Hepatic Oxidative Stress During Aging: Effects of 8% Long-Term Calorie Restriction and Lifelong Exercise

2006 ◽  
Vol 8 (3-4) ◽  
pp. 529-538 ◽  
Author(s):  
Arnold Y. Seo ◽  
Tim Hofer ◽  
Bokyung Sung ◽  
Sharon Judge ◽  
Hae Y. Chung ◽  
...  
2005 ◽  
Vol 288 (4) ◽  
pp. E674-E684 ◽  
Author(s):  
Kevork Hagopian ◽  
Mary-Ellen Harper ◽  
Jesmon J. Ram ◽  
Stephen J. Humble ◽  
Richard Weindruch ◽  
...  

Calorie restriction (CR) without malnutrition increases maximal life span in diverse species. It has been proposed that reduction in energy expenditure and reactive oxygen species (ROS) production could be a mechanism for life span extension with CR. As a step toward testing this theory, mitochondrial proton leak, H2O2 production, and markers of oxidative stress were measured in liver from FBNF1 rats fed control or 40% CR diets for 12 or 18 mo. CR was initiated at 6 mo of age. Proton leak kinetics curves, generated from simultaneous measures of oxygen consumption and membrane potential, indicated a decrease in proton leak after 18 mo of CR, while only a trend toward a proton leak decrease was observed after 12 mo. Significant shifts in phosphorylation and substrate oxidation curves also occurred with CR; however, these changes occurred in concert with the proton leak changes. Metabolic control analysis indicated no difference in the overall pattern of control of the oxidative phosphorylation system between control and CR animals. At 12 mo, no significant differences were observed between groups for H2O2 production or markers of oxidative stress. However, at 18 mo, protein carbonyl content was lower in CR animals, as was H2O2 production when mitochondria were respiring on either succinate alone or pyruvate plus malate in the presence of rotenone. These results indicate that long-term CR lowers mitochondrial proton leak and H2O2 production, and this is consistent with the idea that CR may act by decreasing energy expenditure and ROS production.


Biology Open ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. bio047282
Author(s):  
Ellen Mayara Souza Cruz ◽  
Juliana Maria Bitencourt de Morais ◽  
Carlos Vinícius Dalto da Rosa ◽  
Mellina da Silva Simões ◽  
Jurandir Fernando Comar ◽  
...  

2021 ◽  
Vol 750 ◽  
pp. 141569
Author(s):  
Branka R. Gavrilović ◽  
Tamara G. Petrović ◽  
Tijana B. Radovanović ◽  
Svetlana G. Despotović ◽  
Jelena P. Gavrić ◽  
...  

IUBMB Life ◽  
2019 ◽  
Vol 71 (12) ◽  
pp. 1973-1985 ◽  
Author(s):  
Munevver B. Cicekdal ◽  
Bilge G. Tuna ◽  
Mohammad Charehsaz ◽  
Margot P. Cleary ◽  
Ahmet Aydin ◽  
...  

Author(s):  
Arindam Bhattacharyya ◽  
Debaprasad Mandal ◽  
Lakshmishri Lahiry ◽  
Sankar Bhattacharyya ◽  
Sreya Chattopadhyay ◽  
...  

2021 ◽  
Author(s):  
Jingda Li ◽  
Tianqi Wang ◽  
Panpan Liu ◽  
Fuyuan Yang ◽  
Xudong Wang ◽  
...  

Hesperetin as a major bioflavonoid in citrus fruits improves NAFLD by suppressing hepatic oxidative stress and inflammation.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bailey Hiles-Murison ◽  
Andrew P. Lavender ◽  
Mark J. Hackett ◽  
Joshua J. Armstrong ◽  
Michael Nesbit ◽  
...  

AbstractRepeated sub-concussive impact (e.g. soccer ball heading), a significantly lighter form of mild traumatic brain injury, is increasingly suggested to cumulatively alter brain structure and compromise neurobehavioural function in the long-term. However, the underlying mechanisms whereby repeated long-term sub-concussion induces cerebral structural and neurobehavioural changes are currently unknown. Here, we utilised an established rat model to investigate the effects of repeated sub-concussion on size of lateral ventricles, cerebrovascular blood–brain barrier (BBB) integrity, neuroinflammation, oxidative stress, and biochemical distribution. Following repeated sub-concussion 3 days per week for 2 weeks, the rats showed significantly enlarged lateral ventricles compared with the rats receiving sham-only procedure. The sub-concussive rats also presented significant BBB dysfunction in the cerebral cortex and hippocampal formation, whilst neuromotor function assessed by beamwalk and rotarod tests were comparable to the sham rats. Immunofluorescent and spectroscopic microscopy analyses revealed no significant changes in neuroinflammation, oxidative stress, lipid distribution or protein aggregation, within the hippocampus and cortex. These data collectively indicate that repeated sub-concussion for 2 weeks induce significant ventriculomegaly and BBB disruption, preceding neuromotor deficits.


Antioxidants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 25
Author(s):  
Lara Macchioni ◽  
Davide Chiasserini ◽  
Letizia Mezzasoma ◽  
Magdalena Davidescu ◽  
Pier Luigi Orvietani ◽  
...  

Age-related retinal degenerations, including age-related macular degeneration (AMD), are caused by the loss of retinal pigmented epithelial (RPE) cells and photoreceptors. The pathogenesis of AMD, deeply linked to the aging process, also involves oxidative stress and inflammatory responses. However, the molecular mechanisms contributing to the shift from healthy aging to AMD are still poorly understood. Since RPE cells in the retina are chronically exposed to a pro-oxidant microenvironment throughout life, we simulated in vivo conditions by growing ARPE-19 cells in the presence of 10 μM H2O2 for several passages. This long-term oxidative insult induced senescence in ARPE-19 cells without affecting cell proliferation. Global proteomic analysis revealed a dysregulated expression in proteins involved in antioxidant response, mitochondrial homeostasis, and extracellular matrix organization. The analyses of mitochondrial functionality showed increased mitochondrial biogenesis and ATP generation and improved response to oxidative stress. The latter, however, was linked to nuclear factor-κB (NF-κB) rather than nuclear factor erythroid 2–related factor 2 (Nrf2) activation. NF-κB hyperactivation also resulted in increased pro-inflammatory cytokines expression and inflammasome activation. Moreover, in response to additional pro-inflammatory insults, senescent ARPE-19 cells underwent an exaggerated inflammatory reaction. Our results indicate senescence as an important link between chronic oxidative insult and detrimental chronic inflammation, with possible future repercussions for therapeutic interventions.


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