نتایج جستجو برای: cigarette smoking extracts cse cytochrome c release isolated mitochondria

تعداد نتایج: 1738220  

Common techniques for the treatment of Hepatocellular carcinoma (HCC) have not been successful, and thus the design and discovery of new compounds with better anti-cancer function are needed. Snake venom is among the most important compounds used by researchers to the treatment of various cancers. This study was designed to evaluate the toxicity effect of Persian Gulf snake venom (Enhydrina sch...

2017
Minghui Ji Yudong Zhang Na Li Chao Wang Rong Xia Zhan Zhang Shou-Lin Wang

Cytochrome P450 2A13 (CYP2A13), an extrahepatic enzyme mainly expressed in the human respiratory system, has been reported to mediate the metabolism and toxicity of cigarette smoke. We previously found that nicotine inhibited 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) metabolism by CYP2A13, but its influence on other components of cigarette smoke remains unclear. The nicotine componen...

2011
Junmin Zhou Erika A. Eksioglu Nicole R. Fortenbery Xianghong Chen Huaquan Wang Pearlie K. Epling-Burnette Julie Y. Djeu Sheng Wei

Several reports link cigarette smoking with leukemia. However, the effects of cigarette smoke extract (CSE) on bone marrow hematopoiesis remain unknown. The objective of this study was to elucidate the direct effects of cigarette smoke on human bone marrow hematopoiesis and characterize the inflammatory process known to result from cigarette smoking. Bone marrow mononuclear cells (BMCs) from he...

Multiple Sclerosis (MS) is a neurodegenerative and autoimmune disease that it’s molecular etiology and factors involving in its progression remains unknown. In this study for evaluation effect of mercuric on progression of MS we investigated the additive effect of mercuric sulfide on the brain mitochondrial dysfunction in experimental autoimmune encephalomyelitis (EAE) model of MS in C57BL/6 mi...

Multiple Sclerosis (MS) is a neurodegenerative and autoimmune disease that it’s molecular etiology and factors involving in its progression remains unknown. In this study for evaluation effect of mercuric on progression of MS we investigated the additive effect of mercuric sulfide on the brain mitochondrial dysfunction in experimental autoimmune encephalomyelitis (EAE) model of MS in C57BL/6 mi...

Journal: :The Journal of Cell Biology 1999
Ruth M. Kluck Mauro Degli Esposti Guy Perkins Christian Renken Tomomi Kuwana Ella Bossy-Wetzel Martin Goldberg Terry Allen Michael J. Barber Douglas R. Green Donald D. Newmeyer

During apoptosis, an important pathway leading to caspase activation involves the release of cytochrome c from the intermembrane space of mitochondria. Using a cell-free system based on Xenopus egg extracts, we examined changes in the outer mitochondrial membrane accompanying cytochrome c efflux. The pro-apoptotic proteins, Bid and Bax, as well as factors present in Xenopus egg cytosol, each in...

Journal: :Cancer research 2000
M Watabe K Machida H Osada

We reported previously that a synthetic compound, MT-21, induced apoptosis by activating c-Jun-NH2-terminal kinase via the Krs/MST protein, which is activated by caspase-3 cleavage dependent on reactive oxygen species production. Here we examine the activation mechanism of caspase-3, an important cysteine aspartic protease, during MT-21-induced apoptosis. We found that MT-21 activated caspase-3...

2017
Chao Song Bailing Luo Li Gong

PURPOSE The aim of this study was to investigate the effect of resveratrol (RSV) on cigarette smoke extract (CSE)-induced cell apoptosis and mitochondrial dysfunction in vitro, as well as changes in the MFN2 expression level. METHODS Cultured human bronchial epithelial (HBE) cells were initially treated with CSE to induce apoptosis, followed by incubation either with or without RSV. Numerous ...

2013
Roland F Hoffmann Sina Zarrintan Simone M Brandenburg Arjan Kol Harold G de Bruin Shabnam Jafari Freark Dijk Dharamdajal Kalicharan Marco Kelders Harry R Gosker Nick HT ten Hacken Johannes J van der Want Antoon JM van Oosterhout Irene H Heijink

BACKGROUND Cigarette smoking is the major risk factor for COPD, leading to chronic airway inflammation. We hypothesized that cigarette smoke induces structural and functional changes of airway epithelial mitochondria, with important implications for lung inflammation and COPD pathogenesis. METHODS We studied changes in mitochondrial morphology and in expression of markers for mitochondrial ca...

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