Cytotechnology最新文献

{"title":"The impact of graphene quantum dots on osteogenesis potential of Wharton's jelly mesenchymal stem cells in fibrin hydrogel scaffolds.","authors":"Kaveh Khazaeel, Abbas Sadeghi, Fatemeh Khademi Moghaddam, Tayebeh Mohammadi","doi":"10.1007/s10616-024-00672-9","DOIUrl":"10.1007/s10616-024-00672-9","url":null,"abstract":"<p><p>Bone tissue engineering is a promising approach to overcome the limitations of traditional autograft bone transplantation. Graphene quantum dots (GQDs) have been suggested as an enhancement for osteogenic differentiation. This study aimed to investigate the ability of the fibrin hydrogel scaffold in the presence of graphene quantum dots to promote osteogenic differentiation of human Wharton's jelly-derived mesenchymal stem cells (hWJ-MSCs). The hWJ-MSCs were isolated from the Wharton's jelly of the human umbilical cord using a mechanical method. Fibrin hydrogel scaffolds were prepared by mixing 15 µl of thrombin solution with fibrinogen solution. GQDs were incorporated into the scaffolds at concentrations of 0, 5, and 10 µg/ml. Cell viability was determined through DAPI staining and the MTT assay. Osteogenic differentiation was assessed by measuring alkaline phosphatase (ALP) activity, quantifying calcium deposition using Alizarin Red S staining, and analyzing the gene expression of BGLAP, COL1A1, Runx-2 and ALP via qPCR. Scanning electron microscopy (SEM) was employed to analyze the scaffold architecture. SEM analysis revealed that the fibrin hydrogel exhibited a suitable architecture for tissue engineering, and DAPI staining confirmed cell viability. The MTT results indicated that the GQDs and fibrin hydrogel scaffold exhibited no cytotoxic effects. Furthermore, the incorporation of GQDs at a concentration of 10 µg/ml significantly enhanced ALP activity, calcium deposition, and the expression of osteogenesis-related genes compared to the control. The findings suggest that the combination of fibrin hydrogel and GQDs can effectively promote the osteogenic differentiation of hWJ-MSCs, contributing to the advancement of bone tissue engineering.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"14"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11628478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurotrophomodulatory effect of TNF-α through NF-κB in rat cortical astrocytes.","authors":"Langhnoja Jaldeep, Buch Lipi, Pillai Prakash","doi":"10.1007/s10616-024-00698-z","DOIUrl":"10.1007/s10616-024-00698-z","url":null,"abstract":"<p><p>Tumor necrosis factor alpha (TNF-α) is a well-known pro-inflammatory cytokine originally recognized for its ability to induce apoptosis and cell death. However, recent research has revealed that TNF-α also plays a crucial role as a mediator of cell survival, influencing a wide range of cellular functions. The signaling of TNF-α is mediated through two distinct receptors, TNFR1 and TNFR2, which trigger various intracellular pathways, including NF-κB, JNK, and caspase signaling cascades. Both TNFR1 and TNFR2 are expressed in astrocytes, which are specialized glial cells essential for maintaining the structural and functional integrity of the central nervous system (CNS). Astrocytes support neuronal function by regulating brain homeostasis, maintaining synaptic function, and supplying metabolic substrates. In addition, astrocytes are known to secrete a variety of growth factors and neurotrophins, such as nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and NT-4/5. These neurotrophins play a critical role in supporting neuronal survival, synaptic plasticity, and myelination within the brain. The present study focuses on the role of TNF-α in modulating neurotrophin expression and secretion in rat cortical astrocytes. We demonstrate that TNF-α induces the upregulation of neurotrophins, particularly NGF and BDNF, in cultured astrocytes. This effect is accompanied by an increase in the expression of their respective receptors (TrkA & TrkB), further suggesting a functional modulation of neurotrophic signaling pathways. Notably, we show that the modulation of neurotrophin expression by TNF-α is mediated via the NF-κB signaling pathway. Additionally, we observed that TNF-α also regulates the secretion levels of NGF and BDNF into the culture media of astrocytes in a dose-dependent manner, indicating that TNF-α can modulate both the production and release of these growth factors. Taken together, our findings highlight a previously underexplored neuroprotective role of TNF-α in astrocytes. Specifically, we propose that TNF-α, through the upregulation of neurotrophins, may contribute to maintaining neuronal health and supporting neuroprotection under disease conditions.