Studies on lipid peroxidation and protein oxidation in the aging brain

Cini, M.; Moretti, Antonio

doi:10.1016/0197-4580(95)80007-e

Cited by 127 publications

(75 citation statements)

References 29 publications

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“…However, there are conflicting studies in the literature concerning age-dependent increases of oxidative stress within the brain. Some studies have reported age-related increases in oxidative stress (Aksenova et al, 1998, and some studies have reported no change with aging (Cao and Cutler, 1995,Cini and Moretti, 1995,Goto et al, 1999,Davies et al, 2001. In a review on oxidative stress and aging, Stadtman notes how differing results may have to do with animal breeding conditions or that the animals may have adapted over time to become more resistant to oxidative stress (Stadtman, 2002).…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress and dopamine depletion in an intrastriatal 6-hydroxydopamine model of Parkinson’s disease

Smith

Cass

2007

Neuroscience

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Although the etiology of Parkinson's disease (PD) is unknown, a common element of most theories is the involvement of oxidative stress, either as a cause or effect of the disease. There have been relatively few studies that have characterized oxidative stress in animal models of PD. In the present study a 6-hydroxydopamine (6-OHDA) rodent model of PD was used to investigate the in vivo production of oxidative stress after administration of the neurotoxin. 6-OHDA was injected into the striatum of young adult rats and the production of protein carbonyls and 4-hydroxynonenal (HNE) was measured at 1, 3, 7, and 14 days after administration. A significant increase in both markers was found in the striatum 1 day after neurotoxin administration, and this increase declined to basal levels by day 7. There was no significant increase found in the substantia nigra at any of the time points investigated. This same lesion paradigm produced dopamine depletions of 90-95% in the striatum and 63-80% in the substantia nigra by 14 to 28 days post 6-OHDA. Protein carbonyl and HNE levels were also measured in middle-aged and aged animals 1 day after striatal 6-OHDA. Both protein carbonyl and HNE levels were increased in the striatum of middle-aged and aged animals treated with 6-OHDA, but the increases were not as great as those observed in the young adult animals. Similar to the young animals, there were no increases in either marker in the substantia nigra of the middle-aged and aged animals. There was a trend for an age-dependent increase in basal amounts of oxidative stress markers when comparing the non-lesioned side of the brains of the three age groups. These results support that an early event in the course of dopamine depletion following intrastriatal 6-OHDA administration is the generation of oxidative stress. Keywordsreactive oxygen species; protein carbonyls; 4-hydroxynonenal; striatum; substantia nigra; aging; Fischer-344 rat Parkinson's disease (PD) stems from the loss of dopamine (DA) caused by the degeneration of the dopaminergic neurons of the substantia nigra. The nature of this degeneration remains unclear, although current theories suggest that reactive oxygen species (ROS) are involved in some capacity early in the disease process (Jenner, 2003). One of the earliest changes in patients with PD and incidental Lewy body disease is the loss of glutathione (Sian et al., 1994,Owen et al., 1996. Post mortem tissue from PD patients has been shown to contain elevated levels Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Yoritaka et al., 1996), protein carbonyls (Alam et...

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Section: Discussionmentioning

confidence: 99%

Oxidative stress and dopamine depletion in an intrastriatal 6-hydroxydopamine model of Parkinson’s disease

Smith

Cass

2007

Neuroscience

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“…In other tissues it is not clear how rates of production and removal of oxidized protein relate to the elevated levels measured ; proteins in extracts of gerbil tissues show increased sensitivity to radiolytic oxidation with aging [243], but this is not the case for rat tissue extracts undergoing endogenous or metal-ion-catalysed oxidation [244]. Since the mechanisms of degradation of oxidized proteins are not established, it is perhaps premature to relate changes in the activity of individual proteolytic systems to the accumulation of oxidized proteins in aging (cf.…”

