Microplastic Size-Dependent Toxicity, Oxidative Stress Induction, and p-JNK and p-p38 Activation in the Monogonont Rotifer (Brachionus koreanus)

2016 ◽  
Vol 50 (16) ◽  
pp. 8849-8857 ◽  
Author(s):  
Chang-Bum Jeong ◽  
Eun-Ji Won ◽  
Hye-Min Kang ◽  
Min-Chul Lee ◽  
Dae-Sik Hwang ◽  
...  
Gene ◽  
2012 ◽  
Vol 505 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Jae-Sung Rhee ◽  
Ryeo-Ok Kim ◽  
Bo-Mi Kim ◽  
Hans-Uwe Dahms ◽  
Jae-Seong Lee

2014 ◽  
Vol 280 (1) ◽  
pp. 97-106 ◽  
Author(s):  
Irene Riezzo ◽  
Emanuela Turillazzi ◽  
Stefania Bello ◽  
Santina Cantatore ◽  
Daniela Cerretani ◽  
...  

2016 ◽  
Vol 97 (3) ◽  
pp. 387-391 ◽  
Author(s):  
Eun-Ji Won ◽  
Jeonghoon Han ◽  
Atsushi Hagiwara ◽  
Shoji Oda ◽  
Hiroshi Mitani ◽  
...  

Author(s):  
Putri Anggreini ◽  
Chrismawan Ardianto ◽  
Mahardian Rahmadi ◽  
Junaidi Khotib

Abstract Background Oxidative stress plays a pivotal role in the pathophysiology and pathogenesis of mental diseases, such as depression or anxiety. Psychological stress induced by predatory stimulus is one of the models that explain how induced affective behavior is manifested as a depression-like state. Quercetin is a flavonoid that exhibits potential pharmacological activity on mental diseases. Thus, the present study was designed to investigate the effect of quercetin on innate fear and affective behavior induced by repeated predator stress exposure on mice. Materials and methods ICR mice were exposed to predatory stress for 3 days. Quercetin at a dose of 50 mg/kg was given intraperitoneally along with stress induction. The freezing behavior during the stress induction was analyzed. The anxiety-like and depressive-like behaviors and cognitive and motor functions were examined on the last day of induction. Results Predatory stress increased the affective behaviors (anxiety-like and depressive-like behaviors) and produced freezing behavior without alterations in the cognitive function and exploratory behavior. Treatment with quercetin 50 mg/kg attenuated the freezing, anxiety-like and depressive-like behaviors. Conclusions Repeated predator stress exposure causes both innate fear and depression-like state for the prey animals. Quercetin may have a protective effect against depression and alleviates the fear of traumatic events.


2020 ◽  
Vol 21 (2) ◽  
pp. 490 ◽  
Author(s):  
Anatoly Nikolaev ◽  
John B. Fiveash ◽  
Eddy S. Yang

Diffuse intrinsic pontine glioma (DIPG) is an aggressive pediatric brainstem tumor with a 5-year survival of <1%. Up to 80% of the DIPG tumors contain a specific K27M mutation in one of the two genes encoding histone H3 (H3K27M). Furthermore, p53 mutations found in >70–80% of H3K27M DIPG, and mutant p53 status is associated with a decreased response to radiation treatment and worse overall prognosis. Recent evidence indicates that H3K27M mutation disrupts tri-methylation at H3K27 leading to aberrant gene expression. Jumonji family histone demethylases collaborates with H3K27 mutation in DIPG by erasing H3K27 trimethylation and thus contributing to derepression of genes involved in tumorigenesis. Since the first line of treatment for pediatric DIPG is fractionated radiation, we investigated the effects of Jumonji demethylase inhibition with GSK-J4, and mutant p53 targeting/oxidative stress induction with APR-246, on radio-sensitization of human H3K27M DIPG cells. Both APR-246 and GSK-J4 displayed growth inhibitory effects as single agents in H3K27M DIPG cells. Furthermore, both of these agents elicited mild radiosensitizing effects in human DIPG cells (sensitizer enhancement ratios (SERs) of 1.12 and 1.35, respectively; p < 0.05). Strikingly, a combination of APR-246 and GSK-J4 displayed a significant enhancement of radiosensitization, with SER of 1.50 (p < 0.05) at sub-micro-molar concentrations of the drugs (0.5 μM). The molecular mechanism of the observed radiosensitization appears to involve DNA damage repair deficiency triggered by APR-246/GSK-J4, leading to the induction of apoptotic cell death. Thus, a therapeutic approach of combined targeting of mutant p53, oxidative stress induction, and Jumonji demethylase inhibition with radiation in DIPG warrants further investigation.


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