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Full-Text Articles in Medicine and Health Sciences
Effects Of Tamoxifen On Mitochondrial Nos Activity: Alteration In The Intramitochondrial Ca2+ Homeostasis, Sandeep S. Joshi
Effects Of Tamoxifen On Mitochondrial Nos Activity: Alteration In The Intramitochondrial Ca2+ Homeostasis, Sandeep S. Joshi
Theses, Dissertations and Capstones
Tamoxifen (Tam) is an anticancer drug that induces oxidative stress and apoptosis via mitochondria- and nitric oxide (NO)-dependent pathways. Here, we report that therapeutic concentrations of Tam stimulate the mitochondrial NO synthase (mtNOS) activity of isolated rat liver mitochondria by increasing the intramitochondrial ionized Ca2+ concentration ([Ca2+]m). Tam decreases transmembrane potential (∆ψ) due to increased [Ca2+]m that neutralizes the negative charges of the inner mitochondrial membrane. Thus, the present study reports a novel mechanism for the widely used anti- caner drug, Tam.
Epileptogenesis Causes Long-Term Plasticity Changes In Calbindin D-28k In The Rat Pilocarpine Model Of Acquired Epilepsy, Anne Johnston Harrison
Epileptogenesis Causes Long-Term Plasticity Changes In Calbindin D-28k In The Rat Pilocarpine Model Of Acquired Epilepsy, Anne Johnston Harrison
Theses and Dissertations
Epilepsy is one of the most common neurological disorders, affecting more than 2% of children and 1% of adults in the U.S. Emerging research has demonstrated that calcium, as a major second messenger system, underlies many of these injury-induced plasticity changes associated with the development of epilepsy. Recent evidence has suggested that long term elevations in neuronal resting calcium levels play a role in initiating and maintaining epileptogenesis (the development of epilepsy). Collaborations between our lab and others have produced microarray data that suggests that a major calcium-binding protein, calbindin D-28k, mRNA levels are decreased in epileptic rats even up …