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"37"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing monoclonal antibody production efficiency using CHO-MK cells and specific media in a conventional fed-batch culture.","authors":"Hisashi Saeki, Kaori Fueki, Naoki Maeda","doi":"10.1007/s10616-024-00669-4","DOIUrl":"10.1007/s10616-024-00669-4","url":null,"abstract":"<p><p>Chinese hamster ovary (CHO) cell lines, derived as subclones from the original CHO cell line, are widely used hosts for current biopharmaceutical productions. Recently, a highly proliferative host cell line, CHO-MK, was established from the Chinese hamster ovary tissue. In this study, we assessed the fundamental culture characteristics and capabilities of CHO-MK cells for monoclonal antibody (mAb) production using specified chemically defined media. To achieve this, we established fed-batch cultures of model CHO-MK cells in shake flasks and ambr15 and 2 L bioreactors under various conditions. The mAb-producing CHO-MK cell line A produced 12.6 g/L of antibody within 7 days in the fed-batch culture using a 2 L bioreactor, with a seeding density of 1 × 10⁶ cells/mL. This performance corresponded to a space-time yield of 1.80 g/L/day, representing a productivity level that could be challengingly attained in fed-batch cultures using conventional CHO cells. In addition, when we subjected six different mAb-producing CHO-MK cell lines to fed-batch culture in the ambr15 bioreactor for 7 days, the antibody production ranged between 5.1 and 10.8 g/L, confirming that combining CHO-MK cells and specified media leads to enhanced versatility. These discoveries underscore that CHO-MK cells combined with specified media might represent a next-generation production platform, which could potentially respond to an increasing demand for antibody drugs, reducing production costs, and shortening antibody drug development times. This study is expected to serve as a benchmark for future production process development using CHO-MK cells.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"1"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11573942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Growth suppressing effect of <i>Fagonia arabica</i> extracts on cancerous cell line.","authors":"Rida Fatima, Aqsa Batool, Tabinda Ijaz, Sajjad Ullah Khan, Yasmin Akhtar, Sezai Ercisli, Saeedah Musaed Almutairi, Mohamed Soliman Elshikh, Aroona Saleem, Muhammad Ammar Javed","doi":"10.1007/s10616-024-00663-w","DOIUrl":"10.1007/s10616-024-00663-w","url":null,"abstract":"<p><p>Homeostasis of tissues requires a complex balance between cell proliferation and cell death. The disruption of this balance leads to tumors. Cancer is a mortal disease that spreads all over the body, it is an irregular cell growth. All the tumors are not cancerous, benign tumors do not spread to all body parts. Cancer is caused when cells start to grow out of control, known as increased proliferation. Cancer is of many kinds and the reason for cancer is the uncontrolled growth of cells that can affect any tissue of the body Conventional plants are precious sources of novel cytotoxic agents and are still in a better role in health concerns. The study aimed to evaluate the effect of in vitro anti-proliferative activity of <i>Fagonia arabica</i> plant extracts against HeLa and HepG2 cell lines and compared with normal BHK cells. <i>Fagonia arabica</i> plant (seed, leaves, fruit peel, fruit pulp, stem, and root) is extracted in their solvent's ethanol, ethyl acetate, and petroleum ether. For the estimation of anti-proliferation, cell viability, and cell death in HeLa, HepG2, BHK, MTT assay was done. The angiogenic potential was checked via Immunocytochemistry and ELISA of VEGF. Immunocytochemistry and ELISA of Annexin-V were performed for the estimation of apoptosis in HeLa cells and BHK. Furthermore, Immunocytochemistry and ELISA for p53 were also performed. Cancer cells (HeLa, HepG2) showed reduced angiogenesis, low proliferation, increased apoptotic level, reduced viability, and increased cell death. It is found that <i>Fagonia arabica</i> plant extract induces apoptosis along with inhibition of proliferation and angiogenesis may strongly have profound effects on growth suppression of HeLa and HepG2 cell lines.