Displaying publications 1 - 20 of 152 in total

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  1. Effects of sirtuins on the riboflavin production in Ashbya gossypii
    Kato T, Azegami J, Kano M, El Enshasy HA, Park EY
    Appl Microbiol Biotechnol, 2021 Oct;105(20):7813-7823.
    PMID: 34559286 DOI: 10.1007/s00253-021-11595-2
    This study focuses on sirtuins, which catalyze the reaction of NAD+-dependent protein deacetylase, for riboflavin production in A. gossypii. Nicotinamide, a known inhibitor of sirtuin, made the color of A. gossypii colonies appear a deeper yellow at 5 mM. A. gossypii has 4 sirtuin genes (AgHST1, AgHST2, AgHST3, AgHST4) and these were disrupted to investigate the role of sirtuins in riboflavin production in A. gossypii. AgHST1∆, AgHST3∆, and AgHST4∆ strains were obtained, but AgHST2∆ was not. The AgHST1∆ and AgHST3∆ strains produced approximately 4.3- and 2.9-fold higher amounts of riboflavin than the WT strain. The AgHST3∆ strain showed a lower human sirtuin 6 (SIRT6)-like activity than the WT strain and only in the AgHST3∆ strain was a higher amount of acetylation of histone H3 K9 and K56 (H3K9ac and H3K56ac) observed compared to the WT strain. These results indicate that AgHst3 is SIRT6-like sirtuin in A. gossypii and the activity has an influence on the riboflavin production in A. gossypii. In the presence of 5 mM hydroxyurea and 50 µM camptothecin, which causes DNA damage, especially double-strand DNA breaks, the color of the WT strain colonies turned a deeper yellow. Additionally, hydroxyurea significantly led to the production of approximately 1.5 higher amounts of riboflavin and camptothecin also enhanced the riboflavin production even through the significant difference was not detected. Camptothecin tended to increase the amount of H3K56ac, but the amount of H3K56ac was not increased by hydroxyurea treatment. This study revealed that AgHst1 and AgHst3 are involved in the riboflavin production in A. gossypii through NAD metabolism and the acetylation of H3, respectively. This new finding is a step toward clarifying the role of sirtuins in riboflavin over-production by A. gossypii.Key points• Nicotinamide enhanced the riboflavin production in Ashbya gossypii.• Disruption of AgHST1 or AgHST3 gene also enhanced the riboflavin production in Ashbya gossypii.• Acetylation of H3K56 led to the enhancement of the riboflavin production in Ashbya gossypii.
    Matched MeSH terms: DNA Damage
  2. Cellular and DNA Toxicity Study of Triphenyltin Ethyl Phenyl Dithiocarbamate and Triphenyltin Butyl Phenyl Dithiocarbamate on K562, Leukemia Cell Line
    Hamid A, Rajab NF, Charmagne Y, Awang N, Jufri NF, Rasli NR
    Anticancer Agents Med Chem, 2024;24(1):58-65.
    PMID: 37921147 DOI: 10.2174/0118715206266851231025054446
    INTRODUCTION: Continuous research for new effective drugs to treat cancer has improved our understanding on the mechanism of action of these drugs and paved new potential for their application in cancer treatments. In this study, organotin compounds known as triphenyltin ethyl phenyl dithiocarbamate and triphenyltin butyl phenyl dithiocarbamate were investigated for their toxicity on leukemia cell line (K562) and non-cancerous cell line (Chang liver cell and lung fibroblast, V79 cell).

    METHODS: MTT assay was performed to evaluate the cytotoxic effects of both compounds toward the cells after 24, 48 and 72 hours of exposure or treatment. The alkaline comet assay was conducted to determine the DNA damage on K562 cells after been exposed to both compounds for 30, 60 and 90 minutes.

    RESULTS: The IC50 values obtained from K562 cells ranged from 0.01 to 0.30 μM, whereas for both Chang liver cell and lung fibroblast V79 cell, the values ranged from 0.10 to 0.40 μM. For genotoxicity evaluation, the percentage of damaged DNA is measured as an average of tail moment, and was found to be within 1.20 to 2.20 A.U while the percentage of DNA intensity ranging from 1.50 to 3.50% indicating no genotoxic effects.