Section: Protein Oxidation In Aging and In Selected Pathologies Agingmentioning

confidence: 99%

Biochemistry and pathology of radical-mediated protein oxidation

Dean

Stocker

et al. 1997

Biochemical Journal

1,546

982

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Radical-mediated damage to proteins may be initiated by electron leakage, metal-ion-dependent reactions and autoxidation of lipids and sugars. The consequent protein oxidation is O2-dependent, and involves several propagating radicals, notably alkoxyl radicals. Its products include several categories of reactive species, and a range of stable products whose chemistry is currently being elucidated. Among the reactive products, protein hydroperoxides can generate further radical fluxes on reaction with transition-metal ions; protein-bound reductants (notably dopa) can reduce transition-metal ions and thereby facilitate their reaction with hydroperoxides; and aldehydes may participate in Schiff-base formation and other reactions. Cells can detoxify some of the reactive species, e.g. by reducing protein hydroperoxides to unreactive hydroxides. Oxidized proteins are often functionally inactive and their unfolding is associated with enhanced susceptibility to proteinases. Thus cells can generally remove oxidized proteins by proteolysis. However, certain oxidized proteins are poorly handled by cells, and together with possible alterations in the rate of production of oxidized proteins, this may contribute to the observed accumulation and damaging actions of oxidized proteins during aging and in pathologies such as diabetes, atherosclerosis and neurodegenerative diseases. Protein oxidation may also sometimes play controlling roles in cellular remodelling and cell growth. Proteins are also key targets in defensive cytolysis and in inflammatory self-damage. The possibility of selective protection against protein oxidation (antioxidation) is raised.

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“…Increased levels of ROS and other reactive oxidants have been reported to cause oxidative modifications of lipids, proteins, and DNA in aged animals (Miquel and Weber, 1990;Chen et al, 2000). However, the results of studies investigating oxidative stress in ageing are still controversial (Cini and Moretti, 1995). In humans, there are limited and conflicting results in the literature (Kasapoglu and Ö zben, 2001;Balkan et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Age-related oxidative stress and antioxidant parameters in middle-aged and older European subjects: the ZENITH study

et al. 2005

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Objective: Oxidative stress has been reported to increase with ageing. However, the data in healthy humans remain controversial and studies in free-living elderly people are scarce. The objective of the present study was to compare age-related oxidative stress in late middle-aged and older free-living subjects. Design: The effect of ageing on oxidative stress and antioxidant parameters was investigated in 188 middle-aged subjects from Clermont-Ferrand (France) and Coleraine (UK), and in 199 older subjects from Grenoble (France) and Roma (Italy). Plasma thiol (SH) groups, define definition (TBAR's) and total glutathione (GSH), define definition (FRAP), and superoxide dismutase (SOD) activity were measured at baseline of the ZENITH study. Results: Plasma SH groups and FRAP and, surprisingly, TBAR's were significantly lower in free-living older subjects compared to younger subjects (Po0.001, Po0.001, Po0.01, respectively), but there was no significant differences in GSH levels. Conclusion: European free-living healthy older do not appear to be exposed to an acute oxidative stress. However, the highly significant positive correlation between plasma SH group oxidation or decreased FRAP and ageing is predictive of an increased risk of oxidative stress in older subjects. Moreover, the comparison between middle-aged and older subjects regarding oxidative stress parameters suggests also a progressive and slow decline of antioxidant status in healthy free-living older elderly and underline the impact on life-style factors on successful ageing.

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Studies on lipid peroxidation and protein oxidation in the aging brain

Cited by 127 publications

References 29 publications

Oxidative stress and dopamine depletion in an intrastriatal 6-hydroxydopamine model of Parkinson’s disease

Oxidative stress and dopamine depletion in an intrastriatal 6-hydroxydopamine model of Parkinson’s disease

Biochemistry and pathology of radical-mediated protein oxidation

Age-related oxidative stress and antioxidant parameters in middle-aged and older European subjects: the ZENITH study

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