Drug Induced Mitochondrial Dysfunction

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are books media?

This is a book 

http://www.amazon.ca/Drug-Induced-Mitochondrial-Dysfunction-James-Dykens/dp/0470111313

 

"This is the definitive, one-stop resource....... It discusses mitochondrial impairment to organs, skeletal muscle, and nervous systems...

This is the authoritative reference on drug-induced mitochondrial dysfunction for safety assessment professionals in the pharmaceutical industry and for pharmacologists and toxicologists in both drug and environmental health sciences"
 

I did take a look inside the book but all the good stuff was hidden antidepressants had 10 hits inside but I could not view inside... for 212 bucks you can buy it.

 

This may be of interest for some people here who still have access to money. 

 

 

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http://journal.frontiersin.org/article/10.3389/fphar.2014.00038/abstractTheinterplay between iron accumulation, mitochondrial dysfunction, and inflammation during the execution step of neurodegenerative disorders

Pamela J. Urrutia, Natalia P. Mena and Marco T. Núñez*

• Department of Biology and Research Ring on Oxidative Stress in the Nervous System, Faculty of Sciences, University of Chile, Santiago, Chile
  

A growing set of observations points to mitochondrial dysfunction, iron accumulation, oxidative damage and chronic inflammation as common pathognomonic signs of a number of neurodegenerative diseases that includes Alzheimer’s disease, Huntington disease, amyotrophic lateral sclerosis, Friedrich’s ataxia and Parkinson’s disease. Particularly relevant for neurodegenerative processes is the relationship between mitochondria and iron. The mitochondrion upholds the synthesis of iron–sulfur clusters and heme, the most abundant iron-containing prosthetic groups in a large variety of proteins, so a fraction of incoming iron must go through this organelle before reaching its final destination. In turn, the mitochondrial respiratory chain is the source of reactive oxygen species (ROS) derived from leaks in the electron transport chain. The co-existence of both iron and ROS in the secluded space of the mitochondrion makes this organelle particularly prone to hydroxyl radical-mediated damage. In addition, a connection between the loss of iron homeostasis and inflammation is starting to emerge; thus, inflammatory cytokines like TNF-alpha and IL-6 induce the synthesis of the divalent metal transporter 1 and promote iron accumulation in neurons and microglia. Here, we review the recent literature on mitochondrial iron homeostasis and the role of inflammation on mitochondria dysfunction and iron accumulation on the neurodegenerative process that lead to cell death in Parkinson’s disease. We also put forward the hypothesis that mitochondrial dysfunction, iron accumulation and inflammation are part of a synergistic self-feeding cycle that ends in apoptotic cell death, once the antioxidant cellular defense systems are finally overwhelmed.

 

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http://mitochondrialdiseasenews.com/2015/09/18/reduced-cellular-energy-leads-to-cell-dysfunction-in-neurodegenerative-diseases/

A recently published study by a team of researchers at the Gladstone Institutes, titled “The Role of Mitochondrially Derived ATP in Synaptic Vesicle Recycling“, is the first piece of evidence detailing how abnormalities in cell mitochondria can significantly reduce cellular energy and lead to dysfunctional brain cells. This was observed in models of neurodegenerative diseases. While the role of reduced cellular energy in neurodegeneration has long since been a subject of research, this study, authored by Gladstone Institute of Neurological Disease postdoctoral fellow Divya Pathak, Ph.D., is the first to create and successfully utilize a novel assay to quantify brain cell ATP (the energy molecule). The study is currently published and was selected as Paper of the Week in the Journal of Biological Chemistry.

Through a model of Leigh’s disease, a neurometabolic condition that affects cellular mitochondria, the researchers were able to use novel assays to examine cellular energy levels. They found that the cells in this disease, because it compromised mitochondrial output, were notably dysfunctional.

“It was always assumed that defects in mitochondria would result in a depletion of energy levels, which would be toxic to neurons,” said Dr. Pathak in a news release. “But no one had been able to prove this because the necessary assays were not available. Now that we’ve demonstrated the link between impaired mitochondria, a loss of ATP, and neuronal dysfunction, the next step is to see if this connection holds true in conditions like Parkinson’s disease and Alzheimer’s disease.”

Researchers were also successful in determining a cellular energy threshold, which is the minimum amount of energy a cell would need to conduct synaptic vesicle cycling – a process that allows neurotransmitters to function in the brain. They did this by inhibiting glycolysis, in effect forcing the cells to rely only on ATP from mitochondria and yielding more accurate, isolated results across the cycle. They found that cells needed higher amounts of energy during re-uptake of vesicles after the release of neurotransmitters.

The team also compared energy levels in boutons – the docks where neurotransmitters are released – in cells with and without mitochondria present. Interestingly, there was no significant difference in their energy levels, however this led the researchers to believe that under normal conditions, cell energy can shift rapidly from boutons with mitochondria to boutons without them. Further research would be needed to determine if boutons without mitochondria will exhibit dysfunction.

Senior author Ken Nakamura, MD, PhD, an assistant investigator at the Gladstone Institute of Neurological Disease, believes that carrying out these studies in both healthy and diseased cells is vital for interpreting the findings. “We really need to understand the basics of cell biology in a normal setting in order to comprehend changes in disease,” he explained. “It’s worth taking the time to study these underlying biological processes so that we can identify the best therapeutic targets for neurodegenerative disorders.”