    CONCLUSION: Both compounds are cytotoxic toward leukemia cells and non-cancerous cells but do not exert their genotoxic effects towards leukemia cell.

    Matched MeSH terms: DNA Damage
  3. Fulltext Bioactive compounds from nature: Antioxidants targeting cellular transformation in response to epigenetic perturbations induced by oxidative stress
    Bouyahya A, Bakrim S, Aboulaghras S, El Kadri K, Aanniz T, Khalid A, et al.
    Biomed Pharmacother, 2024 May;174:116432.
    PMID: 38520868 DOI: 10.1016/j.biopha.2024.116432
    Oxidative stress results from a persistent imbalance in oxidation levels that promotes oxidants, playing a crucial role in the early and sustained phases of DNA damage and genomic and epigenetic instability, both of which are intricately linked to the development of tumors. The molecular pathways contributing to carcinogenesis in this context, particularly those related to double-strand and single-strand breaks in DNA, serve as indicators of DNA damage due to oxidation in cancer cases, as well as factors contributing to epigenetic instability through ectopic expressions. Oxidative stress has been considered a therapeutic target for many years, and an increasing number of studies have highlighted the promising effectiveness of natural products in cancer treatment. In this regard, we present significant research on the therapeutic targeting of oxidative stress using natural molecules and underscore the essential role of oxidative stress in cancer. The consequences of stress, especially epigenetic instability, also offer significant therapeutic prospects. In this context, the use of natural epi-drugs capable of modulating and reorganizing the epigenetic network is beginning to emerge remarkably. In this review, we emphasize the close connections between oxidative stress, epigenetic instability, and tumor transformation, while highlighting the role of natural substances as antioxidants and epi-drugs in the anti-tumoral context.
    Matched MeSH terms: DNA Damage/drug effects
  4. Fulltext Long term Tai Chi exercise reduced DNA damage and increased lymphocyte apoptosis and proliferation in older adults
    Goon JA, Noor Aini AH, Musalmah M, Yasmin Anum MY, Wan Ngah WZ
    Med J Malaysia, 2008 Oct;63(4):319-24.
    PMID: 19385493 MyJurnal
    Effect of Tai Chi exercise on the level of DNA damage using the comet assay, lymphocyte viability and frequency of sister chromatid exchange (SCE) were determined in adults aged above 45. Tai Chi participants of 7 years (n=35), showed higher level of normal DNA and lower level of mild and severely damaged DNA as compared to the sedentary subjects (n=35). The former are suggested to have effective DNA repair mechanism as their frequency of SCE was markedly lower. Higher lymphocyte apoptosis and proliferation found in the Tai Chi participants also indicated that the exercise promotes renewal and regeneration of lymphocytes.
    Matched MeSH terms: DNA Damage*
  5. E-Cigarette effects on oral health: A molecular perspective
    Ganapathy V, Jaganathan R, Chinnaiyan M, Chengizkhan G, Sadhasivam B, Manyanga J, et al.
    Food Chem Toxicol, 2025 Feb;196:115216.
    PMID: 39736445 DOI: 10.1016/j.fct.2024.115216
    Electronic cigarettes (e-cigarettes) have emerged as a potential alternative to traditional smoking and may aid in tobacco harm reduction and smoking cessation. E-cigarette use has notably increased, especially among young non-tobacco users, raising concerns due to the unknown long-term health effects. The oral cavity is the first and one of the most crucial anatomical sites for the deposition of e-cigarette aerosols. E-cigarette aerosols contain nicotine, flavors, volatile organic compounds, heavy metals, carcinogens, and other hazardous substances. These aerosols impact the oral cavity, disrupting host-microbial interactions and triggering gingivitis and systemic diseases. Furthermore, oral inflammation and periodontitis can be caused by proinflammatory cytokines induced by e-cigarette aerosols. The toxic components of e-cigarette aerosols increase the cellular reactive oxygen species (ROS) levels, reduce antioxidant capacity, increase DNA damage, and disrupt repair processes, which may further contribute to harmful effects on oral epithelum, leading to inflammatory and pre-malignant oral epithelial lesions. In this review, we analyze the toxicological properties of compounds in e-cigarette aerosols, exploring their cytotoxic, genotoxic, and inflammatory effects on oral health and delving into the underlying molecular mechanisms. Further research is essential to understand the impact of e-cigarettes on oral health and make informed regulatory decisions based on reliable scientific evidence.
