Cell Biochemistry and Biophysics最新文献

{"title":"Microplastics - A Growing Concern as Carcinogens in Cancer Etiology: Emphasis on Biochemical and Molecular Mechanisms.","authors":"Naveen Kumar, Mridul Lamba, Ashok Kumar Pachar, Sonal Yadav, Arbind Acharya","doi":"10.1007/s12013-024-01436-0","DOIUrl":"https://doi.org/10.1007/s12013-024-01436-0","url":null,"abstract":"<p><p>In today's world, the widespread presence of microplastics is undeniable, with concentrations found in various environments, including up to 1000 particles per liter in seawater and up to 10 particles per cubic meter in the atmosphere. Originating from diverse sources, both intentional and unintentional, these minuscule fragments, measuring less than 5 mm, pose significant threats to environmental and human health. Recent research has uncovered a concerning link between microplastics and cancer, prompting urgent investigation. Studies demonstrate microplastics can infiltrate cells, disrupt biological processes, and potentially foster carcinogenic environments. From inducing DNA damage and oxidative stress to triggering inflammatory responses and dysregulating cellular pathways, microplastics exhibit a multifaceted capability in contributing to cancer development. Furthermore, microplastics act as carriers for a range of contaminants, compounding their impact on human health. Their accumulation within tissues and organs raises concerns for short and long-term health consequences, including chronic diseases, reproductive issues, and developmental abnormalities. This review explores the biochemical and molecular mechanisms underlying the interaction between microplastics and cellular systems, providing insights into routes of exposure and health effects, with a focus on lung, skin, and digestive system cancers. As we confront this pressing environmental and public health challenge, a deeper understanding of the microplastic-cancer relationship is crucial to safeguarding the well-being of present and future generations.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141730898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamics of Inflammatory and Pathological Changes Induced by Single Exposure of Particulate Matter (PM_2.5) in Mice: Potential Implications in COPD.","authors":"Jitender Chandel, Amarjit S Naura","doi":"10.1007/s12013-024-01433-3","DOIUrl":"https://doi.org/10.1007/s12013-024-01433-3","url":null,"abstract":"<p><p>Chronic Obstructive Pulmonary Disease (COPD) is a progressive disorder of lungs marked by chronic bronchitis and emphysema. Particulate matter (PM_2.5), a major component of air pollution has been correlated with COPD incidence. The present work aimed to understand dynamics of cellular/molecular players behind PM_2.5-mediated COPD pathogenesis in mice by conducting dose and time-course studies. Single intratracheal exposure of PM_2.5 at a dose of either 100 or 200 μg induced inflammatory response in lungs at 4 days. Time course studies showed that inflammation once triggered by PM_2.5 is progressive in nature as reflected by data on BALF inflammatory cells at 7/14 days. Similarly, various cytokines/chemokines (KC/IL-6/TNF-α/IL-1β/G-CSF/MCP-1) peak at either 7 or 14 days. However, inflammation declined sharply at 21 days. Data on LPO/GSH and activities of SOD/Catalase show induction of continuous oxidative stress in lung tissue. Next, enhanced mtROS in the CD11b⁺ inflammatory cells confirms the redox imbalance in neutrophils/macrophages. A continuous decline in lung function was observed till 28 days. Further, histological analysis of lung tissues at 28 days confirmed the presence of emphysematous lesions, validating the potency of PM_2.5 to cause irreversible damage to lungs through complex interplay of various cellular/molecular players which may be exploited as potential preventive/therapeutic targets.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141730894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FOXM1 Upregulates O-GlcNAcylation Level Via The Hexosamine Biosynthesis Pathway to Promote Angiogenesis in Hepatocellular Carcinoma.","authors":"Xiaorong Zhang, Yifan Zhong, Qing Yang","doi":"10.1007/s12013-024-01393-8","DOIUrl":"https://doi.org/10.1007/s12013-024-01393-8","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) presents significant challenges in treatment and prognosis because of its aggressive nature and high metastatic potential. This study aims to investigate the role of the hexosamine biosynthesis pathway (HBP) and its association with HCC progression and prognosis. We identified SPP1 and FOXM1 as hub genes within the HBP pathway, showing their correlation with poor prognosis and late-stage progression. In addition, the analysis uncovered the complex participation of the HBP pathway in nutrients and oxygen reactions, PI3K-AKT signaling, AMPK activation, and angiogenesis regulation. The disruption of these pathways is pivotal in influencing the growth and progression of HCC. Targeting the HBP presents a promising therapeutic approach to modulate the tumor microenvironment, thereby enhancing the efficacy of immunotherapy. In addition, FOXM1 was identified as the HBP pathway regulator, influencing cellular O-GlcNAcylation level and VEGF secretion, thereby promoting angiogenesis in HCC. Inhibition of O-GlcNAcylation significantly hindered angiogenesis, which is suggested as a potential avenue for therapeutic intervention. Our research demonstrates the practicality of using the HBP-related gene as a prognostic marker in liver cancer patients and suggests targeting FOXM1 as a novel avenue for personalized therapy.