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Source: Toxicology Letters

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Total 86 results found since Jan 2013.

Involvement of aryl hydrocarbon receptor in the cytotoxicity of corannulene and its derivatives.
Abstract Despite numerous studies on the toxicities of planar polycyclic aromatic hydrocarbons (PAHs), very little is known about the toxicological profiles of non-planar PAHs. In the present study, the cytotoxicity of corannulene (COR), a typical bowl-shaped PAH with a myriad of applications in the area of material chemistry, and benzo[a]pyrene (BaP), a typical planar PAH with similar molecular weight, were systematically compared in various cell lines. Compared with BaP, exposure to COR resulted in less cytotoxic responses in both human (HepG2) and murine (Hepa1-6) hepatoma cells, which was characterized with a ...
Source: Toxicology Letters - December 8, 2019 Category: Toxicology Authors: Li G, Ma R, Xing Y, Wei J, Bi Y, Li C, Xiong H, Baldridge KK, Huang J, Siegel JS, Zhang Y Tags: Toxicol Lett Source Type: research

NIX compensates lost role of Parkin in Cd-induced mitophagy in HeLa cells through phosphorylation.
Abstract Our previous study demonstrated that cadmium (Cd) is an effective inducer of mitophagy, which is mainly mediated by PINK1/Parkin pathway. However, the role of other mitophagy pathways in Cd-induced mitophagy remains elusive. The present study employed HeLa cells, lacking fully functional Parkin, as a cell model to study Parkin-independent mitophagy pathway induced by Cd. Our results showed that BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like (Bnip3L/NIX), an outer mitochondrial membrane mitophagy receptor, could provide an alternate pathway for Cd-induced mitophagy in HeLa cells. Specifica...
Source: Toxicology Letters - March 2, 2020 Category: Toxicology Authors: Naeem S, Qi Y, Tian Y, Zhang Y Tags: Toxicol Lett Source Type: research

Decrease in ADAR1 expression by exposure to cigarette smoke enhances susceptibility to oxidative stress.
In conclusion, we show that ADAR1 expression is decreased by cigarette smoking and is a factor that contributes to the enhanced intracellular oxidative stress caused by cigarette smoking. PMID: 32439581 [PubMed - as supplied by publisher]
Source: Toxicology Letters - May 17, 2020 Category: Toxicology Authors: Takizawa M, Nakano M, Fukami T, Nakajima M Tags: Toxicol Lett Source Type: research

High mobility group box-1 protects against Aflatoxin G1-induced pulmonary epithelial cell damage in the lung inflammatory environment.
Abstract Aflatoxin G1 (AFG1) is a member of the carcinogenic aflatoxin family. Our previous studies indicated that oral administration of AFG1 caused tumor necrosis factor (TNF)-〈-dependent inflammation that enhanced oxidative DNA damage in alveolar epithelial cells, which may be related to AFG1-induced lung carcinogenesis. High mobility group box-1 (HMGB1) is a nuclear DNA-binding protein; the intracellular and extracellular roles of HMGB1 have been shown to contribute to DNA repair and sterile inflammation. The role of HMGB1 in DNA damage in an aflatoxin-induced lung inflammatory environment was investigated i...
Source: Toxicology Letters - May 20, 2020 Category: Toxicology Authors: Kang L, Guo N, Liu X, Wang X, Guo W, Xie SM, Liu C, Lv P, Xing L, Zhang X, Shen H Tags: Toxicol Lett Source Type: research

Cr (VI) induced mitophagy via the interaction of HMGA2 and PARK2.
Abstract Chromium (Cr) (VI) is a proven toxin, mutagen and carcinogen. Here, the role of high mobility group A2 (HMGA2) mediating Cr (VI)-induced mitophagy was investigated. Cr (VI)-treatment caused the formation of double membrane autophagic vesicles (AVs) engulfing mitochondria and increased the expression of PINK1, PARK2, LC3 as well as HMGA2 particularly in mitochondria in A549 cells. Silencing of HMGA2 by siRNA decreased expression of PINK1, PARK2 and LC3 II especially in mitochondria, while over-expression of HMGA2 increased the expression of them in A549 cells. It indicated that HMGA2 played a critical role...
Source: Toxicology Letters - August 27, 2020 Category: Toxicology Authors: Gao Z, Mei J, Yan X, Jiang L, Geng C, Li Q, Shi X, Liu Y, Cao J Tags: Toxicol Lett Source Type: research