    Matched MeSH terms: DNA Damage/drug effects
  6. Afterword: An update on clinical utility and diagnostic value of various andrological techniques
    Durairajanayagam D, Agarwal A, Baskaran S, Vij S
    Andrologia, 2021 Mar;53(2):e13819.
    PMID: 33620116 DOI: 10.1111/and.13819
    Matched MeSH terms: DNA Damage
  7. Genotoxicity and apoptotic effect of silver(I) complexes with mixed-ligands of thiosemicarbazones and diphenyl(p-tolyl)phosphine on malignant melanoma cells, SK-MEL-28
    Ooi TC, Nordin FJ, Rahmat NS, Abdul Halim SN', Sarip R, Chan KM, et al.
    Mutat Res Genet Toxicol Environ Mutagen, 2023;886:503581.
    PMID: 36868695 DOI: 10.1016/j.mrgentox.2022.503581
    Complexes of coinage metals can potentially be used as alternatives to platinum-based chemotherapeutic drugs. Silver is a coinage metal that can potentially improve the spectrum of efficacy in various cancers treatment, such as malignant melanoma. Melanoma is the most aggressive form of skin cancer that is often diagnosed in young and middle-aged adults. Silver has high reactivity with skin proteins and can be developed as a malignant melanoma treatment modality. Therefore, this study aims to identify the anti-proliferative and genotoxic effects of silver(I) complexes with mixed-ligands of thiosemicarbazones and diphenyl(p-tolyl)phosphine ligands in the human melanoma SK-MEL-28 cell line. The anti-proliferative effects of a series of silver(I) complex compounds labelled as OHBT, DOHBT, BrOHBT, OHMBT, and BrOHMBT were evaluated on SK-MEL-28 cells by using the Sulforhodamine B assay. Then, DNA damage analysis was performed in a time-dependent manner (30 min, 1 h and 4 h) by using alkaline comet assay to investigate the genotoxicity of OHBT and BrOHMBT at their respective IC50 values. The mode of cell death was studied using Annexin V-FITC/PI flow cytometry assay. Our current findings demonstrated that all silver(I) complex compounds showed good anti-proliferative activity. The IC50 values of OHBT, DOHBT, BrOHBT, OHMBT, and BrOHMBT were 2.38 ± 0.3 μM, 2.70 ± 0.17 μM, 1.34 ± 0.22 μM, 2.82 ± 0.45 μM, and 0.64 ± 0.04 μM respectively. Then, DNA damage analysis showed that OHBT and BrOHMBT could induce DNA strand breaks in a time-dependent manner, with OHBT being more prominent than BrOHMBT. This effect was accompanied by apoptosis induction in SK-MEL-28, as evaluated using Annexin V-FITC/PI assay. In conclusion, silver(I) complexes with mixed-ligands of thiosemicarbazones and diphenyl(p-tolyl)phosphine exerted anti-proliferative activities by inhibiting cancer cell growth, inducing significant DNA damage and ultimately resulting in apoptosis.
    Matched MeSH terms: DNA Damage
  8. Lymphocyte micronuclei frequencies in skin, haematological, prostate, colorectal and esophageal cancer cases: A systematic review and meta-analysis
    Dhillon VS, Deo P, Bonassi S, Fenech M
    Mutat Res Rev Mutat Res, 2021;787:108372.
    PMID: 34083057 DOI: 10.1016/j.mrrev.2021.108372
    Micronucleus (MN) assay has been widely used as a biomarker of DNA damage, chromosomal instability, cancer risk and accelerated aging in many epidemiological studies. In this narrative review and meta-analysis we assessed the association between lymphocyte micronuclei (MNi) and cancers of the skin, blood, digestive tract, and prostate. The review identified nineteen studies with 717 disease subjects and 782 controls. Significant increases in MRi for MNi were observed in the following groups: subjects with blood cancer (MRi = 3.98; 95 % CI: 1.98-7.99; p = 0.000) and colorectal cancer (excluding IBD) (MRi = 2.69; 95 % CI: 1.82-3.98, p DNA damage and chromosomal instability in people with haematological or colorectal cancers. However, the MRi for lymphocyte MNi in subjects with cancers of skin, prostate, esophagus was not significantly increased. More case-control and prospective studies are warranted to further verify the observed trends and to better understand the role of lymphocyte MNi as a biomarker of cancer risk in blood, skin, digestive tract and prostate.
