Journal of Biochemical and Molecular Toxicology最新文献

Protective Effects of Berberine on Bortezomib-Induced Hepatorenal Toxicity in Sprague Dawley Rats: Biochemical, Molecular and Histological Evaluation. 小檗碱对硼替佐米所致大鼠肝肾毒性的保护作用：生化、分子和组织学评价。

IF 2.8 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-10-01 DOI: 10.1002/jbt.70552

Ozge Kandemir, Cihan Gur, Selim Comakli, Sefa Kucukler, Fatih Mehmet Kandemir

{"title":"Protective Effects of Berberine on Bortezomib-Induced Hepatorenal Toxicity in Sprague Dawley Rats: Biochemical, Molecular and Histological Evaluation.","authors":"Ozge Kandemir, Cihan Gur, Selim Comakli, Sefa Kucukler, Fatih Mehmet Kandemir","doi":"10.1002/jbt.70552","DOIUrl":"https://doi.org/10.1002/jbt.70552","url":null,"abstract":"This study investigated the potential of herbal-derived berberine (BBR) to reduce hepatorenal toxicity induced by the proteasome inhibitor bortezomib (BTZ) in male Sprague-Dawley rats. For this purpose, after BTZ and BBR administration to rats, oxidative stress, endoplasmic reticulum stress, inflammation and apoptosis markers in liver and kidney tissues were analyzed by biochemical, qRT-PCR and ELISA methods. Moreover, to serum biochemistry analyses, histopathological and immunohistochemical examinations were performed on tissues. The data obtained showed that BBR alleviated the oxidative stress induced by BTZ in liver and kidney tissues. Additionally, ER stress markers upregulated by BTZ were suppressed by BBR. In liver and kidney tissues, inflammatory genes NF-κB, TLR-4, TNF-α, IL-1β and apoptotic genes P53, Apaf-1, Bax, Casp-3, Casp-6 and Casp-9 were triggered by BTZ administration, while BBR suppressed these genes. In immunohistochemical examinations, 8-OHdG stains in liver tissue and KIM-1 stains in kidney tissue increased with BTZ administration and decreased after BBR administration. Histopathological examinations showed that BTZ negatively affected the liver and kidney architecture, while tissue recovery occurred after BBR treatment. The improvement of the integrity of the damaged liver and kidney tissues with BBR treatment was also confirmed by the results of ALT, AST, Urea and creatinine. As a result, it was observed in the study that BTZ caused toxicity in liver and kidney tissues and may cause dysfunction in the tissues, while BBR may have a protective feature in this BTZ-induced toxicity.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 10","pages":"e70552"},"PeriodicalIF":2.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145232673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Characterization of the Chromatin Accessibility in the Hearts of Mice With Lipopolysaccharide (LPS)-Induced Sepsis. 脂多糖（LPS）诱导脓毒症小鼠心脏染色质可及性的表征。

IF 2.8 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-10-01 DOI: 10.1002/jbt.70543

Hao-Jie Xu, Rui-Zhi Yang, Jian-Jun Yu, Ya-Yi Lin, Jin-Shuang Qu, Chao-Mei Yuan, Ying-Yi Lin, Hang Yang, Kai Zeng

{"title":"Characterization of the Chromatin Accessibility in the Hearts of Mice With Lipopolysaccharide (LPS)-Induced Sepsis.","authors":"Hao-Jie Xu, Rui-Zhi Yang, Jian-Jun Yu, Ya-Yi Lin, Jin-Shuang Qu, Chao-Mei Yuan, Ying-Yi Lin, Hang Yang, Kai Zeng","doi":"10.1002/jbt.70543","DOIUrl":"https://doi.org/10.1002/jbt.70543","url":null,"abstract":"This study investigates the transcription and expression of genes associated with Sepsis-induced cardiac dysfunction (SICD) in a sepsis mouse model by examining chromatin accessibility. The assay for transposase-accessible chromatin by sequencing (ATAC-seq) was employed to investigate chromatin reshaping associated with SICD in the sepsis mouse model. ATAC-seq data were generated from the hearts of sepsis mice, and the relationship between chromatin accessibility and gene expression was analyzed in conjunction with RNA sequencing. RNA-seq results indicated that the most differentially expressed genes were present 1 day post-induction. We identified 2389 increased and 5065 decreased sepsis-associated chromatin-accessible regions in the heart tissues of sepsis mice. At 1 day post-induction, 877 genes were upregulated, and 881 were downregulated. Notably, an enhanced ATAC-seq signal was observed in approximately 1311 genes, with 93 showing upregulated mRNA levels. The signatures of numerous transcription factors, including ERG, ETV2, Mef2c, and JunB, were enriched in the SICD-associated accessible chromatin regions. This study demonstrates that alterations in chromatin accessibility may serve as an initial mechanism in sepsis-induced cardiac dysfunction.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 10","pages":"e70543"},"PeriodicalIF":2.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145232596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epigenetic Regulation of Manganese-Induced Hepatotoxicity Uncovering Histone Demethylation-Associated Gene Networks. 锰诱导肝毒性的表观遗传调控揭示组蛋白去甲基化相关基因网络。