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"36"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KDM1A-mediated ZFP64 demethylation activates CENPL to promote epithelial ovarian cancer progression.","authors":"Jie Wang, Xinjian Fang, Yajun Xing, Meiqing Ding, Liangxue Zhu, Mingyun Wang","doi":"10.1007/s10616-024-00671-w","DOIUrl":"10.1007/s10616-024-00671-w","url":null,"abstract":"<p><p>Lysine-specific histone demethylase 1A (KDM1A) has emerged as an attractive therapeutic target for treating various cancers, owing to its observed overexpression. However, its function in epithelial ovarian cancer (EOC) remains uncertain. The current study sought to investigate the function of KDM1A on malignant phenotypes of EOC cells as well as the underlying mechanism. Colony formation assay, cell counting kit-8, wound healing, Transwell assays, and TUNEL assays were performed to investigate the effects of KDM1A, Zinc finger protein 64 (ZFP64), and centromere protein L (CENPL) in vitro, while subcutaneous tumor formation models were established in nude mice to evaluate their roles in vivo. KDM1A, ZFP64, and CENPL were overexpressed in EOC tissues and cells. Knockdown of KDM1A, ZFP64, or CENPL inhibited the biological behavior of EOC cells. In addition, chromatin immunoprecipitation showed that KDM1A stimulated ZFP64 expression by removing the H3K9me2 mark from its promoter. Restoration of ZFP64 promoted EOC cell malignant phenotype in the presence of KDM1A knockdown. ZFP64 activated CENPL transcription. Reactivation of CENPL promoted the growth of EOC cells in vivo inhibited by knockdown of ZFP64. Collectively, KDM1A promoted EOC cell proliferation, migration, and invasion, and reduced apoptosis by activating the ZFP64/CENPL axis, which triggered EOC progression.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-024-00671-w.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"10"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11609140/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CBX3 contributes to pancreatic adenocarcinoma progression via promoting KIF20A expression.","authors":"Xiaohui Wang, Ping Meng, Huili Liu, Jinhua Tan, Yu Liu, Xu Li","doi":"10.1007/s10616-024-00684-5","DOIUrl":"10.1007/s10616-024-00684-5","url":null,"abstract":"<p><p>Pancreatic adenocarcinoma (PAAD) is one of the malignant tumors with poor prognosis. This study aims to inquiry the effects of Chromobox homologue 3 (CBX3) on PAAD progression. Pan-cancer analysis of CBX3 and its correlation with PAAD progression were investigated by informatics analysis. The role of CBX3 in PAAD was explored in vitro and in vivo. Cell viability, proliferation, migration and invasion were inspected by CCK-8 assay, EdU staining, scratch test and transwell assay, respectively. The morphology of tumors was observed by hematoxylin-eosin staining. Immunohistochemistry (Ki67) was performed to inspect the proliferation of tumor tissue. The protein levels were measured by western blot. Moreover, the downstream genes of CBX3 were screened, and the effects of target gene on PAAD was investigated in vitro. CBX3 was overexpressed in multi cancers, and high CBX3 expression indicated poor prognosis in PAAD. Through the in vitro assays, knockdown of CBX3 suppressed the viability, migration and invasion of PAAD cells, and restrained tumor growth in vivo. Subsequently, kinesin family member 20A (KIF20A) was screened as the downstream gene of CBX3, which was up-regulated in PAAD and related to low overall survival. Mechanistically, we discovered that CBX3 could regulate KIF20A expression. Knockdown of CBX3 promoted the oncogenic effects of KIF20A silencing on PAAD cells, and attenuated the pro-oncogenic effects of KIF20A overexpression on PPAD. Collectively, silencing CBX3 suppressed PAAD progression through regulating KIF20A expression, providing an underlying target for PAAD treatment.