    Matched MeSH terms: DNA Damage/genetics; DNA Damage/physiology
  9. Fulltext The chromosomal DNA damage in buccal mucosa cells among schools children in the vicinity of mobile base stations in Selangor
    Raihanah Chokeli, Nur Azira Baharuddin, Vivien How, Nurul Syazani Yuswir, Shariza Afini Mohd Noor, Ho Yu Bin, et al.
    Malaysian Journal of Medicine and Health Sciences, 2019;15(204):124-129.
    MyJurnal
    Introduction: The increased use of mobile phones has increased the mobile base stations (MBS) deployment. While understanding of radiation protection is growing among the public, questions regarding early-life exposure to ra- diofrequency radiation (RFR) from MBS in children are of importance as to whether it will raise the chances of developing chronic diseases during adulthood. Taking into account the sitting location of MBS, the purpose of this study is to evaluate the chromosomal DNA damage in buccal mucosal cells between school children exposed to RFR emitted from base station antennas. Method: This is a comparative cross-sectional study in which two group of school children were sampled i.e. exposed groups are children whose school located near MBS (200 meters); un- exposed groups are children whose school located distant far from the MBS (>200 meters). Digital RF Analyzer was used to measure RFR at the school surrounding. Buccal mucosa cells from the oral cavity were sampled to examine the level of micronuclei (MN) frequencies. Results: This study found that the densities of the RFR energy differed in range. Although all measurements showed the RFR reading below the acceptable exposure level, there were still sig- nificant variations at each location assessed. Statistically, the MN frequency is significantly different when compared to the exposed and non-exposed group. Conclusion: To understand the mechanism of health effects from exposure to low-level RFR emited from MBS, further study should consider environmental factors influencing MBS sitting on RFR emission, as well as examining the health effects into molecular levels.
    Matched MeSH terms: DNA Damage
  10. Fulltext P53/MDM2 co-expression correlates with the tumour differentiation in oral squamous cell carcinoma - a retrospective study and a systematic review
    Choon, Y.F., Ramanathan, A., Ali, H., Ghani, W.M.N., Cheong, S.C., Zain, R.B.
    Ann Dent, 2011;18(1):8-17.
    MyJurnal
    Background: MDM2 and p53 are involved in a negative feedback loop where p53 regulates MDM2 at the transcriptional level. MDM2, in turn, downregulates p53. This co-ordinated interaction between these proteins is set to play an important role in the regulation of cell cycle progression following DNA damage to cells. The over-expression of both p53 and MDM2 has been reported in various cancers. However there are only few studies discussing the co-expression of MDM2 with p53 in oral squamous cell carcinoma Aim: The purpose of this study was to determine the correlation of co-expression of p53, MDM2, and Ki-67 proteins with clinico-pathological factors in oral squamous cell carcinoma (OSCC) and to conduct a systematic review of the co-expression of p53/MDM2.

    Method: This is a retrospective descriptive study and a systematic review. Formalin-fixed paraffinembedded tissues from 45 OSCC cases were stained by immunohistochemistry (IHC) for p53, MDM2, and Ki-67 proteins.

    Results: Immuno-reactivity for p53, MDM2, and Ki-67 was seen in 75.6%, 97.8%, and 62.2% cases of OSCC respectively. The co-expression of p53 and MDM2 (p53/MDM2) was detected in 97.1%, however there was no significant correlation between p53 and MDM2 expression. Notably, p53/MDM2 coexpression was significantly associated with tumour differentiation (p-value = 0.045). The Ki-67LI was not significantly associated with neither MDM2 nor p53/MDM2 co-expression (p-value = 0.268, 0.916 respectively).

    Conclusion: The expression of MDM2 was not signif icantly associated with p53 expression suggesting that MDM2 expression is mediated by p53-independent pathways or mutated p53 could not induce the expression of MDM2 in this set of OSCCs. The only clinico-pathological parameter that correlates significantly with co-expression of p53/MDM2 is tumour differentiation where it is suggestive that the co-expression of these 2 proteins is indicative of aggressive tumour behavior.
