Effects of exercise induced oxidative stress on glutathione levels in Parkinson’s disease on and off medication

Abstract

Resting plasma glutathione (GSH) levels are lower in individuals with Parkinson's disease (PD) than any other neurological condition. Medications used to treat PD have also been shown to further decrease this depletion. Acute exercise has been shown to be an effective tool to produce oxidative stress in other populations as reflected in lowering levels of GSH. The purpose of this study was to determine how PD responds to acute exercise stress and how medication affects these responses. Fourteen men with PD and 14 men without PD underwent an exercise stress test. Subjects with PD performed the test once off PD medication (PD-Off-med) for 12 h then again 1 week later on PD medication (PD-On-med). GSH and glutathione disulfide (GSSG), were collected via blood draws at rest and after peak exercise along with peak VO(2). At rest and at peak exercise GSH levels and the GSH:GSSG ratio were significantly lower in the PD-On-med and PD-Off-med as compared to controls. GSSG levels were significantly higher in both medication conditions at rest and peak exercise compared to controls. When comparing PD-On-med vs. PD-Off-med at rest and peak exercise, the PD-On-med had lower GSH levels, a lower GSH:GSSG ratio and higher GSSG levels. VO(2) correlated positively with GSH levels. Subjects with PD have lower plasma GSH levels than healthy controls at rest and at peak exercise.

Treadmill exercise activates Nrf2 antioxidant system to protect the nigrostriatal dopaminergic neurons from MPP+ toxicity

“…It has been shown that the activation of brainderived neurotrophic factor and its receptor TrkB signaling pathway is involved in the neuroprotective effect of exercise against brain injury (Gerecke et al, 2012;Wu et al, 2011). On the other hand, reports demonstrate that long-term moderate exercise induces low level of reactive oxygen species (ROS), which may activate the endogenous antioxidant defense system (Elokda et al, 2010;Somani et al, 1995), though highintensity acute exercise increases oxidative stress and vulnerability to brain injury (Aguiar et al, 2010;Teixeira et al, 2009). The induction of adaptive antioxidant defense by regular exercise has therefore been suggested to be able to prevent oxidative stress-associated aging (Navarro et al, 2004) and neurodegeneration (Cechetti et al, 2012;Garcia-Mesa et al, 2012).…”

An Overview of Target Specific Neuro-Protective and Neuro-Restorative Strategies

“…The metabolism of dopamine (DA) itself creates a favorable environment for oxidative damage through intermediates such as DA-quinone and 3, 4-dihydroxy phenylacetaldehyde (Jackson and Smeyne , 2005). On the other hand reduced plasma levels of anti-oxidants such as glutathione and uric acid have been reported in PD patients (Elokda et al, 2010). …”

Nutritional Supplementation, Diet, and Genetics and Their Impact on Parkinson’s Disease (PD), a Review of Studies

“…The lower levels of glutathione were interpreted as a result of oxidative stress. 34 A study was conducted by Elokda et al, 35 to establish the effects of exercise induced oxidative stress on glutathione levels in Parkinson's disease during off and on medication. The study was conducted on the findings that show resting plasma GSH levels to be lower in people suffering from PD in comparison to other neurological conditions.…”

“…Thus the findings showed that PD patients had lower levels of plasma GSH compared to healthy people at rest and peak exercise. 35 A study was conducted by Chen et al, 36 to establish whether increased oxidative damage in peripheral blood correlates with severity of PD. Basing their research on the findings that show neuronal dysfunction due to increased oxidative stress in PD patents, the researchers sought to investigate whether the pathological changes that occur in the brain of PD patients are also present in peripheral tissues.…”