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Plos One : Nelfinavir Inhibits Intra-mitochondrial Calcium Influx and Protects Brain Against Hypoxic-ischemic Injury in Neonatal Mice, Volume 8

By Kihara, Alexandre, Hiroaki

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Book Id: WPLBN0003963732
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos One : Nelfinavir Inhibits Intra-mitochondrial Calcium Influx and Protects Brain Against Hypoxic-ischemic Injury in Neonatal Mice, Volume 8  
Author: Kihara, Alexandre, Hiroaki
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection (Contemporary)
Historic
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Publisher: Plos

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Kihara, A. H. (n.d.). Plos One : Nelfinavir Inhibits Intra-mitochondrial Calcium Influx and Protects Brain Against Hypoxic-ischemic Injury in Neonatal Mice, Volume 8. Retrieved from http://kindle.worldlibrary.net/


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Description : Nelfinavir (NLF), an antiretroviral agent, preserves mitochondrial membranes integrity and protects mature brain against ischemic injury in rodents. Our study demonstrates that in neonatal mice NLF significantly limits mitochondrial calcium influx, the event associated with protection of the brain against hypoxic-ischemic insult (HI). Compared to the vehicletreated mice, cerebral mitochondria from NLF-treated mice exhibited a significantly greater tolerance to the Ca2+-induced membrane permeabilization, greater ADP-phosphorylating activity and reduced cytochrome C release during reperfusion. Pre-treatment with NLF or Ruthenium red (RuR) significantly improved viability of murine hippocampal HT-22 cells, reduced Ca2+ content and preserved membrane potential (Ym) in mitochondria following oxygen-glucose deprivation (OGD). Following histamine-stimulated Ca2+ release from endoplasmic reticulum, in contrast to the vehicle-treated cells, the cells treated with NLF or RuR also demonstrated reduced Ca2+ content in their mitochondria, the event associated with preserved Ym. Because RuR inhibits mitochondrial Ca2+ uniporter, we tested whether the NLF acts via the mechanism similar to the RuR. However, in contrast to the RuR, in the experiment with direct interaction of these agents with mitochondria isolated from naı¨ve mice, the NLF did not alter mitochondrial Ca2+ influx, and did not prevent Ca2+ induced collapse of the Ym. These data strongly argues against interaction of NLF and mitochondrial Ca2+ uniporter. Although the exact mechanism remains unclear, our study is the first to show that NLF inhibits intramitochondrial Ca2+ flux and protects developing brain against HI-reperfusion injury. This novel action of NLF has important clinical implication, because it targets a fundamental mechanism of post-ischemic cell death : intramitochondrial Ca2+ overload R mitochondrial membrane permeabilization R secondary energy failure.

 

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