%, Warri North, Delta State) had the highest percentage increase of fragmented DNA followed by MN628024 (395.04%, Oshimili North, Delta State), MN628015 (345.54%; Aniocha North, Delta State) and MN627984 (342.04%; Ikpoba Okha, Edo State) while accession MN628010 (7.32%; Akoko Edo, Edo State) had the lowest. Accession MN628010 which possessed the highest amount of phenolic content had the lowest percentage increase of fragmented DNA and accession MN627984 which possessed the highest nitric oxide radical scavenging inhibitory effect was among the accessions with the highest percentage increase of fragmented DNA. The findings of this study suggest that the observed lowest percentage of fragmented DNA of A. cepa roots growth induced with the solution of ethidium bromide and treated with V. amygdalina accessions MN628010 extracts (antigenotoxic) could be as a result of the high antioxidant activities in the V. amygdalina accessions. In summary, the findings of this study showed that the 52 V. amygdalina accessions obtained from different locations of Nigeria will help to combat ethidium bromide induced genoxicities and any other genotoxicant that may lead to different complications in plant (A. cepa roots), as all the accessions possessed antioxidant and antigenotoxic properties, as such, possessed comparable amount of natural antioxidant activities and antigenotoxicity. Key words: Antioxidant, antigenotoxicity, bitter leaf, accessions, ethidium bromide, Allium cepa

Novel deoxyribonucleic acid methylation perturbations in workers exposed to vinyl chloride

To explore the epigenetic mechanism of deoxyribonucleic acid (DNA) damage induced by vinyl chloride (VC), we studied the micronuclei of peripheral blood lymphocytes in 193 subjects (92 in a VC exposure group employed in a chlorine-alkali plant; 101 in a control group employed in a power plant) and selected three pairs from the subjects (exposed and control) for whole-genome bisulfite sequencing (WGBS). The results showed that the rate ofmicronucleus formation in the VC exposure group was higher than that of control group (6.05 ± 3.28‰ vs. 2.01 ± 1.79‰). A total of 9534 differentially methylated regions (DMRs) were identified by WGBS, of which 4816 were hypomethylated and 4718 were hypermethylated. The Kyoto encyclopedia of genes and genomes (KEGG) pathway and gene ontology (GO) analyses showed the top three KEGG pathways were cancer , neuroactive ligand-receptor interaction, and axon guidance, and the top three GO-BP pathways enriched were multicellular organismal process, developmental process, and anatomical structure development. In the most enriched DMR pathway (pathways in cancer), we found that BCL2, TJP2, TAOK1, PFKFB3, LIPI, and LIPH were hypermethylated, and the methylation levels of BNIP1 and GRPEL2 were decreased. The methylation of differentially methylated genes (DMGs) mentioned above were verified by methylation-specific PCR (MSP) and agarose gel electrophoresis (AGE) in 50 pairs of subjects, where the coincidence rate was 60-100%. In conclusion, the epigenetic perturbations of specific DMGs (BCL2, TJP2, TAOK1, PFKFB3, LIPI, LIPH, BNIP1, and GRPEL2) may be associated with DNA damage from vinyl chloride exposure.

Evaluation of heavy metals and biomarkers of deoxyribonucleic acid damage in state employment and expenditure for result contract workers in Yenagoa