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"25"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142902673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA NORAD sponging to miR-26b-5p represses the progression of Alzheimer's disease in vitro by upregulating MME expression.","authors":"Lizhu Chen, Xiaoqiong Yan","doi":"10.1007/s10616-024-00691-6","DOIUrl":"10.1007/s10616-024-00691-6","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurological condition that causes brain shrinkage and cell death. This study aimed to identify the role of the NORAD/miR-26b-5p axis in AD. StarBase was used to examine the binding sequences of miR-26b-5p to LncRNA NORAD or its target genes, which were verified by a double luciferase reporter assay. PC12 cells were processed with Aβ_1-42 to construct an AD model in vitro, and LncRNA NORAD and miR-26b-5p levels in PC12 cells were identified by RT-qPCR. Cell viability and apoptosis were measured using the MTT assay and flow cytometry, respectively. LDH release and oxidative stress-related indicators (MDA, SOD, and CAT) were detected using the corresponding kits, and the levels of Bcl-2 and Bax were assessed by western blotting and RT-qPCR. Aβ_1-42 distinctly decreased LncRNA NORAD and membrane metalloendopeptidase (MME) levels in PC12 cells, while miR-26b-5p was generally increased. The LncRNA NORAD can adsorb miR-26b-5p, and the target gene of miR-26b-5p is neprilysin (MME). In the Aβ_1-42 induced AD model, PC12 cell activity decreased, LDH release and apoptosis increased, oxidative stress level increased, Bax expression increased, and Bcl-2 expression decreased. LncRNA NORAD plays a protective role in AD cell models by abrogating miR-26b-5p levels. Inhibition of MME expression eliminated the protective effects of the miR-26b-5p inhibitor in AD cell models. LncRNA NORAD inhibits AD progression in vitro by modulating the miR-26b-5p-MME signaling axis. The LncRNA NORAD/miR-26b-5p is expected to be a prospective therapeutic candidate for AD.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-024-00691-6.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"41"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The protective role of baicalin regulation of autophagy in cancers.","authors":"Qi Zhang, Shiyun Guo, Hangwei Ge, Honggang Wang","doi":"10.1007/s10616-024-00689-0","DOIUrl":"10.1007/s10616-024-00689-0","url":null,"abstract":"<p><p>Autophagy is a conservative process of self degradation, in which abnormal organelles, proteins and other macromolecules are encapsulated and transferred to lysosomes for subsequent degradation. It maintains the intracellular balance, and responds to cellular conditions such as hunger or stress. To date, there are mainly three types of autophagy: macroautophagy, microautophagy and chaperone-mediated autophagy. Autophagy plays a key role in regulating multiple physiological and pathological processes, such as cell metabolism, development, energy homeostasis, cell death and hunger adaptation, and so on. Increasing evidence indicates that autophagy dysfunction participates in many kinds of cancers, such as liver cancer, pancreatic cancer, prostate cancer, and so on. However, the relevant mechanisms are not yet fully understood. Baicalin is a natural flavonoid compound extracted from the traditional Chinese medicine <i>Scutellaria baicalensis</i>. The research has shown that after oral or intravenous administration of baicalin, it is delivered to various organs through the systemic circulation, with the highest volume in the kidneys and lungs. More and more evidence suggests that baicalin has antioxidant, anticancer, anti-inflammatory, anti-apoptotic, immunomodulatory and antiviral effects. Therefore, baicalin plays an important role in various diseases, such as cancers, lung diseases, liver diseases, cardiovascular diseases, ans so on. However, the relevant mechanisms have not yet been fully clear. Recently, increasing evidence indicates that baicalin participates in different cancer by regulating autophagy. Herein, we reviewed the current knowledge about the role and mechanism of baicalin regulation of autophagy in multiple types of cancers to lay the theoretical foundation for future related researches.