IF 2.8 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-10-01 DOI: 10.1002/jbt.70556

Bing Yang, Xiaofeng Li

{"title":"Epigenetic Regulation of Manganese-Induced Hepatotoxicity Uncovering Histone Demethylation-Associated Gene Networks.","authors":"Bing Yang, Xiaofeng Li","doi":"10.1002/jbt.70556","DOIUrl":"https://doi.org/10.1002/jbt.70556","url":null,"abstract":"Excessive manganese (Mn) exposure can result in significant liver toxicity in humans and animals. Histone demethylation, a crucial epigenetic modification, is believed to play a pivotal role in liver disease progression. However, the involvement of histone demethylation-associated genes in Mn-induced hepatotoxicity remains poorly understood. This study aimed to identify these genes related to Mn exposure. We analyzed gene expression data, which included liver samples treated with manganese chloride (MnCl2) and control samples. Our analysis revealed 351 differentially expressed genes (DEGs) on Day 3 and 494 DEGs on Day 5 in livers treated with 700 mg/kg MnCl2. Notably, we identified 24 overlapping histone demethylation-associated DEGs across both time points. Biological process analysis indicated that these DEGs are linked to organ regeneration, cell proliferation, responses to xenobiotic substances and toxins, bile transport, fatty acid metabolism, and posttranscriptional regulation. Pathway analysis identified associations with IL-17 signaling, cAMP pathways, chemical carcinogenesis, and parathyroid hormone synthesis and action. Furthermore, we highlighted several histone demethylation-associated hub genes, including CDKN1A, PPARA, CYP7A1, CAV1, GDF15, and GRP, implicated in Mn-induced hepatotoxicity.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 10","pages":"e70556"},"PeriodicalIF":2.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Downregulation of MUC1 Enhances Antitumor Response in Colon Cancer Model by Decreasing PD-L1 Expression In Vivo and In Vitro. 下调MUC1通过降低体内和体外PD-L1表达增强结肠癌模型的抗肿瘤反应

IF 2.8 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-10-01 DOI: 10.1002/jbt.70538

Daguang Fan, Huanfang Liang, Shan Luo, Yuanyuan Zhang, Jingwei Yan, Dawei Xu, Chongxiao Qu, Jianfang Ma

{"title":"Downregulation of MUC1 Enhances Antitumor Response in Colon Cancer Model by Decreasing PD-L1 Expression In Vivo and In Vitro.","authors":"Daguang Fan, Huanfang Liang, Shan Luo, Yuanyuan Zhang, Jingwei Yan, Dawei Xu, Chongxiao Qu, Jianfang Ma","doi":"10.1002/jbt.70538","DOIUrl":"https://doi.org/10.1002/jbt.70538","url":null,"abstract":"Colorectal cancer (CRC) is a cancer with poor 5-year survival rates. The exploration of biomarkers and potential mechanisms for the diagnosis and treatment of CRC is crucial in clinical practice. The transmembrane glycoprotein Mucin 1 (MUC1), as a glycoprotein, is essential for controlling tumor metabolism. Multiple studies demonstrate that MUC1 has an antitumor effect in prostate, breast, and gastric cancers. However, the mechanism of MUC1 in CRC is still unclear. This study was to explore MUC1's putative molecular mechanism in CRC. The expression of MUC1 in the tumor specimens or normal tissues was identified by immunohistochemistry and Western blot. MUC1 knockdown or exogenous expression and miR-200c were performed to confirm MUC1 function. The molecular mechanism of MUC1 was revealed through quantitative real-time PCR (Q-PCR), western blot, immunoprecipitation assays, and flow cytometry. Our results showed positive correlation between the expression of PD-L1 and MUC1, which is increased in colon carcinoma tissues. MUC1 upregulation can promote CD8 + T cell immune tolerance and immune failure, as well as increased infiltration of Treg, MDSCs and ATM cells. Furthermore, MUC1 downregulated PD-L1 expression by NF-κB p65 and miR-200c. MUC1 downregulation improved antitumor immune response of CD8 + T cells and decreased the proportion of Treg, MDSCs, and ATM cell infiltration. Downregulating MUC1 enhances antitumor immune response through NF-κB p65, and mirR-200c by reducing PD-L1 expression.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 10","pages":"e70538"},"PeriodicalIF":2.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Can Acetaminophen be Used as a Chemotherapeutic Agent in the Kidney? 对乙酰氨基酚可以作为肾脏化疗药物吗？

