Deoxyribonucleic Acid Damage Research Articles

Inflammatory Bowel Disease and Colorectal Cancer: An Eternal Fire in a Beautiful Garden

Inflammatory bowel disease (IBD), encompassing Crohn's disease and ulcerative colitis, significantly increases the risk of colitis-associated cancer (CAC). Chronic inflammation, a key contributor to carcinogenesis, disrupts immune surveillance, induces deoxyribonucleic acid (DNA) damage, and alters genetic and epigenetic pathways. Molecular pathways such as STAT3, mTOR, and NF-κB drive CAC progression, while unique microbiome alterations—loss of Faecalibacterium prausnitzii and increases in Escherichia coli and Fusobacterium species—exacerbate the inflammatory milieu. CAC accounts for 2% of all colon cancers and up to 15% of IBD-related deaths. Risk correlates with IBD duration, increasing approximately 1% annually after the first decade. Surveillance via colonoscopy is crucial, with chromoendoscopy recommended for high-risk cases. Preventive drugs, including aminosalicylates, thiopurines, and biologics, offer modest benefits but lack conclusive evidence. Post-CAC diagnosis, immunosuppressants are discontinued in favor of corticosteroids, with 5-aminosalicylates continued as needed. The use of immune checkpoint inhibitors remains controversial due to exacerbation of colitis. Emerging insights into the gut microbiota's role in IBD and CAC may revolutionize prevention and management strategies. Advances in screening, surveillance, and therapeutic approaches have reduced CAC mortality, underscoring the importance of personalized medicine and ongoing research to address these complex conditions.

Galangin Ameliorates Gamma Radiation-induced DNA Damage and Subsequent Chromosomal Aberrations in Human Blood Lymphocytes

Background Natural compounds with radioprotective properties have gained attention due to their potential to reduce health risks associated with radiation exposure. Galangin (GA), a flavonoid recognized for its antioxidant activity, has been investigated for its capacity to alleviate oxidative stress. Purpose This study aimed to explore the radioprotective effects of GA against gamma radiation-induced double-strand breaks (DSBs), dicentric chromosomes (DCs), and cytokinesis-block micronuclei (CBMN) in human blood lymphocytes. Methods Human blood peripheral lymphocytes (HBPLs) were treated with varying concentrations of GA (1, 5, and 10 µM) for 24 h before being exposed to gamma radiation (3 Gy). Following radiation exposure, the cells were incubated for another 24 h to evaluate deoxyribonucleic acid (DNA) damage. Cytogenetic assays were performed to measure DC and CBMN frequencies, while DSBs were assessed using γ-H2AX analysis. Additionally, the phosphorylation of ATM (p-ATM) was analyzed through Western blotting, and DNA repair gene expression was examined using a polymerase chain reaction (PCR) array. Statistical methods were employed to analyze the data and determine the significance of GA’s protective effects. Results Gamma radiation exposure markedly increased the incidence of DCs and CBMN in HBPLs in a dose-dependent manner. Pretreatment with GA, however, significantly reduced these effects in a concentration-dependent fashion. GA also decreased radiation-induced DSBs, as demonstrated by reduced levels of γ-H2AX and p-ATM. Furthermore, GA-treated cells exhibited a downregulation of DNA repair-related gene expression compared to cells exposed solely to radiation. Among the tested concentrations, 10 µM GA provided the greatest protective effect. Discussion GA effectively mitigates gamma radiation-induced DNA damage in human lymphocytes by lowering the incidence of DSBs, DCs, and CBMN. The protective effects appear to be mediated through modulation of the DNA damage response and the reduction of oxidative stress. Conclusion This study highlights GA’s potential as a radioprotective agent and suggests its relevance in radiation therapy and preventive applications. Further research is warranted to fully elucidate its mechanisms and therapeutic potential.

