Human & experimental toxicology最新文献_第8页

Effects of polycyclic aromatic hydrocarbon exposure on mitochondrial DNA copy number. 多环芳烃暴露对线粒体DNA拷贝数的影响。

Human & experimental toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231216968

Sun-Haeng Choi, Bolormaa Ochirpurev, Hwa Yeong Jo, Jong-Uk Won, Akira Toriba, Heon Kim

{"title":"Effects of polycyclic aromatic hydrocarbon exposure on mitochondrial DNA copy number.","authors":"Sun-Haeng Choi, Bolormaa Ochirpurev, Hwa Yeong Jo, Jong-Uk Won, Akira Toriba, Heon Kim","doi":"10.1177/09603271231216968","DOIUrl":"10.1177/09603271231216968","url":null,"abstract":"Airborne polycyclic aromatic hydrocarbon (PAH) exposure can adversely affect human health by generating reactive oxygen species (ROS) and increasing oxidative stress, which causes changes in mitochondrial DNA copy number (mtDNAcn), a key indicator of mitochondrial damage and dysfunction. This study aimed to determine the effects of atmospheric benzo[a]pyrene (BaP) and 1-nitropyrene (1-NP) exposure on mtDNAcn in humans. One hundred and eight adults living in Cheongju, South Korea, were included in this study. Atmospheric BaP and 1-NP concentrations and urinary 6-hydroxy-1-nitropyrene (6-OHNP), N-acetyl-1-aminopyrene (1-NAAP), and 1-hydroxypyrene concentrations were measured. Blood samples were also collected to assess mtDNAcn. The mean mtDNAcn was 9.74 (SD 4.46). mtDNAcn decreased significantly with age but was not significantly associated with sex, sampling season, or smoking habit. While there was a borderline significant increase in mtDNAcn with increasing ambient total PAH levels, ambient PAH or urinary 1-hydroxypyrene concentrations showed no significant association with mtDNAcn. However, urinary 6-OHNP or 1-NAAP concentrations, 1-NP metabolites, were significantly associated with mtDNAcn. These results suggest that the metabolism of absorbed NPs generates excess ROS, which damages mitochondrial DNA, resulting in increased mtDNAcn.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"42 ","pages":"9603271231216968"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138292639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction Notice: "Sulforaphane triggers iron overload-mediated ferroptosis in gastric carcinoma cells by activating the PI3K/IRP2/DMT1 pathway". 撤回通知：“硫福拉芬通过激活PI3K/IRP2/DMT1途径触发胃癌细胞中铁过载介导的脱铁性贫血”。

Human & experimental toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231212067

引用次数: 0

Increased FGFR3 is involved in T-2 toxin-induced lesions of hypertrophic cartilage associated with endemic osteoarthritis. FGFR3的增加与T-2毒素诱导的与地方性骨关节炎相关的肥大软骨病变有关。

Human & experimental toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231219480

Ying Zhang, Qian Fang, Yinan Liu, Dan Zhang, Ying He, Fei Liu, Kun Sun, Jinghong Chen

{"title":"Increased FGFR3 is involved in T-2 toxin-induced lesions of hypertrophic cartilage associated with endemic osteoarthritis.","authors":"Ying Zhang, Qian Fang, Yinan Liu, Dan Zhang, Ying He, Fei Liu, Kun Sun, Jinghong Chen","doi":"10.1177/09603271231219480","DOIUrl":"10.1177/09603271231219480","url":null,"abstract":"This study evaluated the effect of fibroblast growth factor receptor 3 (FGFR3) on damaged hypertrophic chondrocytes of Kashin-Beck disease (KBD). Immunohistochemical staining was used to evaluate FGFR3 expression in growth plates from KBD rat models and engineered cartilage. In vitro study, hypertrophic chondrocytes were pretreated by FGFR3 binding inhibitor (BGJ398) for 24 h before incubation at different T-2 toxin concentrations. Differentiation -related genes (Runx2, Sox9, and Col Ⅹ) and ECM degradation -related genes (MMP-13, Col Ⅱ) in the hypertrophic chondrocytes were analyzed using RT-PCR, and the corresponding proteins were analyzed using western blotting. Hypertrophic chondrocytes death was detected by the Annexin V/PI double staining assay. The integrated optical density of FGFR3 staining was increased in knee cartilage of rats and engineered cartilage treated with T-2 toxin. Both protein and mRNA levels of Runx2, Sox9, Col Ⅱ, and Col Ⅹ were decreased in a dose-dependent manner when exposed to the T-2 toxin and significantly upregulated by 1 μM BGJ398. The expression of MMP-1, MMP-9, and MMP-13 increased in a dose-dependent manner when exposed to T-2 toxin and significantly reduced by 1 μM BGJ398. 1 μM BGJ398 could prevent early apoptosis and necrosis induced by the T-2 toxin. Inhibiting the FGFR3 signal could alleviate extracellular matrix degradation, abnormal chondrocytes differentiation, and excessive cell death in T-2 toxin-induced hypertrophic chondrocytes.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"42 ","pages":"9603271231219480"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138500612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Environmental contaminants, endocrine disruption, and transgender: Can "born that way" in some cases be toxicologically real? 环境污染物、内分泌紊乱和变性：在某些情况下，“那样出生”在毒理学上是真实的吗？

