منابع مشابه
Toxicity of atorvastatin on isolated brain mitochondria
Background: Although the bio kinetics, metabolism and chemical toxicity of Atorvastatin are well known, until recently little attention was paid to the potential neurotoxic effect of Atorvastatin (Atv). Regarding the concrete evidences indicating Atv may reduce Coenzyme Q10 (CoQ10) levels through blockage of metalonate cycle, the present work aims to determine if Atorvastatin may provide toxic...
متن کاملMetabolic stages, mitochondria and calcium in hypoxic/ischemic brain damage.
Cerebral hypoxia/ischemia leads to mitochondrial dysfunction due to lack of oxygen leaving the glycolytic metabolism as a main pathway for ATP production. Inhibition of mitochondrial respiration thus triggers generation of lactate and hydrogen ions (H+), and furthermore dramatically reduces ATP generation leading to disregulation of cellular ion metabolism with subsequent intracellular calcium ...
متن کاملCalcium signaling, mitochondria and acute pancreatitis: avenues for therapy
Pancreatic necrosis, systemic inflammatory response syndrome, multiple organ failure and sepsis are characteristic of severe acute pancreatitis, which results in death of one in four patients and is without specific drug therapy (59, 62). As the pancreatic acinar cell is an initial site of injury (41, 59), commonly initiated by bile or ethanol excess, investigation of its behaviour in response ...
متن کاملNSAIDs, Mitochondria and Calcium Signaling: Special Focus on Aspirin/Salicylates
Aspirin (acetylsalicylic acid) is a well-known nonsteroidal anti-inflammatory drug (NSAID) that has long been used as an anti-pyretic and analgesic drug. Recently, much attention has been paid to the chemopreventive and apoptosis-inducing effects of NSAIDs in cancer cells. These effects have been thought to be primarily attributed to the inhibition of cyclooxygenase activity and prostaglandin s...
متن کاملMitochondria-controlled signaling mechanisms of brain protection in hypoxia
The article is focused on the role of the cell bioenergetic apparatus, mitochondria, involved in development of immediate and delayed molecular mechanisms for adaptation to hypoxic stress in brain cortex. Hypoxia induces reprogramming of respiratory chain function and switching from oxidation of NAD-related substrates (complex I) to succinate oxidation (complex II). Transient, reversible, compe...
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ژورنال
عنوان ژورنال: Journal of Biological Chemistry
سال: 2009
ISSN: 0021-9258
DOI: 10.1074/jbc.m808066200