Products of Selenite/Thiols Interaction Have Reducing Properties, Cleave Plasmid DNA and Decrease Rat Blood Pressure and Tension of Rat Mesenteric Artery
In conclusion, we found that the thiol/selenite interaction products exhibited significant reducing properties which can be used in further studies of the treatment of pathological conditions caused by oxidative stress. The results of decreased rat blood pressure and the tension of mesenteric artery may be perspective in studies focused on cardiovascular disease and their prevention.PMID:38676879 | DOI:10.1007/s12011-024-04196-3 (Source: Biological Trace Element Research)
Source: Biological Trace Element Research - April 27, 2024 Category: Biology Authors: Marian Grman Peter Balis Andrea Berenyiova Helena Svajdlenkova Lenka Tomasova Sona Cacanyiova Zuzana Rostakova Iveta Waczulikova Miroslav Chovanec Enrique Dom ínguez-Álvarez Karol Ondrias Anton Misak Source Type: research

Products of Selenite/Thiols Interaction Have Reducing Properties, Cleave Plasmid DNA and Decrease Rat Blood Pressure and Tension of Rat Mesenteric Artery
In conclusion, we found that the thiol/selenite interaction products exhibited significant reducing properties which can be used in further studies of the treatment of pathological conditions caused by oxidative stress. The results of decreased rat blood pressure and the tension of mesenteric artery may be perspective in studies focused on cardiovascular disease and their prevention.PMID:38676879 | DOI:10.1007/s12011-024-04196-3 (Source: Biological Trace Element Research)
Source: Biological Trace Element Research - April 27, 2024 Category: Biology Authors: Marian Grman Peter Balis Andrea Berenyiova Helena Svajdlenkova Lenka Tomasova Sona Cacanyiova Zuzana Rostakova Iveta Waczulikova Miroslav Chovanec Enrique Dom ínguez-Álvarez Karol Ondrias Anton Misak Source Type: research

Poisoning by paracetamol
Paracetamol overdose is common. If left untreated, liver and/or renal failure can develop. Administration of the antidote, acetylcysteine, within 8 –10 hours of overdose minimizes or prevents liver damage. After overdose, the tests used to identify that patients are at risk of liver injury are well established but have limitations. Once liver injury has occurred, important prognostic factors are the presence of hepatic encephalopathy, the int ernational normalized ratio, acid–base status and renal function. (Source: Medicine)
Source: Medicine - April 27, 2024 Category: Internal Medicine Authors: James W Dear Tags: Poisonous substances Source Type: research

Exploration of beauvericin's toxic effects and mechanisms in human astrocytes and N-acetylcysteine's protective role
In conclusion, our findings suggest that BEA-induced cytotoxicity in GHA cells involves oxidative stress-associated apoptosis. Furthermore, NAC demonstrates potential as a protective agent against BEA-induced oxidative damage.PMID:38670497 | DOI:10.1016/j.toxicon.2024.107734 (Source: Toxicon)
Source: Toxicon - April 26, 2024 Category: Toxicology Authors: Wei-Zhe Liang Yuan-Yi Chia Huai-Jhih Sun Gwo-Ching Sun Source Type: research

Roles of AhR/CYP1s Signal Pathway Mediated ROS Production in Uremic Cardiomyopathy
CONCLUSION: This study provides evidence that the AhR/CYP1s pathway is activated in UCM rats, and this activation is correlated with the uremic toxin IS. In vitro studies indicate that IS can stimulate the AhR translocation in cardiomyocyte, triggering to the production of intracellular ROS via CYP1s. This process leads to prolonged oxidative stress stimulation and thus contributes to the progression of uremic toxin-mediated cardiomyopathy.PMID:38670245 | DOI:10.1016/j.toxlet.2024.04.005 (Source: Toxicology Letters)
Source: Toxicology Letters - April 26, 2024 Category: Toxicology Authors: Wei Lu Shi Cheng Jiarui Xu Zilong Xiao Yong Yu Qiwen Xie Yi Fang Ruizhen Chen Bo Shen Yeqing Xie Xiaoqiang Ding Source Type: research

Preparation and evaluation of inhalable S-allylmercapto-N-acetylcysteine and nintedanib co-loaded liposomes for pulmonary fibrosis
Eur J Pharm Sci. 2024 Apr 24:106779. doi: 10.1016/j.ejps.2024.106779. Online ahead of print.ABSTRACTOrally marketed products nintedanib (NDNB) and pirfenidone (PFD) for pulmonary fibrosis (PF) are administered in high doses and have been shown to have serious toxic and side effects. NDNB can cause the elevation of galectin-3, which activates the NF-κB signaling pathway and causes the inflammatory response. S-allylmercapto-N-acetylcysteine (ASSNAC) can alleviate the inflammation response by inhibiting the TLR-4/NF-κB signaling pathway. Therefore, we designed and prepared inhalable ASSNAC and NDNB co-loaded liposomes for t...
Source: European Journal of Pharmaceutical Sciences - April 26, 2024 Category: Drugs & Pharmacology Authors: Qinxiu Zhang Genju Li Guozhi Zhao Chongzheng Yan Huaiyou Lv Yaqing Fu Yuhan Li Zhongxi Zhao Source Type: research