Homology Modeling of Human DNA Repair Protein RAD51 Homolog 3 (RAD51C) in Breast Cancer

Breast cancer is known as one of the most predominant cancers that affect both females and males worldwide. The most crucial risk factor in breast cancer is the mutations in the RAD51C gene that have been considered in most hereditary breast cancers. RAD51C, the RAD51 paralogs, is also a deoxyribonucleic acid (DNA) repair protein related to breast and ovarian cancers. DNA double-strand breaks (DSBs) account for the significant detrimental form of DNA damage. RAD51C mutants also have been recognized in breast/ovarian cancer patients. However, the role of the RAD51C protein in hereditary breast cancer and its three-dimensional (3D) structures remains unclear. Thus, this study was conducted to identify the 3D structure of RAD51C protein from its amino acid sequences. The homology modeling for the 3D structure of the RAD51C protein was carried out by using three automated webservers: I-TASSER, SWISS-MODEL, and Phyre2. PyMOL was applied to visualize the 3D structure of RAD51C protein. Next, the MolProbity, ProSA, and SAVES v6.0 programs have been employed to check the stereo-chemical quality of RAD51C protein. The RAD51C-IT models were found to be the best models for the RAD1C protein after being evaluated and validated, and the models were constructed using full-length RAD51C protein sequences. Thus, these protein models can be utilized as a virtual screening tool in discovering potential inhibitors of RAD51C protein.

Multifunctional Nanoparticles as Radiosensitizers to Overcome Hypoxia-Associated Resistance in Cancer Radiotherapy.

Hypoxia, a phenomenon that occurs when the oxygen level in tissues is lower than average, is commonly observed in human solid tumors. For oncological treatment, the hypoxic environment often results in radioresistance and chemoresistance. In this study, a new multifunctional oxygen carrier, carboxymethyl hexanoyl chitosan (CHC) nanodroplets decorated with perfluorohexane (PFH) and superparamagnetic iron oxide (SPIO) nanodroplets (SPIO@PFH-CHC), was developed and investigated. PFH-based oxygen carriers can augment oxygenation within tumor tissues, thereby mitigating radioresistance. Concurrently, oxygenation can cause deoxyribonucleic acid (DNA) damage via oxygen fixation and consequently suppress cancer cell proliferation. Moreover, these pH-sensitive nanodroplets allow higher cellular uptake with minimal cytotoxicity. Two distinctive mechanisms of SPIO@PFH-CHC nanodroplets were found in this study. The SPIO nanoparticles of the SPIO@PFH-CHC nanodroplets can generate hydroxyl radicals (HO•) and other reactive oxygen species (ROS), which is vital to chemodynamic therapy (CDT) via the Fenton reaction. Meanwhile, the higher X-ray absorption among these nanodroplets leads to a local energy surge and causes more extensive deoxyribonucleic acid (DNA) damage via oxygen fixation. This study demonstrates that low cytotoxic SPIO@PFH-CHC nanodroplets can be an efficient radiosensitizer for radiation therapy.

Chamomile flowers extract protects against thinner inhalation-induced lung toxicity via attenuating cytochrome P2E1 activity, surfactant deficiency, and alveolar structural injury in rats

BackgroundLungs are adversely affected by repeated exposure to thinner fumes. This study aimed to examine the pulmonary toxic effects of chronic thinner inhalation and the possible protection by chamomile administration. Adult male Wistar rats were exposed to thinner fumes for 8 weeks (4 h/day, 6 days/week), while chamomile flower extract (400 mg/kg body weight) was given orally during thinner exposure for the same period.ResultsThe study showed lung damage following chronic thinner exposure through increased cytochrome P2E1 (CYP2E1), superoxide anion (O2•−), hydrogen peroxide (H2O2), and malondialdehyde (MDA), with decreased antioxidant enzymes; superoxide dismutase (SOD), and catalase (CAT). Moreover, an elevation of lung enzymes; alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), and lactate dehydrogenase (LDH) with depletion in total protein and albumin contents in serum and bronchoalveolar lavage fluid were observed. Thinner exposure also exhibited increased lung deoxyribonucleic acid (DNA) damage, transforming growth factor-β1 (TGF-β1), insulin-like growth factor-1 (IGF-1), hydroxyproline (HYP), and collagen type 1 (COL-1), with decreased serum surfactant protein-A (SP-A), total and differential leukocytes (WBCs) count, except for neutrophils. Histological investigations revealed deteriorative changes along with accumulated collagen fibers affecting the lung and other respiratory organs.ConclusionSupplementation of chamomile extract succeeded in preventing thinner-induced lung oxidative stress, enzyme leakage, surfactant deficiency, DNA damage, fibrosis, and histological injury. Therefore, consumption of chamomile extract could be recommended for alleviating thinner-induced health hazards and lung toxicity.

