Toxicological Research最新文献_第4页

A convenient spectrophotometric test for screening skin-sensitizing chemicals using reactivity with glutathione in chemico 利用与谷胱甘肽在化学反应中的反应性筛选皮肤过敏化学物质的便捷分光光度检测法

IF 2.3 4区医学

Toxicological Research Pub Date : 2023-12-13 DOI: 10.1007/s43188-023-00218-9

D. H. Cha, G. Kim, Rahul U. Nepal, M. Nepal, Tae Cheon Jeong

引用次数: 0

Protective effect of cilostazol on vascular injury in rats with acute ischemic stroke complicated with chronic renal failure 西洛他唑对急性缺血性中风并发慢性肾功能衰竭大鼠血管损伤的保护作用

IF 2.3 4区医学

Toxicological Research Pub Date : 2023-12-13 DOI: 10.1007/s43188-023-00217-w

Ru Sun, Qun Gu, Xufeng Zhang, Ruiqi Zeng, Dan Chen, Jingjing Yao, Jingjing Min

引用次数: 0

Association between urinary arsenic concentration and genetic polymorphisms in Korean adults 韩国成年人尿砷浓度与基因多态性之间的关系

IF 2.3 4区医学

Toxicological Research Pub Date : 2023-11-23 DOI: 10.1007/s43188-023-00216-x

S. Lee, Sang-Yong Eom, Ji-Ae Lim, Byung-Sun Choi, Ho-Jang Kwon, Young-Seoub Hong, Yong-Dae Kim, Heon Kim, J. Park

引用次数: 0

Distribution of molybdenum in soft tissues and blood of rats after intratracheal instillation of molybdenum(IV) sulfide nano- and microparticles 经气管内注射硫化钼纳米和微粒后大鼠软组织和血液中钼的分布

4区医学

Toxicological Research Pub Date : 2023-11-14 DOI: 10.1007/s43188-023-00213-0

Renata Kuraś, Maciej Stępnik, Jarosław Grobelny, Emilia Tomaszewska, Magdalena Stanisławska, Katarzyna Domeradzka-Gajda, Wojciech Wąsowicz, Beata Janasik

{"title":"Distribution of molybdenum in soft tissues and blood of rats after intratracheal instillation of molybdenum(IV) sulfide nano- and microparticles","authors":"Renata Kuraś, Maciej Stępnik, Jarosław Grobelny, Emilia Tomaszewska, Magdalena Stanisławska, Katarzyna Domeradzka-Gajda, Wojciech Wąsowicz, Beata Janasik","doi":"10.1007/s43188-023-00213-0","DOIUrl":"https://doi.org/10.1007/s43188-023-00213-0","url":null,"abstract":"Abstract There is still little literature data on the toxicity and safety of the commonly used molybdenum (Mo) disulfide which is present in the working as well as living environments. Thus, an experiment was carried out involving rats, with single and repeated intratracheal exposure (in the latter case, 7 administrations at 2-week intervals with the analysis performed after 90 days) to lower (1.5 mg Mo kg −1 b.w.) and higher (5 mg Mo kg −1 b.w.) doses of molybdenum(IV) sulfide nanoparticles (MoS 2 -NPs) and microparticles (MoS 2 -MPs). The analysis of Mo concentrations in the tail and heart blood as well as in soft tissues (lung, liver, spleen, brain), after mineralization and bioimaging, was meant to facilitate an assessment of its accumulation and potential effects on the body following short- and long-term exposure. The multi-compartment model with an exponential curve of Mo concentration over time with different half-lives for the distribution and elimination phases of MoS 2 -MPs and MoS 2 -NPs was observed. After 24 h of exposure, a slight increase in Mo concentration in blood was observed. Next, Mo concentration indicated a decrease in blood concentration from 24 h to day 14 (the Mo concentration before the second administration), below the pre-exposure concentration. The next phase was linear, less abrupt and practically flat, but with an increasing trend towards the end of the experiment. Significantly higher Mo concentrations in MoS 2 -NPs and MoS 2 -MPs was found in the lungs of repeatedly exposed rats compared to those exposed to a single dose. The analysis of Mo content in the liver and the spleen tissue showed a slightly higher concentration for MoS 2 -NPs compared to MoS 2 -MPs. The results for the brain were below the calculated detection limit. Results were consistent with results obtained by bioimaging technique.","PeriodicalId":23181,"journal":{"name":"Toxicological Research","volume":"25 14","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134991641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Comparative study on estrogen receptor alpha dimerization and transcriptional activity of parabens 对羟基苯甲酸酯雌激素受体α二聚化及转录活性的比较研究