    Matched MeSH terms: DNA Damage
  11. Fulltext Genotoxicity assessment of locally produced dental nanocomposite using Comet assay
    Siti Robayah Mohd Zakri, Kannan, Thirumulu Ponnuraj, Nora Aziz, Siti Fadilah Abdullah, Dasmawati Mohamad, Ismail Ab Rahman, et al.
    Archives of Orofacial Sciences, 2011;6(1):15-20.
    MyJurnal
    The aim of this study was to determine the genotoxicity of a locally produced nanocomposite by Universiti Sains Malaysia, Malaysia using Comet assay. Stem cells from human exfoliated deciduous teeth (SHED) were treated with the nanocomposite at five different concentrations (0.006, 0.0125, 0.025, 0.05, and 0.1 mg/ml) along with concurrent negative (medium alone) and positive control (zinc sulfate heptahydrate) and incubated at 37°C for 24 hours in an incubator at 5% CO2. The tail moment was used to assess the extent of DNA damage. The tail moment for the group of SHED treated with nanocomposite (for all the five different concentrations) was not statistically significant as compared to the negative control, suggesting that the locally produced dental nanocomposite did not induce any DNA damage. Hence, it can be concluded that the locally produced nanocomposite is non-genotoxic on stem cells from human exfoliated deciduous teeth.
    Matched MeSH terms: DNA Damage
  12. Fulltext DNA damaging effect of selected salted and fermented food products against Chang liver cell
    Razinah Sharif, Ahmad Rohi Ghazali, Nor Fadilah Rajab
    Jurnal Sains Kesihatan Malaysia, 2007;5(2):63-77.
    MyJurnal
    DNA damaging effect of the salted and fermented food products (salted fishes, dried shrimps and shrimp pastes) collected from three different locations in Malacca namely Pantai Puteri, Batang Tiga and Kelemak on the DNA of the Chang liver cells were evaluated via Alkaline Comet Assay. Treatment at 62.5 mg/ml following 24 hours of incubation was used based on the preliminary cytotoxicity data. Percentage of damage to the DNA was calculated using software for scoring based on the tail moment and tail intensity (severity of the DNA damage). Hydrogen peroxide was used as positive control at 0.1 mM following 30 minutes of incubation in 4 C. The results showed that the methanol extracts of shrimp pastes and salted fish from Pantai Puteri, exhibited a higher DNA damage (shrimp pastes - TM - 8.33 ± 2.19; TI - 31.67 ± 5.84, salted fishes - TM - 2.25 ± 0.86; TI - 9.25 ± 1.55) and were expressed as (shrimp pastes) 56.66 ± 8.74% of DNA damage and methanol salted fish extracts from the same location showed 13.00 ± 2.84% of the DNA damage on Chang liver cells compared to the other extracts. Values for methanol extract of shrimp pastes from Pantai Puteri were comparable to the positive control - Hydrogen peroxide (TM- 9.50 ± 1.50; TI - 30.50 ± 2.50). On the other hand, aqueous salted fishes extract from Pantai Puteri (TM - 1.33 ± 0.42; TI - 8.67 ± 2.42) and shrimp pastes extracts from Kelemak (methanol extract - TM -1.75 ± 0.15; TI -7.50 ± 0.50, aqueous extract - TM - 1.00 ± 0.00; TI - 5.00 ± 0.00) showed slightly high value for tail moment and tail intensity as compared to negative control (TM - 0.29 ± 0.05; TI - 2.50 ± 0.29). Values for methanol extracts of shrimp pastes from Pantai Puteri were comparable to the positive control (TM- 9.50 ± 1.50; TI - 30.50 ± 2.50). In conclusion, our results demonstrate genotoxic damage induced by few salted and fermented food extracts in Chang liver cell.
    Matched MeSH terms: DNA Damage
  13. Fulltext Phytochemical and In Vitro Genotoxicity Studies of Standardized Ficus deltoidea var. kunstleri Aqueous Extract
    Muhammad H, Omar MH, Rasid ENI, Suhaimi SN, Mohkiar FH, Siu LM, et al.
    Plants (Basel), 2021 Feb 11;10(2).