Designing novel Au(III) complexes based on the structure of diazepam: Achieving a multiaction mechanism against glioma.

Metal-based drugs have been used in the clinical treatment of tumors for over 30 years. However, no metal-based drugs have been clinically approved to treat glioma. Although metal complexes have excellent cytotoxicity, their most critical problem is crossing the blood-brain barrier. Therefore, to enable metal complexes to cross blood-brain barrier and target glioma therapy, herein, we propose to rationally used the basic structure of diazepam (5-chlorobenzophenone) and thiosemicarbazide to synthesize gold (Au) complexes C1, C2 and C3 with antiglioma activity. The C3 complex with two methyl groups attached to the N3 of thiosemicarbazone exhibited excellent cytotoxicity to glioma cells through its multiaction mechanism against glioma, inducing apoptosis, autophagy death, and deoxyribonucleic acid damage. In addition, the synthesized C3 complex can effectively cross the blood-brain barrier and accumulate in glioma, considerably decreasing the untoward reaction in vivo. Our findings provide a novel strategy for designing metal-based complexes for the treatment of glioma.

An organotypic model for investigating drug-radiation responses in the lung

Background: Established in vivo radiobiological models are commonly used to assess anti-tumor effects and normal tissue toxicity. However, these models have notable limitations, and additional models are necessary to gain a deeper insights into drug-radiation interactions. Objective: This study aimed to develop an organotypic ex vivo model by using precision-cut lung slices (PCLSs) to evaluate radiation-induced residual deoxyribonucleic acid (DNA) damage, both alone and in combination with a pharmacological inhibitor of DNA double-strand break (DSB) repair. Methods: Left lungs from female C57BL/6 mice were dissected, perfused with 4% low-gelling-temperature agarose, and sliced into 250 μm sections. Lung slices were then incubated ex vivo for up to 7 days. The slices were irradiated using 137Cs, either with or without a DNA-dependent protein kinase (DNA-PK) inhibitor (NU7441). Tissue sections were subsequently fixed and stained for γH2AX and 53BP1, which serve as histological markers of DNA DSBs. Results: The established conditions preserved tissue viability for up to 7 days and maintained structural integrity for 2 days. DNA damage, detected through γH2AX and 53BP1 staining, was consistent between lungs irradiated ex vivo and their counterparts irradiated in vivo. In the organotypic model, radiation alone in DNA-PK-deficient SCID mice and radiation combined with DNA-PK inhibition in C57BL/6 mice led to increased residual γH2AX and 53BP1 staining. Conclusion: This study demonstrates that residual DNA damage levels following ionizing radiation in lung tissue are comparable between in vivo and ex vivo tissue slices, suggesting that PCLSs serve as a valuable organotypic model for investigating the effects of drug-radiation combinations.

A Molecular‐Targeting Photosensitizer to Inhibit DNA Damage Repair System and Induce cGAS‐STING Pathway Activation for Photo‐Immunotherapy of Ovarian Cancer