4区医学

Toxicological Research Pub Date : 2023-10-05 DOI: 10.1007/s43188-023-00212-1

Jong-Yeon Kim, Yooheon Park, Seok-Hee Lee, Eun‐Jung Park, Hae‐Jeung Lee

引用次数: 0

Molecular mechanism of empagliflozin cardioprotection in 5-fluorouracil (5-FU)-induced cardiotoxicity via modulation of SGLT2 and TNFα/TLR/NF-κB signaling pathway in rats 恩格列净通过调节SGLT2和TNFα/TLR/NF-κB信号通路对5-氟尿嘧啶(5-FU)诱导大鼠心脏毒性的保护作用的分子机制

4区医学

Toxicological Research Pub Date : 2023-10-03 DOI: 10.1007/s43188-023-00204-1

Marwa Monier Mahmoud Refaie, Sayed Shehata, Maram El-Hussieny, Michael Atef Fawzy, Nagwa Zenhom Mustafa Ahmed, Heba Marey, Asmaa Mohammed Hishmat, Turki Alkully, Eman Shaaban Mahmoud Abd El Rahman

{"title":"Molecular mechanism of empagliflozin cardioprotection in 5-fluorouracil (5-FU)-induced cardiotoxicity via modulation of SGLT2 and TNFα/TLR/NF-κB signaling pathway in rats","authors":"Marwa Monier Mahmoud Refaie, Sayed Shehata, Maram El-Hussieny, Michael Atef Fawzy, Nagwa Zenhom Mustafa Ahmed, Heba Marey, Asmaa Mohammed Hishmat, Turki Alkully, Eman Shaaban Mahmoud Abd El Rahman","doi":"10.1007/s43188-023-00204-1","DOIUrl":"https://doi.org/10.1007/s43188-023-00204-1","url":null,"abstract":"Abstract One of the commoly used chemotherapeutic agents is 5-Fluorouracil (5-FU). Unfortunately, the clinical administration of 5-FU is complicated with serious cardiotoxic effects and the safe use becomes an urgent task in cardio-oncology. Till now, there are no studies discussed the role of empagliflozin (EMP) against 5-FU cardiotoxicity. Thus, we investigated this effect and the involved mechanisms in 5-FU induced heart injury. Forty male rats of Wistar albino species were used and divided randomly into four groups. Group I is the control group, group II is EMP given group, group III is 5-FU cardiotoxic group and group IV is 5-FU plus EMP group. 5-FU (150 mg/kg) was administered as a single intraperitoneal (i.p.) dose on 1st day to induce cardiotoxicity with or without EMP (30 mg/kg/d) orally for 5 days. The dose of 5-FU is relevant to the human toxic dose. Our data showed that 5-FU given group caused cardiotoxicity with significant increase of serum cardiac enzymes, toll like receptors, enhancement of nuclear factor kappa B (NF-κB), interleukin1β (IL1β), IL6, myeloid-differentiation-factor 88 (MYD88), heart weight, malondialdehyde (MDA), tumor-necrosis-factor-alpha (TNFα), sodium glucose co-transporter 2 (SGLT2), P53 and caspase3 expression with clear histopathological features of cardiotoxicity. Moreover, there is a significant decrease in reduced glutathione (GSH) and total antioxidant capacity (TAC). Interestingly, co-administration of EMP could ameliorate 5-FU induced biochemical and histopathological changes. This effect may be due to modulation of SGLT2, decreasing inflammation, oxidative stress and apoptosis with downregulation of an essential inflammatory cascade that mediates 5-FU cardiotoxicity; TNFα/TLR/NF-κB.","PeriodicalId":23181,"journal":{"name":"Toxicological Research","volume":"201 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135738937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Comparative metabolism of fargesin in human, dog, monkey, mouse, and rat hepatocytes 胰酶在人、狗、猴、小鼠和大鼠肝细胞中的代谢比较

4区医学

Toxicological Research Pub Date : 2023-09-26 DOI: 10.1007/s43188-023-00211-2

Min Seo Lee, Eun Jeong Park, Yong-Yeon Cho, Joo Young Lee, Han Chang Kang, Hye Suk Lee

引用次数: 0

Neurobehavioral effects of the exposure to mercury vapor and methylmercury during postnatal period on mice 产后暴露于汞蒸气和甲基汞对小鼠神经行为的影响

