Search results for "Acquired diseases"
showing 3 items of 3 documents
Cytomics of Oxidative Stress: Probes and Problems
2017
Oxidative stress has been implicated in cellular senescence and aging, as well as in the onset and progression of many diverse genetic and acquired diseases and conditions. However, reactive oxygen (ROS) and nitrogen (RNS) species initiating oxidative stress also serve important regulatory roles, mediated by intercellular and intracellular signaling, adaptation to endogenous and exogenous stress, and destruction of invading pathogens. Fluorescence-based analysis of oxidative stress and related processes is an important cytomic application; almost 4000 papers were published between 1989 and 2016. To ascertain the specific role of ROS and RNS in oxidative stress studies by cytomic methodologi…
SOLID LIPID NANOPARTICLES FOR APPLICATIONS IN GENE THERAPY: A REVIEW OF THE STATE OF THE ART
2010
Importance of the field. Gene therapy represents a new paradigm in the prevention and treatment of many inherited and acquired diseases, including genetic disorders, such as cystic fibrosis, haemophilia and many somatic diseases, such as tumours, neurodegenerative diseases and viral infections, such as AIDS. Areas covered in this review. Among a large array of non-viral transfection agents used for in-vitro applications, cationic SLNs are the topic of this review, being recently proposed as an alternative carrier for DNA delivery, due to many technological advantages such as large-scale production from substances generally recognized as safe, good storage stability and possibility of steam …
A Deficiency in Respiratory Complex I in Heart Mitochondria from Vitamin A-Deficient Rats Is Counteracted by an Increase in Coenzyme Q
1997
Defects of NADH:coenzyme Q oxidoreductase (complex I) of mitochondria have been described in many congenital and acquired diseases. Administration of coenzyme Q (CoQ, ubiquinone) has been shown to benefit patients with some of these diseases. However, the mechanisms by which CoQ exerts the therapeutic effects are not clearly understood. A reason could be the lack of saturation of CoQ, in kinetic terms, for complex I activity. However, this hypothesis has not been proved in vivo because of the difficulty to incorporate CoQ into the mitochondrial membranes. We have found a deficiency in respiratory complex I in heart mitochondria from vitamin A-deficient rats which was accompanied by high CoQ…