AbstractPoly(ADP‐ribose) polymerase (PARP) inhibitors are commonly utilized in the clinical management of patients with platinum‐sensitive recurrent and late‐stage ovarian cancer, which constitutes a significant proportion of gynecological cancer‐related mortality. Nonetheless, the constraints of their monofunctional properties and limited therapeutic efficacy observed in advanced cancer cases necessitate the exploration of more potent therapeutic strategies for the management of ovarian cancer. The present study describes the development of QTABI, a PARP‐targeting photosensitizer capable of producing reactive oxygen species with light irradiation. Simultaneously, it exhibits significant inhibition of PARP activity, induction of deoxyribonucleic acid (DNA) damage, and consequent synthetic lethality. Furthermore, QTABI can effectively promote the accumulation of cytosolic DNA and activate the cyclicGMP‐AMP synthase (cGAS)‐stimulator of interferon gene (STING) pathway under light irradiation, thereby eliciting potent anti‐tumor immune responses and ultimately boosting anti‐cancer efficacy. Collectively, these findings suggest that QTABI is a multi‐functional photosensitizer, which targets the DNA‐damaging repair system and activates the cGAS‐STING pathway, offering a promising combination photo‐immunotherapy strategy for treating ovarian cancer.

Oxidative DNA Damage and Arterial Hypertension in Light of Current ESC Guidelines.

A new insight into oxidative stress is based on oxidative deoxyribonucleic acid (DNA) damage. DNA is the pivotal biopolymer for life and health. Arterial hypertension (HT) is a globally common disease and a major risk factor for numerous cardiovascular (CV) conditions and non-cardiac complications, making it a significant health and socio-economic problem. The aetiology of HT is multifactorial. Oxidative stress is the main driver. Oxidative DNA damage (oxidised guanosine (8OHdG), strand breaks (SSBs, DSBs)) seems to be the crucial and initiating causal molecular mechanism leading to HT, acting through oxidative stress and the resulting consequences (inflammation, fibrosis, vascular remodelling, stiffness, thickness, and endothelial dysfunction). In light of the current European Society of Cardiology (ESC) guidelines with defined gaps in the evidence, this manuscript, for the first time, (1) summarizes evidence for oxidative DNA damage in HT and other CV risk factors, (2) incorporates them into the context of known mechanisms in HT genesis, (3) proposes the existing concept of HT genesis innovatively supplemented with oxidative DNA damage, and (4) mentions consequences such as promising new targets for the treatment of HT (DNA damage response (DDR) pathways).

Proteomic Analysis of Biomarkers Predicting Treatment Response in Patients with Head and Neck Cancers.

Head and neck cancers (HNCs) are the sixth most commonly diagnosed cancer and the eighth leading cause of cancer-related mortality worldwide, with squamous cell carcinoma being the most prevalent type. The global incidence of HNCs is steadily increasing, projected to rise by approximately 30% per year by 2030, a trend observed in both developed and undeveloped countries. This study involved serum proteomic profiling to identify predictive clinical biomarkers in cancer patients undergoing chemoradiotherapy (CRT). Fifteen HNC patients at Tikur Anbessa Specialized Hospital, Radiotherapy (RT) center in Addis Ababa were enrolled. Serum samples were collected before and after RT, and patients were classified as responders (R) or non-responders (NR). Protein concentrations in the serum were determined using the Bradford assay, followed by nano-HPLC-MS/MS for protein profiling. Progenesis QI for proteomics identified 55 differentially expressed proteins (DEPs) between R and NR, with a significance of p < 0.05 and a fold-change (FC) ≥ 1.5. The top five-up-regulated proteins included MAD1L1, PSMC2, TRIM29, C5, and SERPING1, while the top five-down-regulated proteins were RYR1, HEY2, HIF1A, TF, and CNN3. Notably, about 16.4% of the DEPs were involved in cellular responses to DNA damage from cancer treatments, encompassing proteins related to deoxyribonucleic acid (DNA) damage sensing, checkpoint activation, DNA repair, and apoptosis/cell cycle regulation. The analysis of the relative abundance of ten proteins with high confidence scores identified three DEPs: ADIPOQ, HEY2, and FUT10 as potential predictive biomarkers for treatment response. This study highlighted the identification of three potential predictive biomarkers-ADIPOQ, HEY2, and FUT10-through serum proteomic profiling in HNC patients undergoing RT, emphasizing their significance in predicting treatment response.