<p><strong>Background: </strong>Youth unemployment and poverty in Southern Nigeria is high, thus many youths are easily recruited as dock workers and casual labourers without considering the occupational hazards associated with such jobs. This study evaluated some heavy metals and DNA damage biomarkers in state employment and expenditure for result (SEEFOR) contract workers, in Yenagoa.</p><p><strong>Method: </strong>One hundred subjects between the age range of 20 to 55 years, comprising fifty of SEEFOR contract workers and fifty unexposed individuals as control in the study. Blood samples were collected, separated and sera used for the analyses of heavy metals and DNA damaged biomarkers using enzyme linked immunosorbent assay and atomic absorption spectrophotometry.</p><p><strong>Results: </strong>The result showed statistically non-significant difference (p>0.05) values of cadmium, chromium, vanadium, nickel, arsenic and DNA damage biomarkers at the baseline compared with the control group. Cadmium, vanadium and 8-NO<sub>2</sub>-Gua at the 6<sup>th</sup> month showed statistically significant difference (p<0.05). Statistically significant (p<0.05) increase at 12<sup>th</sup> month were equally observed in cadmium, vanadium, nickel, arsenic, and 8-NO<sub>2</sub>-Gua compared with the control. Heavy metals cadmium, chromium, Vanadium values showed statistically significant (p<0.005) increase in both the 18<sup>th</sup> and 24<sup>th</sup> month. DNA damage biomarkers 8-NO<sub>2</sub>-Gua, 4HNE, and BPDE levels also showed a significant (p<0.005) increase at the 18<sup>th</sup> and 24<sup>th</sup> month when compared with the control group.</p><p><strong>Conclusions: </strong>The study suggest that the probability of occurrence of diseases related to heavy metal bioaccumulation and DNA damage originating from oxidative stress, might be higher among SEEFOR road construction workers with time.</p>

Evaluation of Spontaneous DNA Damage Using the Alkaline Comet Assay in Lymphocyte Cells of Humans Living in the High Level Natural Radiation Area of Mamuju, Indonesia

To evaluate the biological impacts of high background radiation exposures that are represented by spontaneous deoxyribonucleic acid (DNA) damage, an evaluation on lymphocyte cells from residents of Mamuju, West Sulawesi, Indonesia was tested. The mean annual dose received by individuals in this area is about 10.40 mSv. Of the 177 adult subjects studied, 102 were from high-level natural radiation areas of Mamuju and 75 subjects were from a nearby normal-level natural radiation area. Both areas are similar in living situations. DNA strand breaks and other parameters of study and control group were determined using a standardized comet assay. Our results showed that chronic low-level natural radiation had resulted in significantly higher (p<0.001) DNA damage based on the three parameters of the assay (tail length, tail DNA, and tail moment) compared to those of control. There was a positive correlation between the level of DNA damage and age, where people aged 40 years and older had a higher level of DNA damage than those under 40 year. The level of DNA damage was also found to be higher in females compared to that of males. It was concluded that chronic exposure to natural radiation in Mamuju had induced spontaneous DNA damage in human cells after long-term exposure which was dependent on age and sex.

Dependability of the Sperm Chromatin Dispersion (SCD) Assay for Recurrent Sperm DNA Damage Evaluation of Sperm DNA Fragmentation (SDF) in Men with Presentation of Infertility-A Short Communication

How the male attributes in the generation of a healthy embryo, there exists a need for a sperm that is of good quality with minimum genome injury whose estimationis usually are done by the determination of sperm Deoxyribonucleic Acid (DNA) breakdown or the Sperm DNA Fragmentation (SDF). SDF usually guides with regards to the quality of sperm chromatin in case of men with a presentation of infertility. The causes attributed are the capacity of side actions of escalation of SDF amounts on natural fertility, embryo generation along with implantation, risk of miscarriage along with health of the newborn [1]. Earlier we detailed the role of SDF in Intracytoplasmic Sperm Injection (ICSI) with use of Time Lapse Microscopy (TLM) simultaneously [2]. SDF represents a marker of chromatin injury, takes place at the time of spermiogenesis, halt in the epididymis along withpost ejaculation inview of various factors that are not unique like varicocoele, insufficient life style like toxic exposure secondary to occupational along with experimental factors, aging as well as infections [3]. For the birth of a healthy newborn, genomically healthy sperms are necessary, while enhancement of sperms with injured chromatin in the human ejaculate might result in non stabilization of the genome at the time of fertilization as well as embryogenesis [4]. Thus it has been pointed that the evaluation of sperm chromatin at a molecularlevel might aid in its provision of the paternal factor for infertility, besides point to decide what treatment actions might be feasi ble for enhanced sperm chromatin quality [5].