Human & experimental toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231203382

Steven David Holladay

引用次数: 0

Ginsenoside Rk1 prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease via activating silence information regulator 3-mediated Nrf2/HO-1 signaling pathway. 人参皂苷 Rk1 通过激活沉默信息调节因子 3 介导的 Nrf2/HO-1 信号通路，预防 1-甲基-4-苯基-1,2,3,6-四氢吡啶诱发的帕金森病。

Human & experimental toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231220610

Yi Ren, Dan Ye, Yiping Ding, Ning Wei

{"title":"Ginsenoside Rk1 prevents 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease via activating silence information regulator 3-mediated Nrf2/HO-1 signaling pathway.","authors":"Yi Ren, Dan Ye, Yiping Ding, Ning Wei","doi":"10.1177/09603271231220610","DOIUrl":"10.1177/09603271231220610","url":null,"abstract":"Objectives: Ginsenoside Rk1, a novel ginsenoside isolated from red ginseng, has anti-inflammatory and anti-tumor activities. This study was designed to elucidate the role of RK1 in an in vitro 1-methyl-4-phenylpyridinium (MPP+) cell model and an in vivo 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) of Parkinson's disease (PD).Methods: The grasping test, pole-climbing test, and rotarod test were performed to measure the effects of RK1 on MPTP-induced motor disorders. The expression of tyrosine hydroxylase (TH) and IBA-1 were evaluated by western blotting. CCK-8 and flow cytometry assays were utilized to assess cell viability and apoptosis. Reactive oxygen species (ROS), Lactate dehydrogenase (LDH), and superoxide dismutase (SOD) were detected to analyze the effects of RK1 on oxidative stress. The levels of inflammatory cytokines were evaluated by enzyme-linked immunosorbent assay (ELISA).Results: The results showed that RK1 allayed motor deficit elicited by MPTP in a mouse model. RK1 administration augmented tyrosine hydroxylase (TH) expression in the brain striatum and substantia nigra (SN) of MPTP-treated mice. Moreover, RK1 pretreatment promoted viability and suppressed apoptosis in MPP+-induced PC-12 cells. Further, RK1 also attenuated MPP+-stimulated oxidative stress and inflammatory response in PC-12 cells. Besides, RK1 augmented the level of SIRT3, and SIRT3 deletion counteracted RK1-induced repression on MPP+-elicited apoptosis, oxidative stress, and inflammatory response in PC-12 cells via modulating the Nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway.Conclusions: RK1 might exert neuroprotective effects against MPP+/MPTP-induced neurotoxicity via activating SIRT3-mediated Nrf2/HO-1 signaling. RK1 might be a promising candidate against PD.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"42 ","pages":"9603271231220610"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138814276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The effects of esketamine on the intestinal microenvironment and intestinal microbiota in mice. 艾司卡胺对小鼠肠道微环境和肠道微生物群的影响

Human & experimental toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231211894