Potential of epicatechin as antioxidant and antiaging in UV-induced BJ cells by regulating COL1A1, FGF-2, GPX-1, and MMP-1 gene, protein levels, and apoptosis

Background Oxidative stress caused by exposure to ultraviolet (UV) light on the skin can damage deoxyribonucleic acid (DNA) and cause keratinocytes to undergo apoptosis. Endogenous antioxidants which play a role in trapping free radicals are also unable to overcome excess reactive oxygen species (ROS) in the body due to UV exposure, so exogenous antioxidants are needed. Polyphenolic compounds extracted from natural ingredients such as flavonoids, quercetin, and epicatechin have quite strong antioxidant activity. This is influenced by the chemical structure of these compounds which are rich in hydroxyl groups and aromatic groups. This structure allows the compound to become an electron donor so that it can neutralize free radicals. In vitro research was used to see the potential effectiveness of epicatechin as an antiaging and antioxidant. The study aims to confirm the potential of epicatechin as an antiaging by in vitro assay. Methods The viability test of epicatechin on human skin fibroblast (BJ) cells was carried out using the water-soluble tetrazolium (WST) assay. BJ cells were UV-induced as a cell model of premature aging. Epicatechin 6.25, 12.5, and 25 µg/mL were administered to UV-induced BJ cells. The gene expression of Collagen I Alpha 1 (COL1A1), matrix metalloproteinase-1 (MMP-1), fibroblast growth factor-2 (FGF-2), and glutathione peroxidase-1 (GPX-1) were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Elastin (ELN), hyaluronidase (HAase), cyclooxigenase-2 (COX-2), 8-hydroxydeoxyguanosine (8-OhdG), and melatonin (MT) protein levels were analyzed by enzyme-linked immunosorbent assay (ELISA). The apoptosis of BJ cells was analyzed using flow cytometry. Results Treatment with epicatechin increased relative gene expression including COL1A1 (5.94), FGF-2 (8.34), and GPX-1 (8.09), and also decreased MMP-1 (2.90) relative gene expression compared to the UV-induced BJ cells. Epicatechin also increased levels of ELN (107.7 ng/mg protein) and MT (830 ng/mg protein) levels compared to the UV-induced BJ cells. Epicatechin treatment decreased levels of HAase (505.96 ng/mg protein), COX-2 (33.69 ng/mg protein), and 8-OHdG (97.87 ng/mg protein) compared to the UV-induced BJ cells. Epicatechin also succeeded in maintaining the percentage of live cells and reducing apoptosis, necrotic of UV-induced skin fibroblast cells. Conclusions Epicatechin has the potential to be an antiaging agent by in vitro assay.

Assessment of waste anesthetic gas concentrations in the operating theaters and DNA damage in exposed female nurse anesthetists

BackgroundPersonnel that work in operation theaters are at risk of exposure to waste anesthetic gases (WAGs) that can cause deoxyribonucleic acid (DNA) damage. To assess the potential impacts of single strand break levels of nurse anesthetists, WAGs levels, and other factors were investigated. MethodsNon-smoker nurse anesthetists (exposure group) and registered nurses (control group) that have never worked in operating theaters (OT) were matched by age. The WAG concentrations in OT were measured via a direct reading instrument. A blood sample of 2 mL from each volunteer nurse was used to determine the single strand break of DNA damage by comet assay; between July 2014 and January 2016. ResultsIn total 77 nurses participated in this study. Even if the average 8-h TWA of the WAG concentrations were low, N2O peaked at 951 ppm and sevoflurane peaked at 88.3 ppm during the induction phrase of pediatric patients. Multivariate analysis showed that ln (% of DNA) in the tail and ln (tail moment) were positively, significantly associated with N2O and cancer in family history, while ln (tail length) was not. However, dietary consumption of fish, meat and cruciferous vegetable had influence on DNA damage and shift work should not be neglected. ConclusionNurse anesthetists were potentially exposed to very high WAG concentrations; especially in pediatric cases. There were multi-factors associated with DNA damage score. To decrease the DNA damage score, lifestyle and dietary consumption should be of more concern.