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"33"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative stress profile and auto-antibodies production in Tunisian patients with COVID-19.","authors":"Bochra Gargouri, Ichrak Ben Amor, Yosra Ramma, Riad Ben Mansour, Ahmed Bayoudh, Imen Kallel, Hammadi Attia","doi":"10.1007/s10616-024-00683-6","DOIUrl":"10.1007/s10616-024-00683-6","url":null,"abstract":"<p><p>The clinical evidence, complications and the pathogenesis of COVID-19 are not clearly understood. In COVID-19 patients, cellular immune response biomarkers and oxidative stress parameters have been used as gravity markers. Indeed, oxidative stress has been proposed to play an essential role in the genesis of COVID-19. In the present research, we investigated lipid peroxidation, protein oxidation, superoxide dismutase activity and the production of auto-antibodies against superoxide dismutase, in the blood of Tunisian patients with corona virus. To evaluate lipid peroxidation, plasma malondialdehyde and conjugated dienes, have been determined in 69 corona virus patients and 30 controls. To determine protein oxidation the thiol level was measured. Plasma superoxide dismutase activity has been measured in 30 corona virus patients and 30 controls on one hand. Utilizing a standard enzyme-linked immunosorbent assay, the level of immunoglobulin G (IgG), and M (IgM) directed against superoxide dismutase was evaluated. To investigate the implication of auto-antibody production in COVID-19 patients in the generation of oxidative stress, a correlation study between auto-antibodies production and oxidative stress parameters was performed. High levels of both malondialdehyde and conjugated dienes were found in the plasma of patients (p < 0.001, respectively). Protein oxidation was confirmed by the high level of thiol (p < 0.001). Superoxide dismutase activity was not significantly lower in COVID-19 patients (p > 0.05). The level of immunoglobulin G (IgG), and M (IgM) directed against superoxide dismutase is significantly higher in COVID-19 patients than in control group (p < 0.001 respectively). Statistical analyses have demonstrated a positive correlation between superoxide dismutase activity and IgM and IgG isotypes antibodies level against superoxide dismutase (p < 0.001). A strong positive correlation was observed between IgG and malondialdehyde level in all cases (r = 0.368; p ≤ 0.01). In addition, a significant positive correlation was noted between IgM and malondialdehyde (r = 0.290; p = 0.024). Similarly, two significant positive relationship was found between IgG / conjugated dienes (r = 0.356; p = 0.005) and between IgM / conjugated dienes (r = 0.285; p = 0.027).</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"22"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655737/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"S-Sulfocysteine's toxic effects on HT-22 cells are not triggered by glutamate receptors, nor do they involve apoptotic or genotoxicity mechanisms.","authors":"Volkan Tekin, Fatih Altintas, Burak Oymak, Egem Burcu Unal, Melek Tunc-Ata, Levent Elmas, Vural Kucukatay","doi":"10.1007/s10616-024-00697-0","DOIUrl":"10.1007/s10616-024-00697-0","url":null,"abstract":"<p><p>S-Sulfocysteine (SSC) is a metabolite derived from the metabolism of sulfur-containing amino acids. It has been implicated in neurotoxicity observed in children with sulfite oxidase deficiency. The aim of our study was to confirm the neurotoxic effects of SSC using a mouse hippocampal cell line (HT-22) and to investigate the role of apoptosis in these effects, especially in terms of caspase-3 activation and genotoxicity. Based on the viability graph obtained following increasing concentrations of SSC, we determined the LC50 dose of SSC to be 125 µM by probit analysis. The cytotoxic effects of SSC were not reversed by glutamate receptor blocker administration. However, SSC treatment did not induce caspase-3 activation or induce DNA damage. Our results showed that SSC has a cytotoxic effect on neurons like glutamate, but glutamate receptor blockers reversed glutamate-induced toxicity, while these blockers did not protect neurons from SSC toxicity. The absence of caspase-3 activation and DNA fragmentation, which are indicative of apoptosis, in SSC-induced cell death suggests that alternative cell death pathways, such as necrosis and oxytosis may be implicated. Further research is necessary to fully elucidate SSC-induced cell death. The aim of our study was to confirm the neurotoxic effects of SSC using a mouse hippocampal cell line (HT-22) and to investigate the role of apoptosis in these effects, especially in terms of caspase-3 activation and genotoxicity.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 1","pages":"32"},"PeriodicalIF":2.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11688261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}