TNF α enhances trovafloxacin-induced in vitro hepatotoxicity by inhibiting protective autophagy.
TNFα enhances trovafloxacin-induced in vitro hepatotoxicity by inhibiting protective autophagy. Toxicol Lett. 2021 Feb 17;: Authors: Ahn JH, Jegal H, Choi MS, Kim S, Park SM, Ahn J, Han HY, Cho HS, Yoon S, Oh JH Abstract Trovafloxacin (TVX) is associated with idiosyncratic drug-induced liver injury (iDILI) and inflammation-mediated hepatotoxicity. However, the inflammatory stress-regulated mechanisms in iDILI remain unclear. Herein, we elucidated the novel role of tumor-necrosis factor alpha (TNFα), an inflammatory stress factor, in TVX-induced in vitro hepatotoxicity and synergistic toxicity. TVX s...
Source: Toxicology Letters - February 17, 2021 Category: Toxicology Authors: Ahn JH, Jegal H, Choi MS, Kim S, Park SM, Ahn J, Han HY, Cho HS, Yoon S, Oh JH Tags: Toxicol Lett Source Type: research

TNF α enhances trovafloxacin-induced in vitro hepatotoxicity by inhibiting protective autophagy
Toxicol Lett. 2021 Feb 17:S0378-4274(21)00049-7. doi: 10.1016/j.toxlet.2021.02.009. Online ahead of print.ABSTRACTTrovafloxacin (TVX) is associated with idiosyncratic drug-induced liver injury (iDILI) and inflammation-mediated hepatotoxicity. However, the inflammatory stress-regulated mechanisms in iDILI remain unclear. Herein, we elucidated the novel role of tumor-necrosis factor alpha (TNFα), an inflammatory stress factor, in TVX-induced in vitro hepatotoxicity and synergistic toxicity. TVX specifically induced synergistic toxicity in HepG2 cells with TNFα, which inhibits autophagy. TVX-treated HepG2 cells induced prot...
Source: Toxicology Letters - February 20, 2021 Category: Toxicology Authors: Jun-Ho Ahn Hyun Jegal Mi-Sun Choi Soojin Kim Se-Myo Park Jaehwan Ahn Hyoung-Yun Han Hyun-Soo Cho Seokjoo Yoon Jung-Hwa Oh Source Type: research

PPAR γ mediates the anti-pulmonary fibrosis effect of icaritin
CONCLUSIONS: Icaritin has therapeutic potential against pulmonary fibrosis via the inhibition of myofibroblast differentiation, which may be mediated by PPARγ.PMID:34153405 | DOI:10.1016/j.toxlet.2021.06.014
Source: Toxicology Letters - June 21, 2021 Category: Toxicology Authors: Qingzhong Hua Xiaoting Huang Weixi Xie Feiyan Zhao Haipeng Cheng Ziqiang Luo Jianzhong Han Zun Wang Qian Zeng Miao Lin Tingting Zhou Jialu Zhang Can Gu Wei Liu Siyuan Tang Source Type: research

Methamphetamine mediates apoptosis of vascular smooth muscle cells via the Chop-related endoplasmic reticulum stress pathway
We examined the expression of the apoptosis-related proteins Caspase 3 and PARP after METH treatment in vivo and in vitro and detected the expression of endoplasmic reticulum stress-related proteins. After treatment with the endoplasmic reticulum stress inhibitor 4-PBA, changes in the above indicators were examined. C/EBP homologous protein (Chop) expression was also detected, and the relationship between endoplasmic reticulum stress and apoptosis was further determined by siRNA silencing of Chop. The results indicated that METH can induce apoptosis of vascular smooth muscle cells (VSMCs) and upregulate the expression of C...
Source: Toxicology Letters - July 2, 2021 Category: Toxicology Authors: Xiaohui Tan Dunpeng Cai Na Chen Sihao Du Dongfang Qiao Xia Yue Tao Wang Jia Li Weibing Xie Huijun Wang Source Type: research