Significance of hepatic xanthine oxidase and uric acid in aged and dietary restricted rats

Chung, Hae Young; Yu, Byung Pal

doi:10.1007/s11357-000-0013-x

Cited by 8 publications

(2 citation statements)

References 31 publications

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“…In the present study, XO activity significantly increased in control acute exercise group (AE) and GSE supplementation decreased XO activity to the control levels in acute exercise group. In the present study, hepatic XO was estimated as a marker of a free radical producing enzyme, because its acts as an initiator for superoxide anion generation in tissues under stress conditions (Chung and Yu, ). Liver has a very high metabolic rate (200 kcal/kg organ mass/day (Divald and Powell, )), which is associated with high oxygen flux, but this is significantly decreased during exercise.…”

Section: Discussionmentioning

confidence: 99%

Effects of Grape Seed Polyphenols on Oxidative Damage in Liver Tissue of Acutely and Chronically Exercised Rats

Belviranlı

Gökbel

Okudan

et al. 2012

Phytotherapy Research

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The objective of the present study was to investigate the effects of grape seed extract (GSE) supplementation on oxidative stress and antioxidant defense markers in liver tissue of acutely and chronically exercised rats. Rats were randomly assigned to six groups: Control (C), Control Chronic Exercise (CE), Control Acute Exercise (AE), GSE‐supplemented Control (GC), GSE‐supplemented Chronic Exercise(GCE) and GSE‐supplemented Acute Exercise (GAE). Rats in the chronic exercise groups were subjected to a six‐week treadmill running and in the acute exercise groups performed an exhaustive running. Rats in the GSE supplemented groups received GSE (100 mg.kg−1.day−1) in drinking water for 6 weeks. Liver tissues of the rats were taken for the analysis of malondialdehyde (MDA), nitric oxide (NO) levels and total antioxidant activity (AOA) and xanthine oxidase (XO) activities. MDA levels decreased with GSE supplementation in control groups but increased in acute and chronic exercise groups compared to their non‐supplemented control. NO levels increased with GSE supplementation. XO activities were higher in AE group compared to the CE group. AOA decreased with GSE supplementation. In conclusion, while acute exercise triggers oxidative stress, chronic exercise has protective role against oxidative stress. GSE has a limited antioxidant effect on exercise‐induced oxidative stress in liver tissue. Copyright © 2012 John Wiley & Sons, Ltd.

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Section: Discussionmentioning

confidence: 99%

Effects of Grape Seed Polyphenols on Oxidative Damage in Liver Tissue of Acutely and Chronically Exercised Rats

Belviranlı

Gökbel

Okudan

et al. 2012

Phytotherapy Research

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show abstract

“…Consequently, soluble analogs have also been synthesized, studied, and shown to be neuroprotective in ischemic brain injury in mice (Haberman et al , 2007). Dietary restriction, an intervention known to increase ischemic tolerance, has also been shown to increase uric acid levels thereby augmenting the anti-oxidative defense system with aging (Chung and Yu, 2000). …”

Section: Pharmacologic Therapiesmentioning

confidence: 99%

Mitochondrial function in hypoxic ischemic injury and influence of aging

Ham

Raju

2017

Progress in Neurobiology

260

205

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Mitochondria are a major target in hypoxic/ischemic injury. Mitochondrial impairment increases with age leading to dysregulation of molecular pathways linked to mitochondria. The perturbation of mitochondrial homeostasis and cellular energetics worsens outcome following hypoxic-ischemic insults in elderly individuals. In response to acute injury conditions, cellular machinery relies on rapid adaptations by modulating posttranslational modifications. Therefore, post-translational regulation of molecular mediators such as hypoxia-inducible factor 1α (HIF-1α), peroxisome proliferator-activated receptor γ coactivator α (PGC-1α), c-MYC, SIRT1 and AMPK play a critical role in the control of the glycolytic-mitochondrial energy axis in response to hypoxic-ischemic conditions. The deficiency of oxygen and nutrients leads to decreased energetic reliance on mitochondria, promoting glycolysis. The combination of pseudohypoxia, declining autophagy, and dysregulation of stress responses with aging adds to impaired host response to hypoxic-ischemic injury. Furthermore, intermitochondrial signal propagation and tissue wide oscillations in mitochondrial metabolism in response to oxidative stress are emerging as vital to cellular energetics. Recently reported intercellular transport of mitochondria through tunneling nanotubes also play a role in the response to and treatments for ischemic injury. In this review we attempt to provide an overview of some of the molecular mechanisms and potential therapies involved in the alteration of cellular energetics with aging and injury with a neurobiological perspective.

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Molecular inflammation hypothesis of aging based on the anti‐aging mechanism of calorie restriction

Chung

Kim

et al. 2002

Microscopy Res & Technique

Self Cite

272

186

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Accumulating evidence strongly suggests that oxidative stress underlies aging processes. Research provides consistent evidence that calorie restriction (CR) reduces age-related oxidative stress and has anti-inflammatory properties. However, information is lacking on the molecular mechanism that would better define the interrelation of reactive oxygen species and nitrogen species and the pro-inflammatory states of the aging process. In this review, the biochemical and molecular bases of the inflammatory process in the aging process are analyzed to delineate the molecular inflammation hypothesis of aging. The key players involved in the proposed hypothesis are the age-related upregulation of NF-kappa B, IL-1 beta, IL-6, TNFalpha, cyclooxygenase-2, and inducible NO synthase, all of which are attenuated by CR. Furthermore, age-related NF kappa B activation is associated with phosphorylation by I kappa B kinase/NIK and MAPKs, while CR blocked these activation processes. The modulation of these factors provides molecular insights of the anti-inflammatory action of CR in relation to the aging process. Based on available finding and our recent supporting evidence, we prefer to use "molecular inflammation" to emphasize the importance of the molecular reaction mechanisms and their aberrance, predisposing to fully expressed chronic inflammatory phenomena. It was further proposed that CR's major force of the regulation of redox-sensitive inflammation may well be its life-prolonging action.

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Significance of hepatic xanthine oxidase and uric acid in aged and dietary restricted rats

Cited by 8 publications

References 31 publications

Effects of Grape Seed Polyphenols on Oxidative Damage in Liver Tissue of Acutely and Chronically Exercised Rats

Effects of Grape Seed Polyphenols on Oxidative Damage in Liver Tissue of Acutely and Chronically Exercised Rats

Mitochondrial function in hypoxic ischemic injury and influence of aging

Molecular inflammation hypothesis of aging based on the anti‐aging mechanism of calorie restriction

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