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141730897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sinensetin Inhibits Angiogenesis in Lung Adenocarcinoma via the miR-374c-5p/VEGF-A/VEGFR-2/AKT Axis.","authors":"Tao Ji, Lin Ye, Erping Xi, Ying Liu, Xiumei Wang, Sha Wang","doi":"10.1007/s12013-024-01352-3","DOIUrl":"https://doi.org/10.1007/s12013-024-01352-3","url":null,"abstract":"<p><p>Sinensetin is a product isolated from Orthosiphon aristatus, and its antitumor activities have been well established. This study focused on the role and mechanism of sinensetin in lung adenocarcinoma (LUAD). LUAD cells were treated with various concentrations of sinensetin. The proliferation, migration, invasion, and angiogenesis of LUAD cells were detected using colony formation, transwell, and tube formation assays, respectively. The protein levels of VEGF-A, VEGFR-2, and phosphorylated AKT (ser473) were measured by western blotting. The targeted relationship between VEGF-A and miR-374c-5p was verified by luciferase reporter assay. BALB/c nude mice inoculated with A549 cells were treated with sinensetin (40 mg/kg/day) by gavage for 21 days to investigate the effect of sinensetin on tumor growth and angiogenesis in vivo. We found that sinensetin reduced proliferation, migration, invasion, angiogenesis, and cancer stem characteristics of LUAD cells. Sinensetin also suppressed LUAD tumor growth and angiogenesis in vivo. Sinensetin downregulated VEGF-A expression in LUAD cells by enhancing miR-374c-5p expression. MiR-374c-5p inhibited the VEGF-A/VEGFR-2/AKT pathway in LUAD cells. The antitumor effect of sinensetin was reversed by overexpression of VEGF-A or inhibition of miR-374c-5p. Overall, sinensetin upregulates miR-374c-5p to inhibit the VEGF-A/VEGFR-2/AKT pathway, thereby exerting antitumor effect on LUAD.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141726650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cratoxylum formosum ssp. pruniflorum induces gastric cancer cell apoptosis and pyroptosis through the elevation of ROS and cell cycle arrest.","authors":"Yaya Song, Chunlin Long, Weizhe Chen, Hao Li, Haofeng Zhao, Liya Liu","doi":"10.1007/s12013-024-01408-4","DOIUrl":"https://doi.org/10.1007/s12013-024-01408-4","url":null,"abstract":"<p><p>Cratoxylum formosum ssp. pruniflorum (CF), a traditional medicinal plant in Southern China, is widely recognized as a popular medicinal and tea plant traditionally utilized by diverse linguistic groups in the region for the treatment of gastrointestinal ailments. The objective of this study was to explore the active components and mechanisms of CF against gastric cancer (GC). The chemical ingredients of CF were obtained by using UPLC-MS/MS-based metabolomics. MGC-803 and HGC-27 cells were employed to investigate the direct anti-GC effect. The potential targets and signaling pathway of CF were identified through network pharmacology and proteomics, followed by subsequent experimental validation. Through UPLC-MS/MS metabolomics analysis, a total of 197 chemical ingredients were identified in CF leaves. Network pharmacology and proteomics techniques revealed 25 potential targets for GC, with a protein-protein interaction (PPI) network highlighting 12 cores targets, including CTNNB1, CDK2, et al. Furthermore, seven key CF ingredients - vismione B, feruloylcholine, α-amyrin, vanillic acid, galangin, cinnamic acid, and caffeic acid - were found to mediate anti-GC effects through pathways such as reactive oxygen species (ROS) and cell cycle signaling pathway. In vitro experiments demonstrated that CF significantly inhibited the proliferation and migration of GC cells, increased intracellular reactive oxygen species (ROS), malondialdehyde (MDA) and lactate dehydrogenase (LDH) levels, arrested the cell cycle at the S-phase, induced apoptosis and pyroptosis, and upregulated expression of apoptosis proteins (Bax, Bax/Bcl-2, cleaved-Caspase-3/Caspase-3), and pyroptosis proteins (GSDMD-N/GSDMD and GSDME-N/GSDME), while downregulating expression of cell cycle proteins (CDK2 and cyclin A1) as well as necroptosis proteins (RIP1 and MLKL). Collectively, these findings reveal CF's therapeutic potential against GC by the augmentation of ROS production, cell cycle arrest, promotion of apoptosis, and pyroptosis, offering valuable evidence for the development and utilization of CF in clinical settings.