Oxygen free radicals and Parkinson's disease

Adams, James D.; Odunze, Ifeoma N.

doi:10.1016/0891-5849(91)90009-r

Cited by 289 publications

(120 citation statements)

References 73 publications

Supporting

Mentioning

115

Contrasting

Unclassified

Order By: Relevance

“…The decrease in the antioxidant capacity caused by the nutrient deficiency was likely to result in the accumulation of free radicals in muscle, liver and spleen. As containing an iron-sulfur center, the accumulation of free radicals in muscle, liver and spleen would cause the oxidation of bio-molecules (e.g., protein, amino acids, lipid and DNA), which further lead to cell injury and death (Adams & Odunze, 1991;Bachowski et al, 1997). This may be one of the main reasons for the growth retardation of liver, spleen and muscle of kids in energy and/or protein restriction groups.…”

Section: The Antioxidant Capacity In Tissuesmentioning

confidence: 99%

Effects of Protein and/or Energy Restriction for Six Weeks, Followed with Nutritional Recovery on the Antioxidant Capacity and Development of Liver, Spleen and Muscle of Weaned Kids

Yang¹,

Sun²,

He³

et al. 2012

JAS

View full text Add to dashboard Cite

The effects of protein and/or energy restrictions on the antioxidant capacity and development of liver, spleen and muscle were investigated in kids. Sixty Liuyang Black kids, weaned at 28-day old, were allocated to four treatments: control, either energy or protein restriction, and combined energy and protein restriction. The experimental period consisted of six weeks of nutritional restriction followed with nine weeks of nutritional recovery. On day 42, energy restriction decreased the activity of glutathione peroxidase (GSH-Px) in spleen, the superoxide dismutase (SOD) mRNA level in muscle and spleen, and the ratio of RNA to DNA in liver (P < 0.05); protein restriction decreased the activity of glutathione reductase (GR) in muscle and liver, the ratio of RNA to DNA in liver, and the N concentration and the ratio of N to DNA in spleen and muscle (P < 0.05); combined restriction of energy and protein decreased the activities of catalase and GR and the ratio of RNA to DNA in muscle, and the activities of SOD, GSH-Px and GR in spleen (P < 0.05). On day 105, there was no difference in the antioxidant parameters among four groups (P > 0.05); however, the weights of liver and spleen in groups of pre-protein restriction and pre-combined restriction of energy and protein were still less than those of kids in control. The results indicate that six weeks of nutritional restriction can reduce the antioxidant capacity of muscle, spleen and liver, retard the development of liver and spleen, and the retarded development partly continues even after nine weeks of nutritional recovery.

show abstract

Section: The Antioxidant Capacity In Tissuesmentioning

confidence: 99%

Effects of Protein and/or Energy Restriction for Six Weeks, Followed with Nutritional Recovery on the Antioxidant Capacity and Development of Liver, Spleen and Muscle of Weaned Kids

Yang¹,

Sun²,

He³

et al. 2012

JAS

View full text Add to dashboard Cite

show abstract

“…Two age-associated neurodegenerative diseases, i.e., AD and PD, have been of special interest to free radical biologists since they have both been speculated to involve oxidative damage to neurons (87,(112)(113)(114)(115).…”

Section: Age-related Disease Models In Which Melatonin Has Been Testedmentioning

confidence: 99%

“…The loss of nigrostriatal dopaminergic neurons due to cytotoxic free radicals is believed to account, in part, for the neurodegenerative movement disorder of PD (24,114). Assuming that melatonin, because of its antioxidative actions, may assist in reducing neuronal damage due to the autooxidation of dopamine, Miller et al (119) tested this possibility using what has come to be known as the oxygen radical absorbance capacity (ORAC) assay; this method measures the oxidation of the fluorescent protein porphyridium cruentum 13-phycoerythrin (13-PE) in the presence of oxidizing agents such as dopamine.…”

Section: Age-related Disease Models In Which Melatonin Has Been Testedmentioning

confidence: 99%

Aging and oxygen toxicity: Relation to changes in melatonin

Reíter

1997

AGE

View full text Add to dashboard Cite

Melatonin (N-acetyl-5-methoxytryptamine) is a chemical mediator produced in the pineal gland and other sites in the body. The melatonin found in the blood is derived almost exclusively from the pineal gland. Since the pineal synthesizes melatonin primarily at night, blood levels of the indole are also higher at night (5-15 fold) than during the day. Some individuals on a nightly basis produce twice as much melatonin as others of the same age. Throughout life, the melatonin rhythm gradually wanes such that, in advanced age, melatonin production is usually at a minimum. Melatonin was recently found to be a free radical scavenger and antioxidant. It has been shown, in the experimental setting, to protect against both free radical induced DNA damage and oxidative stress-mediated lipid peroxidation. Pharmacologically, melatonin has been shown to reduce oxidative damage caused by such toxins as the chemical carcinogen safrole, carbon tetrachloride, paraquat, bacterial lipopolysaccharide, kainic acid, 8-aminolevulinic and amyloid 13 peptide of AIzheimer's disease as well as a model of Parkinson's disease involving the drug 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Additionally, the oxidative damage caused by agents such as ionizing radiation and excessive exercise is reduced by melatonin. Since free radical-induced molecular injury may play a significant role in aging, melatonin's ability to protect against it suggests a potential function of melatonin in deferring aging and agerelated, free radical-based diseases. Besides its ability to abate oxidative damage, other beneficial features of melatonin may be important in combating the signs of aging; these include melatonin's immune-stimulating function, its sleep-promoting ability, its function as an anti-viral agent, and general protective actions at the cellular level. Definitive tests of the specific functions of physiological levels of melatonin in processes of aging are currently being conducted.