Cold Atmospheric Plasma in Cancer Therapy: Molecular Insights, Novel Concepts, and Future Opportunities

Over the past 2 decades, cold atmospheric plasma (CAP) has been playing increasingly pivotal roles in cutting edge biomedical applications and has developed into an innovative field of research of growing importance. One promising new medical application of CAP is cancer treatment. Being able to richly induce both reactive oxygen and nitrogen species, CAP has been shown to effectively control events critical to cancer initiation/progression; selectively inducing Deoxyribonucleic acid (DNA) damage and apoptotic cell deaths, reducing tumor volume and vasculature, halting metastasis and conferring anti-tumor effects by taking advantage of e.g., synergies among and between chemotherapeutic drugs and nanoparticles. This paper discusses molecular and immunological mechanisms of CAP treatment as a potential tool against cancers, with a focus on the novel mechanisms by which CAP interacts with chemotherapeutic drugs and nanotechnology. We then attempt to draw parallels between what is already known about the mechanisms of CAP activity, some novel concepts and attempts of CAP synergy, and the knowledge we would need to develop CAP as a potential therapeutic strategy in oncotherapy. HIGHLIGHTS This article focused on critical review of cold atmospheric plasma’s (CAP) application in cancer therapy. CAP technology in cancer treatment has been expected to cause a medical and therapeutic implications. CAP has strong anticancer efficacy and has been reported about the cell migration and apoptosis. The major role of reactive oxygen and nitrogen species of plasma discharge is to control the core state of cancer transition. GRAPHICAL ABSTRACT

Significant role of secondary electrons in the formation of a multi-body chemical species spur produced by water radiolysis.

Scientific insights into water photolysis and radiolysis are essential for estimating the direct and indirect effects of deoxyribonucleic acid (DNA) damage. Secondary electrons from radiolysis intricately associated with both effects. In our previous paper, we simulated the femtosecond (1 × 10- 15s) dynamics of secondary electrons ejected by energy depositions of 11-19eV into water via high-energy electron transport using a time-dependent simulation code. The results contribute to the understanding of simple "intra-spur" chemical reactions of tree-body chemical species (hydrated electrons, hydronium ion and OH radical) in subsequent chemical processes. Herein, we simulate the dynamics of the electrons ejected by energy depositions of 20-30eV. The present results contribute to the understanding of complex "inter-spur" chemical reactions of the multi-body chemical species as well as for the formation of complex DNA damage with redox site and strand break on DNA. The simulation results present the earliest formation mechanism of an unclear multi-body chemical species spur when secondary electrons induce further ionisations or electronic excitations. The formation involves electron-water collisions, i.e. ionisation, electronic excitation, molecular excitation and elastic scattering. Our simulation results indicate that (1) most secondary electrons delocalise to ~ 12nm, and multiple collisions are sometimes induced in a water molecule at 22eV deposition energy. (2) The secondary electrons begin to induce diffuse band excitation of water around a few nm from the initial energy deposition site and delocalise to ~ 8nm at deposition energies ~ 25eV. (3) The secondary electron can cause one additional ionisation or electronic excitation at deposition energies > 30eV, forming a multi-body chemical species spur. Thus, we propose that the type and density of chemical species produced by water radiolysis strongly depend on the deposition energy. From our results, we discuss formation of complex DNA damage.

The Impact of Exercise on DNA Damage in Athletes: Causes, Mechanisms, and Case Studies

Although physical activity is important for the athlete’s health and performance, it may also lead to Deoxyribonucleic Acid (DNA) damage, which may have long-term health consequences and affect performance. This article summarizes different types of DNA damage that may occur in athletes, including their potential risk causes, such as mechanical stress, heat stress, and oxidative stress. Furthermore, several mechanisms by which physical activity might lead to DNA damage and affect health and performance are also discussed. Various strategies such as diet and nutrition, antioxidant supplements, cooling strategies, and recovery modalities are also presented to mitigate, prevent, and minimize the potential DNA damage upon physical activities. This article also highlights case studies of athletes who have experienced DNA damage and the effects on their performance and health. In summary, this article offers valuable perspectives on the intricate relationship between physical activity and DNA damage as well as the importance of addressing this issue in the context of athletic performance and health. Keywords: athlete, DNA damage, exercise, RONS