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141722766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combination of Vismodegib and Paclitaxel Enhances Cytotoxicity via Bak-mediated Mitochondrial Damage in EGFR-Mutant Non-Small Cell Lung Cancer Cells.","authors":"Wei-Chen Yeh, Yun-Chieh Tu, Pei-Ling Hsu, Chu-Wan Lee, Hsin-Hsien Yu, Bor-Chyuan Su","doi":"10.1007/s12013-024-01438-y","DOIUrl":"https://doi.org/10.1007/s12013-024-01438-y","url":null,"abstract":"<p><p>Half of NSCLC patients harbor epidermal growth factor receptor (EGFR) mutations, and their therapeutic responses are remarkably different from patients with wild-type EGFR (EGFR-WT) NSCLC. We previously demonstrated that the hedgehog inhibitor vismodegib (Vis) potentiates paclitaxel (PTX)-induced cytotoxicity via suppression of Bax phosphorylation, which promotes accumulation of mitochondrial damage and apoptosis in EGFR-WT NSCLC cells. In this study, we further delineated the anticancer activity and underlying mechanisms of this combination treatment in EGFR-mutant NSCLC cells. MTS/PMS activity and trypan blue exclusion assays were used to assess cell viability. Apoptosis was monitored by chromosome condensation, annexin V staining, and cleavage of PARP and caspase-3. Western blots were conducted to track proteins of interest after treatment. Reactive oxygen species (ROS) level was monitored by 2',7'-dichlorodihydrofluorescein diacetate. Mitochondrial status was analyzed by tetramethylrhodamine, ethyl ester. Hedgehog signaling was induced by PTX, which rendered H1975 and PC9 cells insensitive to PTX-induced mitochondrial apoptosis via suppression of Bak. However, Vis enhanced PTX-induced Bak activation, leading to mitochondrial damage, ROS accumulation, and subsequent apoptosis. Our findings suggest that the combination of Vis and PTX could be a potential therapeutic strategy to increase PTX sensitivity of EGFR-mutant NSCLC.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141726649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxic Regulation of the KLK4 Gene in two Different Prostate Cancer Cells Treated with TGF- β.","authors":"Fatma Poyrazlı, Derya Okuyan, Feray Köçkar, Sümeyye Aydoğan Türkoğlu","doi":"10.1007/s12013-024-01396-5","DOIUrl":"https://doi.org/10.1007/s12013-024-01396-5","url":null,"abstract":"<p><p>The human kallikrein-related peptidase (KLK) family which consists of 15 members is associated with prostate cancer and other cancers. It has been reported that overexpression of KLK4 in prostate cancer correlates with bone metastasis or advanced stage. Hypoxia occurs in the early stages of prostate cancer due to the accumulation of acidic metabolites or reactive oxygen species (ROS). In our study, KLK4 gene expression in hypoxic conditions in PC-3 and LNCaP cells which are treated with TGF-β was evaluated with mRNA, protein, and promoter activity levels. A chemical hypoxia model was created and confirmed at mRNA and protein level. No statistically significant cytotoxic effect of CoCl₂ and TGF-β was observed in PC-3 and LNCaP cells with the MTT test. Four different truncated KLK4 gene promoter constructs were cloned in pmetLuc expression vector and basal activities of all promoter fragments were analyzed. The activities of P1 (-447/ + 657), P2 (-103/ + 657), and P3 (-267/ + 657) promoter fragments increased in hypoxic conditions except P4 (+555/ + 657), which does not contain the SMAD and HRE region. KLK4 mRNA levels in both PC-3 and LNCaP cells increased in the hypoxia and hypoxia/TGF groups compared to the non-treated groups. The stimulating effect of TGF-β is correlated with the increase in SMAD2/3 mRNA levels. KLK4 expression is up-regulated by TGF-β, especially under hypoxic conditions, and its interaction with the SMAD pathway is determined with different inhibitor experiments. HIF-1α and SMAD transcription factors bind to the KLK4 promoter showing the direct interaction of HIF-1α (-80/-52) and SMAD (+163/+194) regions with EMSA.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141722767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Imaging Techniques and Biochemical Biomarkers: New Insights into Diagnosis of Pancreatic Cancer.","authors":"Seyed Hamed Jafari, Zahra Sadat Lajevardi, Mohammad Masoud Zamani Fard, Ameneh Jafari, Soroush Naghavi, Fatemeh Ravaei, Seyed Pouya Taghavi, Kimia Mosadeghi, Fatemeh Zarepour, Maryam Mahjoubin-Tehran, Neda Rahimian, Hamed Mirzaei","doi":"10.1007/s12013-024-01437-z","DOIUrl":"https://doi.org/10.1007/s12013-024-01437-z","url":null,"abstract":"<p><p>Pancreatic cancer (PaC) incidence is increasing, but our current screening and diagnostic strategies are not very effective. However, screening could be helpful in the case of PaC, as recent evidence shows that the disease progresses gradually. Unfortunately, there is no ideal screening method or program for detecting PaC in its early stages. Conventional imaging techniques, such as abdominal ultrasound, CT, MRI, and EUS, have not been successful in detecting early-stage PaC. On the other hand, biomarkers may be a more effective screening tool for PaC and have greater potential for