show abstract

“…Although the cause of PD is still unknown, oxidative stress has been implicated as a pathogenetic factor. According to this so called "free radical hypothesis," the degeneration of the nigro-striatal system in PD is related to the relatively high exposure of these neurons to reactive oxygen species (ROS), in particular hydrogen peroxide (H 2 O 2 ), produced during both the enzymatic (monoamine oxidase-catalyzed) and nonenzymatic (auto-oxidative) breakdown of DA (Adams and Odunze, 1991;Olanow, 1992). Thus, DAergic cell death in PD may be caused by an overproduction of ROS and/or a diminished protection against them.…”

Section: Abstract: Parkinson's Disease; Oxidative Stress; Glutathionmentioning

confidence: 99%

Glutathione Is Involved in the Granular Storage of Dopamine in Rat PC12 Pheochromocytoma Cells: Implications for the Pathogenesis of Parkinson’s Disease

Drukarch¹,

Jongenelen²,

Schepens³

et al. 1996

J. Neurosci.

View full text Add to dashboard Cite

Parkinson's disease (PD) is characterized by degeneration of dopamine (DA)-containing nigro-striatal neurons. Loss of the antioxidant glutathione (GSH) has been implicated in the pathogenesis of PD. Previously, we showed that the oxidant hydrogen peroxide inhibits vesicular uptake of DA in nigro-striatal neurons. Hydrogen peroxide is scavenged by GSH and, therefore, we investigated a possible link between the process of vesicular storage of DA and GSH metabolism. For this purpose, we used rat pheochromocytoma-derived PC12 cells, a model system applied extensively for studying monoamine storage mechanisms. We show that depletion of endogenous DA stores with reserpine was accompanied in PC12 cells by a longlasting, significant increase in GSH content the extent of which appeared to be inversely related to the rate of GSH synthesis. A similar increase in GSH content was observed after depletion of DA stores with the tyrosine hydroxylase inhibitor ␣-methylp-tyrosine. In the presence of ␣-methyl-p-tyrosine, refilling of the DA stores by exogenous DA reduced GSH content back to control level. Lowering of PC12 GSH content, via blockade of its synthesis with buthionine sulfoximine, however, led to a significantly decreased accumulation of exogenous [ 3 H]DA without affecting uptake of the acetylcholine precursor [ 14 C]choline. These data suggest that GSH is involved in the granular storage of DA in PC12 cells and that, considering the molecular characteristics of the granular transport system, it is likely that GSH is used to protect susceptible parts of this system against (possibly DA-induced) oxidative damage. Key words: Parkinson's disease; oxidative stress; glutathione; dopamine; PC12 cells; neurotransmitter uptake; vesicular storageParkinson's disease (PD) is characterized primarily by a loss of dopamine (DA) in the striatum caused by degeneration of DAergic neurons in the zona compacta of the substantia nigra (SN) (Gibb and Lees, 1991). Although the cause of PD is still unknown, oxidative stress has been implicated as a pathogenetic factor. According to this so called "free radical hypothesis," the degeneration of the nigro-striatal system in PD is related to the relatively high exposure of these neurons to reactive oxygen species (ROS), in particular hydrogen peroxide (H 2 O 2 ), produced during both the enzymatic (monoamine oxidase-catalyzed) and nonenzymatic (auto-oxidative) breakdown of DA (Adams and Odunze, 1991;Olanow, 1992). Thus, DAergic cell death in PD may be caused by an overproduction of ROS and/or a diminished protection against them. Evidence to support the "free radical hypothesis" has come from postmortem investigations of PD brains, which consistently show an increase in the indices of oxidative stress in the SN at the time of death (Hirsch et al., 1991;Jenner, 1993). One of these indices, possibly even preceding the loss of DA (Dexter et al., 1994), is a decrease in the level of glutathione (GSH) in the Parkinsonian SN (Riederer et al., 1989;Sofic et al., 1992;Jenner, 1993). GSH, the most abund...

show abstract

Oxygen free radicals and Parkinson's disease

Cited by 289 publications

References 73 publications

Effects of Protein and/or Energy Restriction for Six Weeks, Followed with Nutritional Recovery on the Antioxidant Capacity and Development of Liver, Spleen and Muscle of Weaned Kids

Effects of Protein and/or Energy Restriction for Six Weeks, Followed with Nutritional Recovery on the Antioxidant Capacity and Development of Liver, Spleen and Muscle of Weaned Kids

Aging and oxygen toxicity: Relation to changes in melatonin

Glutathione Is Involved in the Granular Storage of Dopamine in Rat PC12 Pheochromocytoma Cells: Implications for the Pathogenesis of Parkinson’s Disease

Contact Info

Product

Resources

About