    PMID: 33670296 DOI: 10.3390/plants10020343
    The present study was carried out to assess the genotoxicity potential of Ficus deltoidea var. kunstleri aqueous extract (FDAE) using standard in vitro assays. The DNA damage of V79B cells was measured using the alkaline comet assay treated at 0.1 mg/mL (IC10) and 0.3 mg/mL (IC25) of FDAE together with positive and negative controls. For in vitro micronucleus assay, the V79B cells were treated with FDAE at five different concentrations (5, 2.5, 1.25, 0.625, and 0.3125 mg/mL) with and without S9 mixture. The bacteria reverse mutation assay of FDAE was performed on Salmonella typhimurium strains TA98, 100, 1535, 1537, and Escherichia coli strain WP2uvrA using pre-incubation method in the presence or in the absence of an extrinsic metabolic system (S9 mixture). FDAE at 0.1 and 0.3 mg/mL significantly increased DNA damage in both comet tail and tail moment (p < 0.05). No significant changes were detected in the number of micronucleated cell when compared to control. Tested at the doses up to 5000 µg/plate, the FDAE did not increase the number of revertant colonies for all strains. In conclusion, further investigation needs to be conducted in animal model to confirm the non-genotoxicity activities of FDAE.
    Matched MeSH terms: DNA Damage
  14. In vitro evaluation of cytotoxicity and genotoxicity of porous nickel titanium dental implants produced by metal injection molding technique
    N W N A M, R A, N H KA, E S, M A A K, M H I, et al.
    J Biomed Mater Res B Appl Biomater, 2024 Jan;112(1):e35306.
    PMID: 37522375 DOI: 10.1002/jbm.b.35306
    Porous NiTi (pNiTi) is a promising biomaterial for functional long-term implantation that has been produced using various manufacturing techniques and tested for biocompatibility. pNiTi produced using a more recent technology of Metal Injection Molding (MIM) has shown better physical and mechanical properties than those produced by earlier manufacturing methods, but its biocompatibility has yet to be determined. Hence, extracts from pNiTi dental implants produced by MIM were tested for cytotoxicity and genotoxicity in this work. Its toxicity was evaluated at the cellular and in vitro levels using elution and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assays. Short-term testing revealed that pNiTi extract was cytocompatible with L-929 fibroblast and V79-4 lung cells, with no cell lysis or reactivity observed, respectively (USP grade 0). Following exposure to varied extract concentrations, good cell viability was observed where the lowest concentration showed the highest optical density (OD) and cell viability (2.968 ± 0.117 and 94%, respectively), and the highest concentration had the least OD and cell viability (2.251 ± 0.054 and 71%, respectively). pNiTi extracts demonstrated genocompatibility in two independent assays: mutagenic potential using a bacterial reverse mutation test and a clastogenic effect on chromosomes using the micronucleus test. Similar to the negative control reactions, there was no significant increase in revertant colonies following exposure to 100% pNiTi extract with and without metabolic activation (p = .00). No DNA clastogenic activity was caused by pNiTi at varied extract concentrations as compared to the negative control when tested with and without metabolic activation (p = .00). As a result, both cytotoxic and genotoxic investigations have confirmed that pNiTi dental implants utilizing the MIM process are cytocompatible and genocompatible in the short term, according to the International Standard, ISO 10993 - Parts 3, 5, and 33.
    Matched MeSH terms: DNA Damage
  15. Fulltext Potential lethal damage repair in glioblastoma cells irradiated with ion beams of various types and levels of linear energy transfer
    Chew MT, Nisbet A, Suzuki M, Matsufuji N, Murakami T, Jones B, et al.
    J Radiat Res, 2019 Jan 01;60(1):59-68.
