International Counseling Values: Recognizing Valued Approaches Identified by International Counseling Professionals Through Qualitative Inquiry.

People may assume that the counseling profession functions with a shared set of values that promote well-being and mental health to individuals, families, and communities across the globe. Common values, such as described in training programs, ethical codes, and other areas, reflect the approach and direction for providing professional counseling services among counseling professionals throughout the world. The researchers designed this qualitative study using a phenomenological approach to explore how counseling values are experienced and implemented across various cultures.

Newly Identified Chemicals Preserve Mitochondrial Capacity and Decelerate Loss of Photoreceptor Cells in Murine Retinal Degeneration Models.

Metabolic stress and associated mitochondrial dysfunction are implicated in retinal degeneration irrespective of the underlying cause. We identified seven unique chemicals from a Chembridge DiverSET screen and tested their protection against photoreceptor cell death in cell- and animal-based approaches. Calcium overload (A23187) was triggered in 661W murine photoreceptor-derived cells, and changes in redox potential and real-time changes in cellular metabolism were assessed using the MTT and Seahorse Biosciences XF assay, respectively.

SAHA is neuroprotective in in vitro and in situ models of retinitis pigmentosa.

Purpose: Recent reports linking HDAC6 to mitochondrial turnover and neurodegeneration led us to hypothesize that an inhibitor such as Vorinostat (suberoylanilide hydroxamic acid, SAHA) may reduce mitochondrial damage found in retinitis pigmentosa (RP), a progressive neurodegenerative disease of the eye. Here we tested the efficacy of SAHA for its ability to protect photoreceptors in in-vitro and in-situ models of RP. As the stressor, we focused on calcium overload.

Small Molecules that Protect Mitochondrial Function from Metabolic Stress Decelerate Loss of Photoreceptor Cells in Murine Retinal Degeneration Models.

One feature common to many of the pathways implicated in retinal degeneration is increased metabolic stress leading to impaired mitochondrial function. We found that exposure of cells to calcium ionophores or oxidants as metabolic stressors diminish maximal mitochondrial capacity. A library of 50,000 structurally diverse "drug-like" molecules was screened for protection against loss of calcium-induced loss of mitochondrial capacity in 661W rod-derived cells and C6 glioblastomas.

Assessment of mitochondrial damage in retinal cells and tissues using quantitative polymerase chain reaction for mitochondrial DNA damage and extracellular flux assay for mitochondrial respiration activity.

Mitochondrial dysfunction and genomic instability are associated with a number of retinal pathologies including age-related macular degeneration, diabetic retinopathy, and glaucoma. Consequences of mitochondrial dysfunction within cells include elevation of the rate of ROS production due to damage of electron transport chain proteins, mitochondrial DNA (mtDNA) damage, and loss of metabolic capacity. Here we introduce the quantitative polymerase chain reaction assay (QPCR) and extracellular flux assay (XF) as powerful techniques to study mitochondrial behavior.

Early alterations in mitochondrial reserve capacity; a means to predict subsequent photoreceptor cell death.

Although genetic and environmental factors contribute to neurodegenerative disease, the underlying etiology common to many diseases might be based on metabolic demand. Mitochondria are the main producer of ATP, but are also the major source of reactive oxygen species. Under normal conditions, these oxidants are neutralized; however, under environmental insult or genetic susceptibility conditions, oxidative stress may exceed cellular antioxidant capacities, leading to degeneration.

Antioxidant and prooxidant effects of polyphenol compounds on copper-mediated DNA damage.

Inhibition of copper-mediated DNA damage has been determined for several polyphenol compounds. The 50% inhibition concentration values (IC(50)) for most of the tested polyphenols are between 8 and 480 μM for copper-mediated DNA damage prevention. Although most tested polyphenols were antioxidants under these conditions, they generally inhibited Cu(I)-mediated DNA damage less effectively than Fe(II)-mediated damage, and some polyphenols also displayed prooxidant activity.

Kinetics of iron oxidation upon polyphenol binding.

Polyphenol prevention of iron-mediated DNA damage occurs primarily through iron binding. Once bound, iron in the Fe(2+)-polyphenol complex autooxidizes to Fe(3+) in the presence of O(2). To determine the correlation between the rate of Fe(2+)-polyphenol autooxidation and polyphenol antioxidant ability, kinetic studies at pH = 6.

A review of the antioxidant mechanisms of polyphenol compounds related to iron binding.

In this review, primary attention is given to the antioxidant (and prooxidant) activity of polyphenols arising from their interactions with iron both in vitro and in vivo. In addition, an overview of oxidative stress and the Fenton reaction is provided, as well as a discussion of the chemistry of iron binding by catecholate, gallate, and semiquinone ligands along with their stability constants, UV-vis spectra, stoichiometries in solution as a function of pH, rates of iron oxidation by O(2) upon polyphenol binding, and the published crystal structures for iron-polyphenol complexes. Radical scavenging mechanisms of polyphenols unrelated to iron binding, their interactions with copper, and the prooxidant activity of iron-polyphenol complexes are briefly discussed.

Predicting how polyphenol antioxidants prevent DNA damage by binding to iron.

Prevention of oxidative DNA damage due to hydroxyl radical is important for the prevention and treatment of disease. Because of their widely recognized antioxidant ability, 12 polyphenolic compounds were assayed by gel electrophoresis to directly quantify the inhibition of DNA damage by polyphenols with Fe(2+) and H2O2. All of the polyphenol compounds have IC50 values ranging from 1-59 microM and inhibit 100% of DNA damage at 50-500 microM concentrations.

The central role of metal coordination in selenium antioxidant activity.

Oxidative DNA damage occurs in vivo by hydroxyl radical generated in metal-mediated Fenton-type reactions. Cell death and mutation caused by this DNA damage are implicated in neurodegenerative and cardiovascular diseases, cancer, and aging. Treating these conditions with antioxidants, including highly potent selenium antioxidants, is of growing interest.