IF 2.8 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-10-01 DOI: 10.1002/jbt.70529

Hartmut Jaeschke, Jephte Y Akakpo, Anup Ramachandran

引用次数: 0

Kaempferide Inhibits the Proliferation and Invasion and Induces Ferroptosis in Melanoma by Inactivating Wnt/β-Catenin Pathway. 山奈哌利通过灭活Wnt/β-Catenin通路抑制黑色素瘤的增殖和侵袭并诱导铁凋亡。

IF 2.8 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-10-01 DOI: 10.1002/jbt.70535

Yonghui Xu, Rui Zhao, Zeping Huang, Yun Zhang, Runping Yang, Jin Zhang

{"title":"Kaempferide Inhibits the Proliferation and Invasion and Induces Ferroptosis in Melanoma by Inactivating Wnt/β-Catenin Pathway.","authors":"Yonghui Xu, Rui Zhao, Zeping Huang, Yun Zhang, Runping Yang, Jin Zhang","doi":"10.1002/jbt.70535","DOIUrl":"https://doi.org/10.1002/jbt.70535","url":null,"abstract":"Melanoma is a type of skin cancers, with the nature of aggression, metastasis and high lethality. Kaempferide (KF), a natural flavonoid, shows anti-cancer in different cancers. However, the activity of KF on melanoma remains unclear. Cell counting kit-8, transwell, iron measurement, the determination of ROS levels and western blot were utilized to examine the impact and mechanism of KF on melanoma. An in vivo investigation employing immunohistochemistry and western blot assays was carried out on tumor-bearing mice. A375 and A2085 cells' E-cadherin expression was boosted whereas N-cadherin expression, invasion count, and cell survival were all decreased by KF. In both A375 and A2085, KF raised the relative Fe2+ level, which was then farther enhanced by the erastin incubation and reduced by the ferrostatin-1 treatment. Besides, KF enhanced the level of ROS while lowering the expression of xCT and GPX4 in the two cells. Mechanically, the application of LiCl reversed the drop in the relative levels of p-GSK3β/GSK3β, c-Myc, and active-β-catenin/β-catenin in melanoma cells caused by KF. LiCl's activation of the Wnt/β-catenin pathway counteracted the impact of KF on melanoma cell proliferation, invasion, and ferroptosis. KF reduced tumor weight and volume in vivo, as well as the expression of c-Myc, p-GSK3β/GSK3β, active-β-catenin/β-catenin, and N-cadherin, GPX4, and xCT, but enhanced the E-cadherin level in mice xenografted with A375 cells. KF inhibited melanoma by attenuating proliferation and invasion and inducing ferroptosis via Wnt/β-catenin axis, highlighting the underlying therapeutical effect of KF on melanoma.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 10","pages":"e70535"},"PeriodicalIF":2.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145232531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Protective Effects of Dose-Dependent Umbelliferone Application on CLP-Induced Acute Lung Injury (ALI) Model. 剂量依赖性伞形酮对clp致急性肺损伤模型的保护作用。

IF 2.8 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-10-01 DOI: 10.1002/jbt.70549

Yusuf Umut Bati, Mert Sezer, Alican Yilmaz, Lale Baser, Ali Guraslan, Pinar Bayram, Murat Karamese

{"title":"The Protective Effects of Dose-Dependent Umbelliferone Application on CLP-Induced Acute Lung Injury (ALI) Model.","authors":"Yusuf Umut Bati, Mert Sezer, Alican Yilmaz, Lale Baser, Ali Guraslan, Pinar Bayram, Murat Karamese","doi":"10.1002/jbt.70549","DOIUrl":"https://doi.org/10.1002/jbt.70549","url":null,"abstract":"This study aimed to evaluate the beneficial effects of umbelliferone (UMB) (25, 50, and 100 mg/kg) in a cecal ligation and puncture (CLP)-induced rat model of sepsis, focusing on inflammation and oxidative stress mechanisms. Thirty-six Wistar albino rats were randomly assigned to six groups: Control, Sham, Sepsis, and Sepsis treated with three different doses of umbelliferone. Inflammatory cytokines were measured by ELISA, oxidative stress markers by tissue biochemistry, while protein expression and immune cell density were assessed using Western blotting and immunohistochemistry. Sepsis markedly increased pro-inflammatory cytokines, oxidative stress parameters, and NF-κB/CD68 immunopositivity, while reducing antioxidant defenses. UMB administration dose-dependently reversed these alterations, reducing pro-inflammatory cytokines, enhancing anti-inflammatory cytokines, restoring antioxidant balance, and significantly decreasing Nrf2 expression. Umbelliferone confers protection against sepsis-induced acute lung injury through multiple mechanisms, including suppression of NF-κB signaling, modulation of cytokine balance, and activation of the Nrf2/Keap1/HO-1 pathway. These findings highlight its potential as a natural therapeutic candidate for sepsis-related organ injury.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 10","pages":"e70549"},"PeriodicalIF":2.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145232683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bisphenol A Treatment Impairs Synaptic Function in Human Cholinergic Neurons. 双酚A处理损害人胆碱能神经元的突触功能。