Effects of Pervari Honey from Türkiye on Proliferation, Oxidative Stress, and Apoptosis of Human Breast Cancer Cells

Breast cancer is one of the most common causes of deaths worldwide. Major obstacles to treatment have contributed to the increasing popularity of complementary or alternative therapies. Although recent results support the mechanism that honey induces cell death, the full mechanisms are still unknown. This study investigates the potential use of Pervari honey (PH) as an in vitro therapeutic agent in breast cancer. Firstly, the antioxidant capacity and total phenolic content of PH were tested. In addition, MCF-7 and MDA-MB-231 breast cancer cells treated with PH were examined for cell viability, reactive oxygen species production, oxidative deoxyribonucleic acid (DNA) damage, and apoptosis. Our results show that PH treatment decreased cell viability dose-dependently and increased reactive oxygen species (ROS) levels, oxidative DNA damage, and apoptosis rate. The present study suggests that honey is a promising source to produce pharmaceuticals and nutraceuticals for breast cancer therapy.

Enhanced skin benefits of EGCG loaded in nonapeptide-1-conjugated mesoporous silica nanoparticles to reverse skin photoaging

Epigallocatechin-3-gallate (EGCG), a catechin present in green tea, has been studied extensively for its potential as a cosmetic ingredient due to its various biological properties. However, the low stability and bioavailability of EGCG have hindered its effective utilization in cosmetic applications. This study, to improve the stability and bioavailability of EGCG for reversing skin photo-aging, nonapeptide-1-conjugated mesoporous silica nanoparticles (EGCG@NP-MSN) were fabricated to load EGCG. MSNs can regulate the EGCG release and provide ultraviolet light (UV) protection to possess excellent photostability. Nonapeptide-1 exhibits melanin transfer interference properties and reduces the melanin content in treated skin areas. In vitro and in vivo results confirmed that the EGCG-loaded MSNs retained antioxidant properties, effectively scavenged the melanin and significantly reduced the deoxyribonucleic acid (DNA) damage in skin cells exposed to UV irradiation. The melanin inhibition rate is 5.22 times and the tyrosinase inhibition rate is 1.57 times that of free EGCG. The utilization of this innovative platform offers the potential for enhanced stability, controlled release, and targeted action of EGCG, thereby providing significant advantages for skin application.This delivery system combines the advantages of antioxidant, anti-aging, and anti-UV radiation properties, paving the way for the cosmetics development with improved efficacy and better performance in promoting skin health and appearance.

Liquid water radiolysis induced by secondary electrons generated from MeV-energy carbon ions.

Fast ion beams induce damage to deoxyribonucleic acid (DNA) by chemical products, including secondary electrons, produced from interaction with liquid water in living cells. However, the production process of these chemical products in the Bragg peak region used in particle therapy is not fully understood. To investigate this process, we conducted experiments to evaluate the radiolytic yields produced when a liquid water jet in vacuum is irradiated with MeV-energy carbon beams. We used secondary ion mass spectrometry to measure the products, such as hydronium cations (H3O+) and hydroxyl anions (OH-), produced along with ·OH radicals, which are significant inducers of DNA damage formation. In addition, we simulated the ionization process in liquid water by incident ions and secondary electrons using a Monte Carlo code for radiation transport. Our results showed that secondary electrons, rather than incident ions, are the primary cause of ionization in water. We found that the production yield of H3O+ or OH- was linked to the frequency of ionization by secondary electrons in water, with these electrons having energies between 10.9 and 550eV. These electrons are responsible for ionizing the outer-shell electrons of water molecules. Finally, we present that the elementary processes contribute to advancing radiation biophysics and biochemistry, which study the formation mechanism of DNA damage.