    PMID: 30452663 DOI: 10.1093/jrr/rry081
    Glioblastoma (GBM), a Grade IV brain tumour, is a well-known radioresistant cancer. To investigate one of the causes of radioresistance, we studied the capacity for potential lethal damage repair (PLDR) of three altered strains of GBM: T98G, U87 and LN18, irradiated with various ions and various levels of linear energy transfer (LET). The GBM cells were exposed to 12C and 28Si ion beams with LETs of 55, 100 and 200 keV/μm, and with X-ray beams of 1.7 keV/μm. Mono-energetic 12C ions and 28Si ions were generated by the Heavy Ion Medical Accelerator at the National Institute of Radiological Science, Chiba, Japan. Clonogenic assays were used to determine cell inactivation. The ability of the cells to repair potential lethal damage was demonstrated by allowing one identical set of irradiated cells to repair for 24 h before subplating. The results show there is definite PLDR with X-rays, some evidence of PLDR at 55 keV/μm, and minimal PLDR at 100 keV/μm. There is no observable PLDR at 200 keV/μm. This is the first study, to the authors' knowledge, demonstrating the capability of GBM cells to repair potential lethal damage following charged ion irradiations. It is concluded that a GBM's PLDR is dependent on LET, dose and GBM strain; and the more radioresistant the cell strain, the greater the PLDR.
    Matched MeSH terms: DNA Damage*
  16. Retinal degeneration rat model: A study on the structural and functional changes in the retina following injection of sodium iodate
    Koh AE, Alsaeedi HA, Rashid MBA, Lam C, Harun MHN, Saleh MFBM, et al.
    J. Photochem. Photobiol. B, Biol., 2019 Jul;196:111514.
    PMID: 31154277 DOI: 10.1016/j.jphotobiol.2019.111514
    Retinal disorders account for a large proportion of ocular disorders that can lead to visual impairment or blindness, and yet our limited knowledge in the pathogenesis and choice of appropriate animal models for new treatment modalities may contribute to ineffective therapies. Although genetic in vivo models are favored, the variable expressivity and penetrance of these heterogeneous disorders can cause difficulties in assessing potential treatments against retinal degeneration. Hence, an attractive alternative is to develop a chemically-induced model that is both cost-friendly and standardizable. Sodium iodate is an oxidative chemical that is used to simulate late stage retinitis pigmentosa and age-related macular degeneration. In this study, retinal degeneration was induced through systemic administration of sodium iodate (NaIO3) at varying doses up to 80 mg/kg in Sprague-Dawley rats. An analysis on the visual response of the rats by electroretinography (ERG) showed a decrease in photoreceptor function with NaIO3 administration at a dose of 40 mg/kg or greater. The results correlated with the TUNEL assay, which revealed signs of DNA damage throughout the retina. Histomorphological analysis also revealed extensive structural lesions throughout the outer retina and parts of the inner retina. Our results provided a detailed view of NaIO3-induced retinal degeneration, and showed that the administration of 40 mg/kg NaIO3 was sufficient to generate disturbances in retinal function. The pathological findings in this model reveal a degenerating retina, and can be further utilized to develop effective therapies for RPE, photoreceptor, and bipolar cell regeneration.
    Matched MeSH terms: DNA Damage/drug effects
  17. Genotoxic effects of Dukhan: A smoke bath from the wood of Acacia seyal used traditionally by Sudanese women
    Elgorashi EE, Eldeen IMS, Makhafola TJ, Eloff JN, Verschaeve L
    J Ethnopharmacol, 2022 Mar 01;285:114868.
    PMID: 34826541 DOI: 10.1016/j.jep.2021.114868
    ETHNOBOTANICAL RELEVANCE: Smoke from the wood of Acacia seyal Delile has been used by Sudanese women for making a smoke bath locally called Dukhan. The ritual is performed to relieve rheumatic pain, smooth skin, heal wounds and achieve general body relaxation.

    AIM OF THE STUDY: The present study was designed to investigate the in vitro anti-inflammatory effect of the smoke condensate using cyclooxygenase -1 (COX-1) and -2 (COX-2) as well as its potential genotoxic effects using the bacterial-based Ames test and the mammalian cells-based micronucleus/cytome and comet assays.

    MATERIAL AND METHODS: The smoke was prepared in a similar way to that commonly used traditionally by Sudanese women then condensed using a funnel. Cyclooxygenase assay was used to evaluate its in vitro anti-inflammatory activity. The neutral red uptake assay was conducted to determine the range of concentrations in the mammalian cells-based assays. The Ames, cytome and comet assays were used to assess its potential adverse (long-term) effects.

    RESULTS: The smoke condensate did not inhibit the cyclooxygenases at the highest concentration tested. All smoke condensate concentrations tested in the Salmonella/microsome assay induced mutation in both TA98 and TA100 in a dose dependent manner. A significant increase in the frequency of micronucleated cells, nucleoplasmic bridges and nuclear buds was observed in the cytome assay as well as in the % DNA damage in the comet assay.