Exploration of beauvericin's toxic effects and mechanisms in human astrocytes and N-acetylcysteine's protective role
In conclusion, our findings suggest that BEA-induced cytotoxicity in GHA cells involves oxidative stress-associated apoptosis. Furthermore, NAC demonstrates potential as a protective agent against BEA-induced oxidative damage.PMID:38670497 | DOI:10.1016/j.toxicon.2024.107734 (Source: Toxicon)
Source: Toxicon - April 26, 2024 Category: Toxicology Authors: Wei-Zhe Liang Yuan-Yi Chia Huai-Jhih Sun Gwo-Ching Sun Source Type: research

Roles of AhR/CYP1s Signal Pathway Mediated ROS Production in Uremic Cardiomyopathy
CONCLUSION: This study provides evidence that the AhR/CYP1s pathway is activated in UCM rats, and this activation is correlated with the uremic toxin IS. In vitro studies indicate that IS can stimulate the AhR translocation in cardiomyocyte, triggering to the production of intracellular ROS via CYP1s. This process leads to prolonged oxidative stress stimulation and thus contributes to the progression of uremic toxin-mediated cardiomyopathy.PMID:38670245 | DOI:10.1016/j.toxlet.2024.04.005 (Source: Toxicology Letters)
Source: Toxicology Letters - April 26, 2024 Category: Toxicology Authors: Wei Lu Shi Cheng Jiarui Xu Zilong Xiao Yong Yu Qiwen Xie Yi Fang Ruizhen Chen Bo Shen Yeqing Xie Xiaoqiang Ding Source Type: research

Preparation and evaluation of inhalable S-allylmercapto-N-acetylcysteine and nintedanib co-loaded liposomes for pulmonary fibrosis
Eur J Pharm Sci. 2024 Apr 24;197:106779. doi: 10.1016/j.ejps.2024.106779. Online ahead of print.ABSTRACTOrally marketed products nintedanib (NDNB) and pirfenidone (PFD) for pulmonary fibrosis (PF) are administered in high doses and have been shown to have serious toxic and side effects. NDNB can cause the elevation of galectin-3, which activates the NF-κB signaling pathway and causes the inflammatory response. S-allylmercapto-N-acetylcysteine (ASSNAC) can alleviate the inflammation response by inhibiting the TLR-4/NF-κB signaling pathway. Therefore, we designed and prepared inhalable ASSNAC and NDNB co-loaded liposomes f...
Source: European Journal of Pharmaceutical Sciences - April 26, 2024 Category: Drugs & Pharmacology Authors: Qinxiu Zhang Genju Li Guozhi Zhao Chongzheng Yan Huaiyou Lv Yaqing Fu Yuhan Li Zhongxi Zhao Source Type: research

Preparation and evaluation of inhalable S-allylmercapto-N-acetylcysteine and nintedanib co-loaded liposomes for pulmonary fibrosis
Eur J Pharm Sci. 2024 Apr 24;197:106779. doi: 10.1016/j.ejps.2024.106779. Online ahead of print.ABSTRACTOrally marketed products nintedanib (NDNB) and pirfenidone (PFD) for pulmonary fibrosis (PF) are administered in high doses and have been shown to have serious toxic and side effects. NDNB can cause the elevation of galectin-3, which activates the NF-κB signaling pathway and causes the inflammatory response. S-allylmercapto-N-acetylcysteine (ASSNAC) can alleviate the inflammation response by inhibiting the TLR-4/NF-κB signaling pathway. Therefore, we designed and prepared inhalable ASSNAC and NDNB co-loaded liposomes f...
Source: European Journal of Pharmaceutical Sciences - April 26, 2024 Category: Drugs & Pharmacology Authors: Qinxiu Zhang Genju Li Guozhi Zhao Chongzheng Yan Huaiyou Lv Yaqing Fu Yuhan Li Zhongxi Zhao Source Type: research