A narrative review of mitochondrial dysfunction and male infertility.

Recent investigations have highlighted mitochondrial dysfunction as a major component in reduced sperm function and male infertility. The creation of energy, control of reactive oxygen species (ROS), apoptosis, and sperm motility are all critically dependent on mitochondria. The health of the male reproductive system may be significantly impacted by any alteration of mitochondrial structure, function, or integrity. This review intends to open the door to better diagnostic methods, novel therapy strategies, and improved reproductive outcomes for infertile couples by clarifying the crucial function of mitochondria. We searched PubMed, Google Scholar, and others for articles related to male infertility and mitochondrial dysfunction from 2014 to 2023. The articles related to the theme were preliminarily screened by abstract, and then the selected literature was read and summarized. In this essay, we examine the research on male infertility and mitochondrial malfunction. We investigate the intricate connection between sperm quality, deoxyribonucleic acid damage, oxidative stress (OS), and mitochondrial bioenergetics. We discuss about how spermatogenesis and sperm function are affected by mitochondrial mutations, deletions, and single nucleotide polymorphisms. We also explore the impact of age-related changes, lifestyle choices, and environmental factors on mitochondrial function and male fertility. This review also clarifies the mechanisms by which mitochondrial dysfunction impacts the viability, morphology, and capacitation of sperm, among other aspects of male reproductive health. Furthermore, we go over the recently developed field of mitochondrial treatments and possible therapeutic approaches that target mitochondrial malfunction to enhance male fertility. Mitochondria are important for sperm: The control of sperm motility, capacitation, and general quality is largely dependent on mitochondria. Deterioration of sperm motility and male infertility may result from disruption of the structure, function, or integrity of the mitochondria. Future studies should focus on figuring out the processes underlying mitochondrial dysfunction as fertility and reproductive health are significantly impacted by it. We discuss the evaluation of infertile men mitochondrial function defects and difficulties, and make recommendations for further study in this area. This article provides a thorough resource for clinicians, researchers, and reproductive biologists to understand the underlying mechanisms of male infertility and explore potential therapeutic interventions.

The Impact of Oleuropein on Cisplatin-Induced Toxicity in Cochlear Cells in Relation to the Expression of Deoxyribonucleic Acid Damage-Associated Genes.

Different organs respond differently to cisplatin (CDDP)-induced toxicity. Oleuropein (OLE) is a natural phenolic antioxidant. The purpose of this study was to determine the potential protective effect of OLE against CDDP-induced ototoxicity by evaluating expression of genes associated with deoxyribonucleic acid (DNA) damage and repair in cochlear cells. House Ear Institute-Organ of Corti 1 (HEI-OC1) cells were treated using CDDP, OLE, and OLE-CDDP. The water-soluble tetrazolium salt assay was used for monitoring cell viability. Deoxyribonucleic acid damage in cells due to the CDDP, OLE, and combination treatments was determined using a flow-cytometric kit. The change in the expression of 84 genes associated with CCDP, OLE, and OLE-CDDP treatments that induced DNA damage was tested using the reverse transcription polymerase chain reaction array. Changes ≥3-fold were considered significant. House Ear Institute-Organ of Corti 1 cell viability was significantly reduced by CDDP. The OLE-CDDP combination restored the cell viability. Cisplatin increased the H2AX ratio, while OLE-CDDP combination decreased it. Some of the DNA damage-associated genes whose expression was upregulated with CDDP were downregulated with OLE-CDDP, while the expression of genes such as Gadd45g and Rev1 was further downregulated. The expression of DNA repair-related Abl1, Dbd2, Rad52, and Trp53 genes was downregulated with CDDP, whereas their expression was upregulated with OLE-CDDP treatment. In cochlear cells, the OLE-CDDP combination downregulated DNA damage-associated gene expression relative to that upregulated mainly by CDDP. The results revealed that OLE has a potential protective effect on CDDP-induced ototoxicity in cochlear cells by altering the expression of DNA damage-related genes.