4区医学

Toxicological Research Pub Date : 2023-09-21 DOI: 10.1007/s43188-023-00210-3

Jin-Yong Lee, Minoru Yoshida, Masahiko Satoh, Chiho Watanabe

引用次数: 0

YPEL3 expression induces cellular senescence via the Hippo signaling pathway in human breast cancer cells. 在人乳腺癌症细胞中，YPEL3的表达通过Hippo信号通路诱导细胞衰老。

IF 1.6 4区医学

Toxicological Research Pub Date : 2023-08-24 eCollection Date: 2023-10-01 DOI: 10.1007/s43188-023-00208-x

Yeonju Kwon, Hyein Lee, Hyemin Park, Boyoung Lee, Tae-Uk Kwon, Yeo-Jung Kwon, Young-Jin Chun

{"title":"YPEL3 expression induces cellular senescence via the Hippo signaling pathway in human breast cancer cells.","authors":"Yeonju Kwon, Hyein Lee, Hyemin Park, Boyoung Lee, Tae-Uk Kwon, Yeo-Jung Kwon, Young-Jin Chun","doi":"10.1007/s43188-023-00208-x","DOIUrl":"10.1007/s43188-023-00208-x","url":null,"abstract":"The Hippo pathway is a signaling pathway that controls organ size in animals by regulating cell proliferation and apoptosis. Yes-associated protein 1 (YAP1), an oncogene associated with the development and progression of breast cancer, is downregulated by the Hippo pathway and is associated with the development and progression of breast cancer. Yippee-like 3 (YPEL3) is a target gene of the tumor suppressor protein p53, and its activation has been shown to inhibit cell growth, induce cellular senescence, and suppress tumor cell metastasis. In this study, we found that YAP1 inhibits the expression of YPEL3 expression in breast cancer cells. Furthermore, a decrease in lamin B1, a marker protein of cellular senescence, coupled with the activation of senescence-associated β-galactosidase indicated that upregulating YPEL3 levels through YAP1 downregulation can induce cellular senescence. Additionally, elevated YPEL3 levels resulted in higher levels of oxygen consumption rate in mitochondria, thus promoting apoptosis. This suggests that YPEL3 plays a crucial role in regulating oxidative stress and cell apoptosis in breast cancer cells. Therefore, the interaction between YAP1 and YPEL3 represents a novel mechanism of cellular senescence mediated by the Hippo signaling pathway. Collectively, our findings suggest that the Hippo signaling pathway plays an important role in regulating cellular senescence, which could have implications for the development of new therapeutic strategies for diseases such as cancer.","PeriodicalId":23181,"journal":{"name":"Toxicological Research","volume":"39 4","pages":"711-719"},"PeriodicalIF":1.6,"publicationDate":"2023-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10541347/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41178390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Effects of toxicants on endoplasmic reticulum stress and hepatic cell fate determination. 毒物对内质网应激和肝细胞命运测定的影响。

IF 1.6 4区医学

Toxicological Research Pub Date : 2023-07-26 eCollection Date: 2023-10-01 DOI: 10.1007/s43188-023-00201-4

Jihoon Tak, Sang Geon Kim

{"title":"Effects of toxicants on endoplasmic reticulum stress and hepatic cell fate determination.","authors":"Jihoon Tak, Sang Geon Kim","doi":"10.1007/s43188-023-00201-4","DOIUrl":"10.1007/s43188-023-00201-4","url":null,"abstract":"Toxicant-induced injury is a significant global health issue. However, the mechanisms through which toxicants such as carbon tetrachloride, acetaminophen, dimethylformamide, cocaine, and morphine induce the death of multiple cell types and contribute to liver toxicity are highly complex. This phenomenon involves intricate signaling pathways in association with oxidative stress, inflammation, and activation of death receptors, which are closely linked to endoplasmic reticulum (ER) stress. ER stress initially triggers the unfolded protein response, which either promotes cell survival or causes cell death at later times, depending on the severity and duration of the stress. Thus, comprehending the molecular basis governing cell fate determination in the context of ER stress may provide key insights into the prevention and treatment of toxicant-induced injury. This review summarizes our current understanding of agents that trigger different forms of ER stress-mediated cell death, necroptosis, ferroptosis, pyroptosis, and apoptosis, and covers the underlying molecular basis of toxicant-induced ER stress, as well as potential target molecules.","PeriodicalId":23181,"journal":{"name":"Toxicological Research","volume":"39 4","pages":"533-547"},"PeriodicalIF":1.6,"publicationDate":"2023-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10541383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41150455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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