Mitochondrial dysfunction in the hippocampus of rats caused by chronic oxidative stress

Rodrı́guez-Martı́nez, Erika; Martı́nez, Federico; Espinosa-García, María Teresa; Maldonado, Perla D.; Rivas‐Arancibia, Selva

doi:10.1016/j.neuroscience.2013.08.018

Cited by 43 publications

(40 citation statements)

References 39 publications

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“…This first stage may be considered to represent an initial process of the conformational changes, even though other studies demonstrate that, during this stage, there is an increase of lipid oxidation and oxidized proteins, as well as an increase in inflammation markers (Rivas-Arancibia et al, 2010; Rodríguez-Martínez et al, 2013). …”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, there exists a clear process of progressive neurodegeneration followed by a major increase of oxidized biomolecules, mitochondrial deficit and a decrease of antioxidant systems (Rodríguez-Martínez et al, 2013). The above may indicate that, unlike Aβ 1–40, which is commonly formed in the brain (Yin et al, 2007), Aβ 1–42 shows a change in its spatial conformation, promoted by oxidative stress (Butterfield et al, 2013; Korshavn et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

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Structural Changes of Amyloid Beta in Hippocampus of Rats Exposed to Ozone: A Raman Spectroscopy Study

Rivas‐Arancibia

Rodrı́guez-Martı́nez

Badillo‐Ramírez

et al. 2017

Front. Mol. Neurosci.

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The aim of this work was to study the effect of oxidative stress on the structural changes of the secondary peptide structure of amyloid beta 1–42 (Aβ 1–42), in the dentate gyrus of hippocampus of rats exposed to low doses of ozone. The animals were exposed to ozone-free air (control group) and 0.25 ppm ozone during 7, 15, 30, 60, and 90 days, respectively. The samples were studied by: (1) Raman spectroscopy to detect the global conformational changes in peptides with α-helix and β-sheet secondary structure, following the deconvolution profile of the amide I band; and (2) immunohistochemistry against Aβ 1–42. The results of the deconvolutions of the amide I band indicate that, ozone exposure causes a progressively decrease in the abundance percentage of α-helix secondary structure. Furthermore, the β-sheet secondary structure increases its abundance percentage. After 60 days of ozone exposure, the β-sheet band is identified in a similar wavenumber of the Aβ 1–42 peptide standard. Immunohistochemistry assays show an increase of Aβ 1–42 immunoreactivity, coinciding with the conformational changes observed in the Raman spectroscopy of Aβ 1–42 at 60 and 90 days. In conclusion, oxidative stress produces changes in the folding process of amyloid beta peptide structure in the dentate gyrus, leading to its conformational change in a final β-sheet structure. This is associated to an increase in Aβ 1–42 expression, similar to the one that happens in the brain of Alzheimer’s Disease (AD) patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Structural Changes of Amyloid Beta in Hippocampus of Rats Exposed to Ozone: A Raman Spectroscopy Study

Rivas‐Arancibia

Rodrı́guez-Martı́nez

Badillo‐Ramírez

et al. 2017

Front. Mol. Neurosci.

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“…This finding suggests that FoxO 3a has a regulatory role in response to increasing oxidative stress generated by exposure to low doses of ozone. Previous experiments by our group have shown that the activity of this enzyme does not correlate with the increased expression demonstrated here; this may suggest a blockade of activity caused by oxidative damage to the enzyme structure [20]. …”

Section: Discussionmentioning

confidence: 55%

Oxidative Stress Activates the Transcription Factors FoxO 1a and FoxO 3a in the Hippocampus of Rats Exposed to Low Doses of Ozone

Gómez-Crisóstomo

Martínez

Rivas‐Arancibia

2014

Oxidative Medicine and Cellular Longevity

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The exposure to low doses of ozone induces an oxidative stress state, which is involved in neurodegenerative diseases. Forkhead box O (FoxO) family of transcription factors are activated by oxidative signals and regulate cell proliferation and resistance to oxidative stress. Our aim was to study the effect of chronic exposure to ozone on the activation of FoxO 1a and FoxO 3a in the hippocampus of rats. Male Wistar rats were divided into six groups and exposed to 0.25 ppm of ozone for 0, 7, 15, 30, 60, and 90 days. After treatment, the groups were processed for western blotting and immunohistochemistry against FoxO 3a, Mn SOD, cyclin D2, FoxO 1a, and active caspase 3. We found that exposure to ozone increased the activation of FoxO 3a at 30 and 60 days and expression of Mn SOD at all treatment times. Additionally, increases in cyclin D2 from 7 to 90 days; FoxO 1a at 15, 30, and 60 days; and activate caspase 3 from 30 to 60 days of exposure were noted. The results indicate that ozone alters regulatory pathways related to both the antioxidant system and the cell cycle, inducing neuronal reentry into the cell cycle and apoptotic death.

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“…Oxidative stress has profound effect on cellular viability and damage in a range of different pathologies (Wang et al 2013a, b;Rodríguez-Martínez et al 2013). Mitochondria have been found to be essential in controlling at least certain apoptosis pathways (Green and Reed 1998).…”

Section: Stress-related Depressionmentioning

confidence: 99%

Role of Stress, Depression, and Aging in Cognitive Decline and Alzheimer’s Disease

Daulatzai

2014

Behavioral Neurobiology of Stress-Related Disorders

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Late-onset Alzheimer's disease (AD) is a chronic neurodegenerative disorder and the most common cause of progressive cognitive dysfunction and dementia. Despite considerable progress in elucidating the molecular pathology of this disease, we are not yet close to unraveling its etiopathogenesis. A battery of neurotoxic modifiers may underpin neurocognitive pathology via deleterious heterogeneous pathologic impact in brain regions, including the hippocampus. Three important neurotoxic factors being addressed here include aging, stress, and depression. Unraveling "upstream pathologies" due to these disparate neurotoxic entities, vis-à-vis cognitive impairment involving hippocampal dysfunction, is of paramount importance. Persistent systemic inflammation triggers and sustains neuroinflammation. The latter targets several brain regions including the hippocampus causing upregulation of amyloid beta and neurofibrillary tangles, synaptic and neuronal degeneration, gray matter volume atrophy, and progressive cognitive decline. However, what is the fundamental source of this peripheral inflammation in aging, stress, and depression? This chapter highlights and delineates the inflammatory involvement-i.e., from its inception from gut to systemic inflammation to neuroinflammation. It highlights an upregulated cascade in which gut-microbiota-related dysbiosis generates lipopolysaccharides (LPS), which enhances inflammation and gut's leakiness, and through a Web of interactions, it induces stress and depression. This may increase neuronal dysfunction and apoptosis, promote learning and memory impairment, and enhance vulnerability to cognitive decline.

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Mitochondrial dysfunction in the hippocampus of rats caused by chronic oxidative stress

Cited by 43 publications

References 39 publications

Structural Changes of Amyloid Beta in Hippocampus of Rats Exposed to Ozone: A Raman Spectroscopy Study

Structural Changes of Amyloid Beta in Hippocampus of Rats Exposed to Ozone: A Raman Spectroscopy Study

Oxidative Stress Activates the Transcription Factors FoxO 1a and FoxO 3a in the Hippocampus of Rats Exposed to Low Doses of Ozone

Role of Stress, Depression, and Aging in Cognitive Decline and Alzheimer’s Disease

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