Ying Zhang, Wenhao Ma, Hao Lin, Xuefeng Gu, Hong Xie

{"title":"The effects of esketamine on the intestinal microenvironment and intestinal microbiota in mice.","authors":"Ying Zhang, Wenhao Ma, Hao Lin, Xuefeng Gu, Hong Xie","doi":"10.1177/09603271231211894","DOIUrl":"10.1177/09603271231211894","url":null,"abstract":"Objective: This study aimed to investigate the impact of esketamine on the intestinal flora and microenvironment in mice using mRNA transcriptome sequencing and 16S rRNA sequencing.Methods: Ten female mice were randomly assigned to two groups. One group received daily intramuscular injections of sterile water, while the other group received esketamine. After 24 days, the mice were sacrificed, and their intestinal tissues and contents were collected for 16S rRNA sequencing and mRNA transcriptome sequencing. The intergroup differences in the mouse intestinal flora were analyzed. Differentially expressed genes were utilized to construct ceRNA networks and transcription factor regulatory networks to assess the effects of esketamine on the intestinal flora and intestinal tissue genes.Results: Esketamine significantly altered the abundance of intestinal microbiota, including Adlercreutzia equolifaciens and Akkermansia muciniphila. Differential expression analysis revealed 301 significantly upregulated genes and 106 significantly downregulated genes. The ceRNA regulatory network consisted of 6 lncRNAs, 44 miRNAs, and 113 mRNAs, while the regulatory factor network included 13 transcription factors and 53 target genes. Gene Ontology enrichment analysis indicated that the differentially expressed genes were primarily associated with immunity, including B-cell activation and humoral immune response mediation. The biological processes in the ceRNA regulatory network primarily involved transport, such as organic anion transport and monocarboxylic acid transport. The functional annotation of target genes in the TF network was mainly related to epithelial cells, including epithelial cell proliferation and regulation.Conclusion: Esketamine induces changes in gut microbiota and the intestinal microenvironment, impacting the immune environment and transport modes.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"42 ","pages":"9603271231211894"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138814396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to "5-Fluorouracil-induced toxicity in both male and female reproductive systems: A narrative review". 5-氟尿嘧啶对男性和女性生殖系统的毒性：叙述性综述 "的更正。

Human & experimental toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231224521

引用次数: 0

Rhamnazin ameliorates 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin-evoked testicular toxicity by restoring biochemical, spermatogenic and histological profile in male albino rats. 鼠李嗪通过恢复雄性白化大鼠的生化、生精和组织学特征，改善2，3，7，8-四氯二苯并对二恶英引起的睾丸毒性。

Human & experimental toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231205859

Muhammad Umar Ijaz, Shama Mustafa, Qurat Ul Ain, Ali Hamza, Shafaqat Ali

{"title":"Rhamnazin ameliorates 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin-evoked testicular toxicity by restoring biochemical, spermatogenic and histological profile in male albino rats.","authors":"Muhammad Umar Ijaz, Shama Mustafa, Qurat Ul Ain, Ali Hamza, Shafaqat Ali","doi":"10.1177/09603271231205859","DOIUrl":"10.1177/09603271231205859","url":null,"abstract":"2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD) is a potential environmental toxin that has the ability to affect male reproductive tract. Rhamnazin is a naturally present flavone that displays multiple medicinal properties. Therefore, the current study was designed to determine the mitigative role of rhamnazin against TCDD induced reproductive damage. 48 adult male albino rats were randomly separated into four groups: control, TCDD (10 µgkg-1), TCDD + rhamnazin (10 µgkg-1 + 5 mgkg-1 respectively) and rhamnazin (5 mgkg-1). The trial was conducted for 56 days. TCDD intoxication notably affected superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GSR) and catalase (CAT) activities, besides reactive oxygen species (ROS) and malondialdehyde (MDA) concentrations were augmented. TCDD administration also lowered sperm motility, viability, sperm number, while it augmented the sperm morphological (tail, neck/midpiece and head) anomalies. Moreover, it decreased the levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and plasma testosterone. Moreover, TCDD reduced steroidogenic enzymes i.e., 17-beta hydroxysteroid dehydrogenase (17β-HSD), steroidogenic acute regulatory protein (StAR) and 3-beta hydroxysteroid dehydrogenase (3β-HSD) as well as B-cell lymphoma 2 (Bcl-2) expressions, but increased the expressions of Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase-3). Furthermore, TCDD exposure also induced histopathological anomalies in testicular tissues. However, the supplementation of rhamnazin recovered all the mentioned damages in the testicles. The outcomes revealed that rhamnazin can ameliorate TCDD induced reproductive toxicity due to its anti-oxidant, anti-apoptotic and androgenic nature.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"42 ","pages":"9603271231205859"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41147346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Punicalagin is cytotoxic to human colon cancer cells by modulating cell proliferation, apoptosis, and invasion. 普尼卡金通过调节细胞增殖、凋亡和侵袭，对人结肠癌细胞具有细胞毒性。

Human & experimental toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231213979

Ding-Ping Sun, Hsuan-Yi Huang, Chia-Lin Chou, Li-Chin Cheng, Wen-Ching Wang, Yu-Feng Tian, Chia-Lang Fang, Kai-Yuan Lin

