S8.7 Cellular metabolic profile and lonidamine-induced cytochrome c release
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چکیده
منابع مشابه
Minocycline blocks c-terminal fragments of amyloid precursor protein-induced neurotoxicity by inhibition of cytochrome c release and caspase-12 activation
Minocycline is a second-generation tetracycline that effectively crosses the blood-brain barrier. It has remarkable neuroprotective qualities in models of cerebral ischaemia, traumatic brain injury, Huntington’s and Parkinson’s diseases. However, there is no evidence about neuroprotective effects of minocycline on AD. Alzheimer’s disease (AD) is a neurodegenerative disorder characterized neurop...
متن کاملMinocycline blocks c-terminal fragments of amyloid precursor protein-induced neurotoxicity by inhibition of cytochrome c release and caspase-12 activation
Minocycline is a second-generation tetracycline that effectively crosses the blood-brain barrier. It has remarkable neuroprotective qualities in models of cerebral ischaemia, traumatic brain injury, Huntington’s and Parkinson’s diseases. However, there is no evidence about neuroprotective effects of minocycline on AD. Alzheimer’s disease (AD) is a neurodegenerative disorder characterized neurop...
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Although the existence of cardiac mitochondrial cGMP has been reported previously [Kimura and Murad (1974) J. Biol. Chem. 249, 6910-6916], the physiological and pathophysiological properties of cGMP in cardiac mitochondria have remained unknown. The aim of the present study was to clarify whether cardiac mitochondrial cGMP regulates the apoptosis of cardiomyocytes. In the presence of GTP, the N...
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Introduction: Cognitive dysfunction is the most common problem of patients with Alzheimer disease (AD). The pathological mechanism of cognitive impairment in AD may contribute to neuronal loss, synaptic dysfunction, and alteration in neurotransmitters receptors. Mitochondrial synapses dysfunction due to the accumulation of amyloid beta (Aβ) is one of the earliest pathological features of AD. Th...
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tBid, the cleaved form of Bid, can induce cytochrome c (Cyt. c) release from rat heart mitochondria more efficiently and reproducibly than that from liver or brain mitochondria. Unlike Bax, such release was not prevented by cyclosphorin A, an inhibitor of the opening of permeability transition pore. Carbonyl-cyanide m-chlorophenyl-hydrazone or oligomycin also have no obvious effect on the relea...
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ژورنال
عنوان ژورنال: Biochimica et Biophysica Acta (BBA) - Bioenergetics
سال: 2008
ISSN: 0005-2728
DOI: 10.1016/j.bbabio.2008.05.195