P53 and taurine upregulated gene 1 promotes the repair of the DeoxyriboNucleic Acid damage induced by bupivacaine in murine primary sensory neurons

ABSTRACT The research aimed to explore the biological role of p53 protein and long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in bupivacaine (bup)-induced neurotoxicity. Our work treated dorsal root ganglion (DRG) cells with bup, detected cell viability through CCK-8, apoptosis through TUNEL assays, DeoxyriboNucleic Acid (DNA) damage through γ-H2AX protein and comet assay, including p53 mRNA, protein and TUG1 expression through q-PCR and western blot, furthermore, cell viability and DNA damage were determined after the silencing of p53 and TUG1, biological information and TUG1 FISH combined with p53 protein immunofluorescence (IF) was performed to determine the cellular localization of these molecule. In vivo experiments, we explored the impact of intrathecal injection of bup on p53 mRNA and protein, TUG1, γ-H2AX protein expression. The results showed that bup was available to signally decreased cell viability, promoted apoptosis rate and DNA damage, additionally, bup increased p53 mRNA and protein and TUG1 expression. P53 siRNA and TUG1 siRNA significantly increased DNA damage. Furthermore, bioinformatics analysis and colocalization experiments revealed that the p53 protein is a transcription factor of TUG1, in vivo experiment, intrathecal injection of bup increased the p53 mRNA, p53 protein, TUG1 and γ-H2AX protein in the murine DRG. In this study, it was found p53 and TUG1 promote the repair of the DNA damage induced by bup in murine dorsal root ganglion cells, suggesting a new strategy for the amelioration of bup-induced neurotoxicity.

Evaluating the relationship between the respiratory exposure to the benzene with the primary damages of deoxyribonucleic acid and total antioxidant capacity in one of the oil companies in Iran.

Benzene is a carcinogenic chemical substance which causes the injuries and damages through producing the free radicals in DNA (deoxyribonucleic acid) and the antioxidants are the agents which reduce the impacts of DNA damages by inhibiting the free radicals. This study was conducted aiming at determination of primary damages of DNA and level of plasma oxidative stress markers resulting from the respiratory exposure to the benzene found in petroleum compounds among the workers at loading platforms of a petroleum products distribution center. This study was an analytical (case control) research conducted among the workers in a working shift serving at the loading platforms of petroleum products. The exposure group included the workers with a history of contact with benzene and the control group was composed of the persons with no history of exposure to benzene. To investigate the level of the personnel's exposure to benzene, NIOSH-1501 method was utilized; to analyze the samples taken from the air, GC mass (gas chromatography-mass spectrometry) was applied; and to determine the average of DNA primary damages, comet assay was used. Total antioxidant capacity was determined by a photometric method. Results indicated that tail length (TL), tail density (TD), tail momentum (TM), percentage of tail in the DNA (%DNA), and %TAC in control group were 78.59, 8.35, 1.20, 10.05, and 25.58 and in the exposure group were 59.21, 75.74, 57.74, 3.5, and 16.58, respectively. The previously mentioned results showed a decrease in the TL, %DNA, and %TAC values among the workers already exposed to benzene while an increase in the TD and TM values of the same group compared to the control non-exposed group. In comparing the averages between two studied groups, all study variables had statistically meaningful difference (p < 0.05). More studies are recommended to be conducted on using the methods which identify the special places of breakage and damage in DNA chain due to the exposure to benzene and consequently prevent the complications and consequences.

DNA Damage in Circulating Hematopoietic Progenitor Stem Cells as Promising Biological Sensor of Frailty.

Frailty is an age-related syndrome that exposes individuals to increased vulnerability. Although it is potentially reversible, in most cases it leads to negative outcomes, including mortality. The different methods proposed identify frailty after the onset of clinical manifestations. An early diagnosis might make it possible to manage the frailty progression better. The frailty pathophysiology is still unclear although mechanisms, in particular, those linked to inflammation and immunosenescence, have been investigated. A common feature of several clinical aspects involved in senescent organisms is the increase of oxidative stress, described as one of the major causes of deoxyribonucleic acid (DNA) damage accumulation in aged cells including the adult stem cell compartment. Likely, this accumulation is implicated in frailty status. The oxidative status of our frail, pre-frail, and non-frail population was characterized. In addition, the DNA damage in hematopoietic cells was evidenced by analyzing the peripheral blood mononuclear cell and their T lymphocyte, monocyte, circulating hematopoietic progenitor stem cell (cHPSC) subpopulations. The phosphorylation of C-terminal of histone H2AX at amino acid Ser 139 (γ-H2AX), which occurs at the DNA double-strand break focus, was evaluated. In our frail population, increased oxidative stress and a high level of DNA damage in cHPSC were found. This study may have potential implications because the increment of DNA damage in cHPSC could be suggestive of an organism impairment preceding the evident frailty. In addition, it may open the possibility for attenuation of frailty progression throughout specific drugs acting on preventing DNA damage or removing damaged cells