{"title":"Punicalagin is cytotoxic to human colon cancer cells by modulating cell proliferation, apoptosis, and invasion.","authors":"Ding-Ping Sun, Hsuan-Yi Huang, Chia-Lin Chou, Li-Chin Cheng, Wen-Ching Wang, Yu-Feng Tian, Chia-Lang Fang, Kai-Yuan Lin","doi":"10.1177/09603271231213979","DOIUrl":"https://doi.org/10.1177/09603271231213979","url":null,"abstract":"Purpose: The purpose of this study was to explore the anticancer effect of punicalagin, an abundant bioactive tannin compound isolated from Punica granatum L., on three colon cancer cell lines, namely, HCT 116, HT-29, and LoVo.Research Design: Normal and colon cancer cells were treated with different concentrations of punicalagin for different periods. Data Collection and Analysis: Cell viability was measured with a CCK-8 assay. Programmed cell death and invasion were analyzed using an annexin V and cell death kit and a cell invasion analysis kit. The expression of active caspase-3, MMP-2, MMP-9, Snail, and Slug were measured by Western blot.Results: The results of the cell viability analysis showed that punicalagin was cytotoxic to colon cancer cells, but it was not to normal cells in a dose- and time-dependent manner. Additionally, punicalagin induced apoptosis in colon cancer cells (shown by the cumulative percentage of colorectal cancer cells in early and late apoptosis). It was found that caspase-3 activity increased following punicalagin treatment. Western blot results also showed that punicalagin increased the expression of activated caspase-3. In contrast, punicalagin inhibited the invasion of colon cancer cells. Further, treatment of colon cancer cells with punicalagin suppressed the expression of MMP-2, MMP-9, Snail, and Slug. Conclusions: These results showed that the activation of caspase-3 and the inhibition of MMP-2, MMP-9, Snail and Slug were involved in the effects of punicalagin on colon cancer cells.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"42 ","pages":"9603271231213979"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71490396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nrf2 attenuates methamphetamine-induced myocardial injury by regulating oxidative stress and apoptosis in mice. Nrf2通过调节氧化应激和细胞凋亡减轻甲基苯丙胺诱导的小鼠心肌损伤。

Human & experimental toxicology Pub Date : 2023-01-01 DOI: 10.1177/09603271231219488

Hao Yu, Yanxia Peng, Wenjuan Dong, Baoyu Shen, Genmeng Yang, Qianyun Nie, Yan Tian, Lixiang Qin, Chunhui Song, Bingzheng Chen, Yongna Zhao, Lihua Li, Shijun Hong

{"title":"Nrf2 attenuates methamphetamine-induced myocardial injury by regulating oxidative stress and apoptosis in mice.","authors":"Hao Yu, Yanxia Peng, Wenjuan Dong, Baoyu Shen, Genmeng Yang, Qianyun Nie, Yan Tian, Lixiang Qin, Chunhui Song, Bingzheng Chen, Yongna Zhao, Lihua Li, Shijun Hong","doi":"10.1177/09603271231219488","DOIUrl":"10.1177/09603271231219488","url":null,"abstract":"Objectives: Methamphetamine (MA) abuse is a serious social problem worldwide. Cardiovascular complications were the second leading cause of death among MA abusers. We aimed to clarify the effects of MA on myocardial injury, oxidative stress, and apoptosis in myocardial cells and to explore the potential mechanism of nuclear factor-erythroid factor 2-related factor 2 (Nrf2) in MA-induced oxidative stress and apoptosis.Methods: An acute cardiac toxicity model of MA was established by intraperitoneal injection of MA (2 mg/kg) for 5 days. Nrf2 activation (by sulforaphane (SFN) 1 h before MA injection) and Nrf2 gene knockout were performed to explore the regulatory effects of Nrf2 on cardiac toxicity.Results: The protein expressions of Nrf2 (p < .001) and heme oxygenase-1 (HO-1) were increased (p < .01), suggesting that MA activated the Nrf2/HO-1 pathway. In the MA group, cardiac injury score (p < .001) and cardiac troponin I (cTnI) protein expression increased (p < .01). Malondialdehyde (MDA) content increased (p < .001), superoxide dismutase (SOD) activity decreased (p < .05). Protein expressions of Caspase-3 (p < .001) and Bax (p < .001) increased, and Bcl-2 decreased (p < .001) as well. These changes were reversed by activation of Nrf2 but became more pronounced after Nrf2 knockout, suggested that the activation and knockout of Nrf2 attenuated and aggravated MA-induced myocardial injury, oxidative stress and apoptosis in myocardial cells, respectively.Conclusions: MA administration induced myocardial injury, oxidative stress, and apoptosis in mice. Nrf2 attenuated MA-induced myocardial injury by regulating oxidative stress and apoptosis, thus playing a protective role.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"42 ","pages":"9603271231219488"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138465186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0