further evaluation compared to imaging. Recent studies on biomarkers and artificial intelligence (AI)-enhanced imaging have shown promising results in the early diagnosis of PaC. In addition to proteins, non-coding RNAs are also being studied as potential biomarkers for PaC. This review consolidates the current literature on PaC screening modalities to provide an organized framework for future studies. While conventional imaging techniques have not been effective in detecting early-stage PaC, biomarkers and AI-enhanced imaging are promising avenues of research. Further studies on the use of biomarkers, particularly non-coding RNAs, in combination with imaging modalities may improve the accuracy of PaC screening and lead to earlier detection of this deadly disease.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141722768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quercetin Attenuates Acute Kidney Injury Caused by Cisplatin by Inhibiting Ferroptosis and Cuproptosis.","authors":"Mengqi Shi, Youchaou Mobet, Hong Shen","doi":"10.1007/s12013-024-01379-6","DOIUrl":"https://doi.org/10.1007/s12013-024-01379-6","url":null,"abstract":"<p><p>Ferroptosis, an iron- and ROS-dependent form of regulated cell death. Cuproptosis is a novel form of cellular demise mode. Quercetin, a natural flavonoid, has demonstrated a range of pharmacological activities, including anti-cancer, anti-inflammatory, and antioxidant properties. In this research, we investigated the quercetin effect on cisplatin-induced acute kidney and its mechanism associated ferroptosis and cuproptosis. The HK-2 cells were used in this research. Cell viability was evaluated using the CCK-8 assay. Acute kidney injury (AKI) models were established to perform in vivo experiments. Renal tissue homogenate was used to determine ROS, LPO, MDA, PA, etc., to assess ferroptosis and cuproptosis. To perform bioinformatic analysis, microarray data from the GEO database was utilized. Real-time PCR analysis and ELISA was explored the mechanism of ferroptosis and cuproptosis. We found that ferroptosis and cuproptosis in AKI were abnormally activated caused by cisplatin, and that quercetin attenuated AKI by inhibiting ferroptosis and cuproptosis. QCT suppressed ferroptosis by reducing malondialdehyde (MDA) and ROS levels and increasing glutathione (GSH) levels and alleviated cuproptosis by reducing copper ion, pyruvate (PA) and HSP70 levels. Moreover, bioinformatic analysis revealed that the ferroptosis-related gene SLC7A11 and the cuproptosis-related genes ATP7B and GLS were the differential expression genes. And QCT significantly increased the expression or activity of SLC7A11, GPX4, ATP7B, and GLS in Cis-AKI mice. Our findings highlight the clinical importance of quercetin, which guards against cisplatin-induced acute kidney injury by suppressing ferroptosis and cuproptosis.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141722769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impacts of 1.5 T MRI Static Magnetic Field on Biochemical and Enzyme Activity Parameters on Radiology Department Workers.","authors":"Thabit Elias Basheer, Suzan Mohammed Haji, Basim S A Al Sulivany","doi":"10.1007/s12013-024-01422-6","DOIUrl":"https://doi.org/10.1007/s12013-024-01422-6","url":null,"abstract":"<p><p>Magnetic Resonance Imaging (MRI) is an important diagnostic technique that uses powerful magnetic fields to generate detailed images of the human body. The aim of this study is to investigate to how static magnetic fields (SMF) affect the levels of trace elements and biochemical parameters in MRI staff' blood serum. This study examines the impacts of these exposures of 18 participants (9 males and 9 females) aged between 25 and 60.on the levels of trace elements in the blood serum and the biochemical parameters of the MRI staff at Azadi Teaching Hospital in Duhok and Zakho General Hospital-Bidari in Zakho City. Eighteen participants, consisting of nine males and nine females aged between 25 and 60, were selected from these hospitals. The researchers obtained blood samples and conducted analysis to determine the presence of trace elements (sodium, potassium, calcium, chloride) as well as numerous biochemical markers. The results showed that potassium and calcium levels increased with age, and older females had considerable deviations. Chloride levels exhibited a significant increase with age in both males and females. Glucose, creatinine, uric acid, and urea levels showed an increase with age, suggesting the possible damage to kidney function caused by continuous exposure to MRI. Increased levels of liver enzymes (GPT, GOT, ALP) and thyroid-stimulating hormone (TSH) were noticed, particularly in older females, indicating potential liver and thyroid dysfunction. These results highlight the importance of applying strict safety protocols and conducting regular health assessments for MRI personnel to minimize the possible hazards.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141632296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}