Synthesis, Molecular Modeling, DNA Damage Interaction, and Antioxidant Potential of Hesperidin Loaded on Gold Nanoparticles

The flavonoglycone hesperidin is recognized as a potent anti-inflammatory, anticancer, and antioxidant agent. However, its poor bioavailability is a crucial bottleneck regarding its therapeutic activity. Gold nanoparticles are widely used in drug delivery because of its unique properties that differ from bulk metal. Hesperidin loaded gold nanoparticles were successfully prepared to enhance its stability and bioactive potential, as well as to minimize the problems associated with its absorption. The free radical scavenging activities of hesperidin, gold nanoparticles, and hesperidin loaded gold nanoparticles were compared with that of Vitamin C and subsequently evaluated in vitro using 2,2-diphenyl-1-picrylhydrazyl assay. The antioxidant pharmacophore-based structure-activity relationship analysis was assessed by the density functional theory as well as quantum chemical calculations. Moreover, the structural properties were utilized using Becke’s three-parameter hybrid exchange and Lee-Yang-Parr’s correction of functional approaches. Hesperidin-loaded gold nanoparticles were found to decrease hydrogen peroxide (H2O2) and thus induce Deoxyribonucleic acid (DNA) instability. In addition, hesperidin-gold nanoparticles were observed to display important antioxidant potential as well as ameliorate the functional activity of macrophages against Escherichia coli, possibly protecting DNA. These particles might be appropriate for clinical trials and could prove useful for the treatment of various life-threatening disorders.

Fu Fang Gang Liu Aqueous Extract Inhibits the Proliferation of Hela Cells by Causing Deoxyribonucleic Acid Damage

Fu Fang Gang Liu Aqueous Extract Inhibits the Proliferation of Hela Cells by Causing Deoxyribonucleic Acid Damage

Citalopram Induced Cardiotoxicity in Rats at Repeated Doses

Although the correlation between citalopram and cardiovascular pathologies was realized via case studies, there is no experimental study that was performed independently of other risk factors related to cardiotoxicity. In the study reported here, we aimed to identify the cardiotoxic effects of citalopram by evaluating serum cardiac biomarkers, such as serum aspartate transaminase, creatine kinase-myoglobin binding, lactate dehydrogenase and troponin-T levels as well as electrocardiogram parameters, deoxyribonucleic acid damage in cardiomyocytes and histological findings of heart tissue in rats that were administered oral doses of 5, 10, or 20 mg/kg of citalopram for 28 d. Additionally, to investigate possible mechanisms underlying cardiotoxicity, glutathione and malondialdehyde levels in cardiac tissue were determined to evaluate oxidative stress. According to our results, heart rates were increased, PR intervals were prolonged, and T wave amplitudes were significantly decreased in the 20 mg/kg citalopram-administered groups when compared with the control group. Additionally, serum aspartate transaminase, lactate dehydrogenase and troponin-T levels were significantly increased in the 10 and 20 mg/kg citalopram-administered group compared to the control group. Significant deoxyribonucleic acid damages were observed in the 10 and 20 mg/kg citalopram-administered groups. Histopathological investigations revealed degenerative changes in the 10 and 20 mg/kg citalopram-administered groups. In heart tissues, glutathione levels were decreased in the 10 and 20 mg/kg citalopram-administered groups significantly when compared with the control group. These findings indicated the relationship between high-dose and subtherapeutic-dose citalopram administration and cardiac morphological, biochemical and functional toxic effects.