IF 2.8 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-10-01 DOI: 10.1002/jbt.70558

Anna Maria Carrese, Rossella Vitale, Manuela Turco, Francesco Aniello, Natasha Petecca, Luisa Cigliano, Emilia Vitale, Aldo Donizetti

{"title":"Bisphenol A Treatment Impairs Synaptic Function in Human Cholinergic Neurons.","authors":"Anna Maria Carrese, Rossella Vitale, Manuela Turco, Francesco Aniello, Natasha Petecca, Luisa Cigliano, Emilia Vitale, Aldo Donizetti","doi":"10.1002/jbt.70558","DOIUrl":"10.1002/jbt.70558","url":null,"abstract":"Bisphenol A (BPA) is a synthetic compound widely used in the production of polycarbonate plastics and epoxy resins, commonly found in food and beverage packaging. Exposure to BPA can occur through several routes, although the primary source is dietary. Due to its ability to cross the placental and blood-brain barriers, the adverse effects of BPA can have implications across the entire human lifespan, from embryonic development to adulthood. While its harmful effect on brain development and function has been extensively documented in animal models, its impact on human mature neurons, particularly concerning synaptic activity, remains poorly understood. In this study, we investigated the effects of BPA on a human cholinergic neuron model. BPA exposure was found to reduce neuritic complexity and alter the expression of key synaptic proteins. These structural changes were accompanied by dysregulation of activity-regulated gene expression, indicating impaired synaptic function. Our findings suggest that even a short-term exposure to BPA can disrupt synaptic integrity, with potential consequences for normal brain functions.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 10","pages":"e70558"},"PeriodicalIF":2.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12499904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Taxifolin Attenuates Cisplatin-Induced Acute Kidney Injury by Promoting Fatty Acid Oxidation. 紫杉醇通过促进脂肪酸氧化减轻顺铂诱导的急性肾损伤。

IF 2.8 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-10-01 DOI: 10.1002/jbt.70559

Xuejin Jin, Lingkun Wang, Miao Yuan, Huanyan Tao, Huiyan Zha, Zheng Xu, Guang Liang, Xiangwei Xu, Qian Zhou

{"title":"Taxifolin Attenuates Cisplatin-Induced Acute Kidney Injury by Promoting Fatty Acid Oxidation.","authors":"Xuejin Jin, Lingkun Wang, Miao Yuan, Huanyan Tao, Huiyan Zha, Zheng Xu, Guang Liang, Xiangwei Xu, Qian Zhou","doi":"10.1002/jbt.70559","DOIUrl":"https://doi.org/10.1002/jbt.70559","url":null,"abstract":"Cisplatin-induced nephrotoxicity frequently manifests as acute kidney injury (AKI), creating a major limitation for its widespread clinical application. Taxifolin, a phytochemical flavonoid, possesses potent free radical-scavenging activity and the ability to modulate inflammatory responses. Our study focused on assessing the renoprotective capacity of taxifolin in the context of cisplatin-induced kidney damage. Cell culture studies showed that taxifolin reduced damage to human tubular epithelial cells caused by cisplatin. Furthermore, we evaluated the protective effect of taxifolin on mice with cisplatin-induced nephrotoxicity. Oral administration of taxifolin effectively mitigated both functional impairment and structural injury in renal tubules, both when administered 2 days before and 2 h following cisplatin injection. Transcriptomic analysis of renal tissues via RNA-seq revealed that taxifolin's nephroprotective effects against cisplatin toxicity may involve Fabp4-regulated lipid metabolism pathways. In both cisplatin-induced AKI mouse models and renal tubular cells, taxifolin enhanced lipid metabolism, restored cellular energy (ATP) production, and upregulated PGC-1α/PPARα expression by reversing Fabp4-impaired suppression of fatty acid beta-oxidation. Collectively, these results indicate that taxifolin exerts nephroprotective effects against cisplatin-induced AKI by modulating Fabp4-dependent fatty acid oxidation pathways, positioning it as a potential therapeutic candidate for cisplatin-associated nephrotoxicity.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 10","pages":"e70559"},"PeriodicalIF":2.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Response to "Letter to Editor". 对“致编辑信”的回应。

IF 2.8 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-10-01 DOI: 10.1002/jbt.70554

Ayse Nur Coskun-Demirkalp, Akın Tekcan, Mustafa Cakir, Hamiyet Donmez-Altuntas

引用次数: 0