    CONCLUSIONS: The findings indicated a dose dependent genotoxic potential of the smoke condensate in the bacterial and human C3A cells and may pose a health risk to women since the smoke bath is frequently practised. The study highlighted the need for further rigorous assessment of the risks associated with the smoke bath practice.

    Matched MeSH terms: DNA Damage/drug effects
  18. Fulltext Association of GSTM1 and GSTT1 with ageing in auto repair shop workers
    Eshkoor SA, Marashi SJ, Ismail P, Rahman SA, Mirinargesi M, Adon MY, et al.
    Genet. Mol. Res., 2012;11(2):1486-96.
    PMID: 22653598 DOI: 10.4238/2012.May.21.5
    We evaluated the possible influence of glutathione S-transferase mu (GSTM1) and glutathione S-transferase theta (GSTT1) genes on genetic damage due to occupational exposure, which contributes to accelerate ageing. This study was conducted on 120 car auto repair workshop workers exposed to occupational hazards and 120 controls without this kind of exposure. The null and non-null genotypes of GSTM1 and GSTT1 genes were determined by multiplex PCR. Micronucleus frequency, Comet tail length and relative telomere length differences between the null and non-null genotypes of the GSTM1 gene were significantly greater in the exposed group. Lack of GSTT1 did not affect the damage biomarkers significantly (P > 0.05), while lack of GSTM1 was associated with greater susceptibility to genomic damage due to occupational exposure. It was concluded that early ageing is under the influence of these genes and the environmental and socio-demographic factors. Duration of working time was significantly associated with micronucleus frequency, Comet tail length and relative telomere length.
    Matched MeSH terms: DNA Damage/genetics
  19. Assessment of genotoxic and molecular mechanisms of cancer risk in smoking and smokeless tobacco users
    Chandirasekar R, Kumar BL, Sasikala K, Jayakumar R, Suresh K, Venkatesan R, et al.
    Mutat Res Genet Toxicol Environ Mutagen, 2014 Jun;767:21-7.
    PMID: 24769293 DOI: 10.1016/j.mrgentox.2014.04.007
    Inexpensive forms of tobacco are widely used in developing countries such as India. We have evaluated genotoxicity endpoints (chromosome aberrations, micronucleus frequency, comet assay) and polymorphisms of the XRCC1 and p53 genes among smokers and smokeless tobacco (SLT) users in rural Tamilnadu, South India. Cytogenetic, DNA damage and SNP analyses were performed on peripheral blood samples; micronucleus frequency was measured in peripheral blood and buccal mucosa exfoliated cells. Both categories of tobacco users had elevated levels of genotoxic damage. SNP analysis of tobacco users revealed that 17% carry the XRCC1 gln399gln genotype and 19% carry the p53 pro72pro genotype. Both genotypes are associated with increased risk of cancer.
    Matched MeSH terms: DNA Damage*
  20. Fulltext Dietary spices protect against hydrogen peroxide-induced DNA damage and inhibit nicotine-induced cancer cell migration
    Jayakumar R, Kanthimathi MS
    Food Chem, 2012 Oct 01;134(3):1580-4.
    PMID: 25005983 DOI: 10.1016/j.foodchem.2012.03.101
    Spices are rich sources of antioxidants due to the presence of phenols and flavonoids. In this study, the DNA protecting activity and inhibition of nicotine-induced cancer cell migration of 9 spices were analysed. Murine fibroblasts (3T3-L1) and human breast cancer (MCF-7) cells were pre-treated with spice extracts and then exposed to H₂O₂ and nicotine. The comet assay was used to analyse the DNA damage. Among the 9 spices, ginger, at 50 μg/ml protected against 68% of DNA damage in 3T3-L1 cells. Caraway, cumin and fennel showed statistically significant (p<0.05) DNA protecting activity. Treatment of MCF-7 cells with nicotine induced cell migration, whereas pre-treatment with spices reduced this migration. Pepper, long pepper and ginger exhibited a high rate of inhibition of cell migration. The results of this study prove that spices protect DNA and inhibit cancer cell migration.
    Matched MeSH terms: DNA Damage/drug effects*
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