1.
Antioxidants, oxidants, and redox impacts on cell function - A tribute to Helmut Sies.
Cadenas, E, Packer, L, Traber, MG
Archives of biochemistry and biophysics. 2016;:94-9
Abstract
This article is in tribute to Helmut Sies and is written by his friends from the Oxygen Club of California with personal recollections from each of us: Enrique Cadenas on "Oxidative Stress and Mentorship", Lester Packer on "The Antioxidant Network", and Maret G. Traber on "Nutrition and Chronic Disease". We conclude with a brief overview of the positive influence Helmut Sies has had on the Oxygen Club of California.
2.
[Radioprotectors: History, Trends and Prospects].
Gudkov, SV, Popova, NR, Bruskov, VI
Biofizika. 2015;(4):801-11
Abstract
The search for ideal protective agents for use in a variety of radiation scenarios has continued for more than six decades. This review describes the history of the major discoveries, shows the chronology of the changes in attitudes, trends and paradigms. The readers are invited to meet with various classes of chemical compounds that have the potential to protect against acute and late effects of ionizing radiation when administered either before or after radiation exposure. The work represents characteristics of radioprotective agents such as a dose reduction factor, time of administration, tissue specificity, toxicity; the mechanisms of their action and practical applications are also described. A separate chapter considers the further development prospects and directions in this field of research.
3.
Therapeutic strategies in Friedreich's ataxia.
Richardson, TE, Kelly, HN, Yu, AE, Simpkins, JW
Brain research. 2013;:91-7
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Abstract
First established as a diagnosis by Nikolaus Friedreich in 1863, Friedreich's ataxia (FA) is an autosomal recessive progressive neurodegenerative disorder cause by a trinucleotide repeat expansion. FA begins with the functional absence of the FXN gene product frataxin, a protein whose exact function still remains unknown. This absence results in impaired intracellular antioxidant defenses, dysregulation of iron-sulfur cluster proteins, depression of aerobic electron transport chain respiration, massive mitochondrial dysfunction, and ultimately cell death in the brain, spinal cord and heart. Herein, we review the molecular and cellular pathogenesis leading to widespread organ system dysfunction, as well as current therapeutic research aimed at preventing the debilitating effects of frataxin loss and preventing the signs and symptoms associated of FA. We also discuss the ongoing treatment strategies employed by our laboratory to prevent mitochondrial damage using synergistic effects of 17β-estradiol and methylene blue, previously shown by our group and others to have protective effects in human FA fibroblasts. This article is part of a Special Issue entitled Hormone Therapy.