Preparation and evaluation of inhalable S-allylmercapto-N-acetylcysteine and nintedanib co-loaded liposomes for pulmonary fibrosis
Eur J Pharm Sci. 2024 Apr 24;197:106779. doi: 10.1016/j.ejps.2024.106779. Online ahead of print.ABSTRACTOrally marketed products nintedanib (NDNB) and pirfenidone (PFD) for pulmonary fibrosis (PF) are administered in high doses and have been shown to have serious toxic and side effects. NDNB can cause the elevation of galectin-3, which activates the NF-κB signaling pathway and causes the inflammatory response. S-allylmercapto-N-acetylcysteine (ASSNAC) can alleviate the inflammation response by inhibiting the TLR-4/NF-κB signaling pathway. Therefore, we designed and prepared inhalable ASSNAC and NDNB co-loaded liposomes f...
Source: European Journal of Pharmaceutical Sciences - April 26, 2024 Category: Drugs & Pharmacology Authors: Qinxiu Zhang Genju Li Guozhi Zhao Chongzheng Yan Huaiyou Lv Yaqing Fu Yuhan Li Zhongxi Zhao Source Type: research

Preparation and evaluation of inhalable S-allylmercapto-N-acetylcysteine and nintedanib co-loaded liposomes for pulmonary fibrosis
Eur J Pharm Sci. 2024 Apr 24;197:106779. doi: 10.1016/j.ejps.2024.106779. Online ahead of print.ABSTRACTOrally marketed products nintedanib (NDNB) and pirfenidone (PFD) for pulmonary fibrosis (PF) are administered in high doses and have been shown to have serious toxic and side effects. NDNB can cause the elevation of galectin-3, which activates the NF-κB signaling pathway and causes the inflammatory response. S-allylmercapto-N-acetylcysteine (ASSNAC) can alleviate the inflammation response by inhibiting the TLR-4/NF-κB signaling pathway. Therefore, we designed and prepared inhalable ASSNAC and NDNB co-loaded liposomes f...
Source: European Journal of Pharmaceutical Sciences - April 26, 2024 Category: Drugs & Pharmacology Authors: Qinxiu Zhang Genju Li Guozhi Zhao Chongzheng Yan Huaiyou Lv Yaqing Fu Yuhan Li Zhongxi Zhao Source Type: research

Honokiol Suppresses Cell Proliferation and Tumor Migration through ROS in Human Anaplastic Thyroid Cancer Cells
CONCLUSION: Taken together, we provided the potential mechanism for treating ATC cells with honokiol, which significantly suppresses tumor proliferation and inhibits tumor metastasis in vitro through reactive oxygen species (ROS) induction.PMID:38659261 | DOI:10.2174/0118715303295608240408082523 (Source: Endocrine, Metabolic and Immune Disorders Drug Targets)
Source: Endocrine, Metabolic and Immune Disorders Drug Targets - April 25, 2024 Category: Endocrinology Authors: Kai-Sheng Liao Ying-Ray Lee Wen-Ying Chao Yen-Ju Huang Hui-Chen Chung Shu-Hsin Chen Yi-Zhen Li Pei-Wen Zhao Hong-Yi Chang Source Type: research

Honokiol Suppresses Cell Proliferation and Tumor Migration through ROS in Human Anaplastic Thyroid Cancer Cells
CONCLUSION: Taken together, we provided the potential mechanism for treating ATC cells with honokiol, which significantly suppresses tumor proliferation and inhibits tumor metastasis in vitro through reactive oxygen species (ROS) induction.PMID:38659261 | DOI:10.2174/0118715303295608240408082523 (Source: Endocrine, Metabolic and Immune Disorders Drug Targets)
Source: Endocrine, Metabolic and Immune Disorders Drug Targets - April 25, 2024 Category: Drugs & Pharmacology Authors: Kai-Sheng Liao Ying-Ray Lee Wen-Ying Chao Yen-Ju Huang Hui-Chen Chung Shu-Hsin Chen Yi-Zhen Li Pei-Wen Zhao Hong-Yi Chang Source Type: research

Honokiol Suppresses Cell Proliferation and Tumor Migration through ROS in Human Anaplastic Thyroid Cancer Cells
CONCLUSION: Taken together, we provided the potential mechanism for treating ATC cells with honokiol, which significantly suppresses tumor proliferation and inhibits tumor metastasis in vitro through reactive oxygen species (ROS) induction.PMID:38659261 | DOI:10.2174/0118715303295608240408082523 (Source: Endocrine, Metabolic and Immune Disorders Drug Targets)
Source: Endocrine, Metabolic and Immune Disorders Drug Targets - April 25, 2024 Category: Endocrinology Authors: Kai-Sheng Liao Ying-Ray Lee Wen-Ying Chao Yen-Ju Huang Hui-Chen Chung Shu-Hsin Chen Yi-Zhen Li Pei-Wen Zhao Hong-Yi Chang Source Type: research