Biological Redox Systems and Oxidative Stress

Sies, Helmut

doi:10.1007/s00018-007-7230-8

Cited by 45 publications

(34 citation statements)

References 24 publications

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“…Oxidative stress is defined as an imbalance between the levels of pro-oxidants and antioxidants, resulting in macromolecular damage and disruption of redox signalling and controls [133]. Macromolecular damage usually occurs via oxidative mechanisms linked to free radicals, including O 2 − , NO and OH − (hydroxyl ions).…”

Section: Ampk and The Oxidative Stress Responsementioning

confidence: 99%

AMP-activated protein kinase, stress responses and cardiovascular diseases

2012

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AMPK (AMP-activated protein kinase) is one of the key players in maintaining intracellular homoeostasis. AMPK is well known as an energy sensor and can be activated by increased intracellular AMP levels. Generally, the activation of AMPK turns on catabolic pathways that generate ATP, while inhibiting cell proliferation and biosynthetic processes that consume ATP. In recent years, intensive investigations on the regulation and the function of AMPK indicates that AMPK not only functions as an intracellular energy sensor and regulator, but is also a general stress sensor that is important in maintaining intracellular homoeostasis during many kinds of stress challenges. In the present paper, we will review recent literature showing that AMPK functions far beyond its proposed energy sensor and regulator function. AMPK regulates ROS (reactive oxygen species)/redox balance, autophagy, cell proliferation, cell apoptosis, cellular polarity, mitochondrial function and genotoxic response, either directly or indirectly via numerous downstream pathways under physiological and pathological conditions.

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Section: Ampk and The Oxidative Stress Responsementioning

confidence: 99%

AMP-activated protein kinase, stress responses and cardiovascular diseases

2012

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“…Oxidative stress reflects an imbalance between reactive oxygen species (ROS) production and antioxidant defense, favoring the oxidant environment [1, 2]. Both intracellular redox status and oxidative stress are known to be involved in inflammation and aging [3–6].…”

Section: Introductionmentioning

confidence: 99%

Redox regulation of SIRT1 in inflammation and cellular senescence

Hwang¹,

Yao²,

Caito³

et al. 2013

Free Radical Biology and Medicine

425

341

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Sirtuin1 (SIRT1) regulates inflammation, aging (lifespan and healthspan), calorie restriction/energetics, mitochondrial biogenesis, stress resistance, cellular senescence, endothelial functions, apoptosis/autophagy, and circadian rhythms through deacetylation of transcription factors and histones. SIRT1 level and activity are decreased in chronic inflammatory conditions and aging where oxidative stress occurs. SIRT1 is regulated by a NAD+-dependent DNA repair enzyme poly(ADP-ribose)-polymerase-1 (PARP-1), and subsequent NAD+ depletion by oxidative stresses may have consequent effects on inflammatory and stress responses as well as cellular senescence. SIRT1 has been shown to undergo covalent oxidative modifications by cigarette smoke-derived oxidants/aldehydes, leading to post-translational modifications, inactivation, and protein degradation. Furthermore, oxidant/carbonyl stress-mediated reduction of SIRT1 leads to the loss of its control on acetylation of target proteins including p53, RelA/p65 and FOXO3, thereby enhancing the inflammatory, pro-senescent and apoptotic responses, as well as endothelial dysfunction. In this review, the mechanisms of cigarette smoke/oxidant-mediated redox post-translational modifications of SIRT1 and its role in PARP1, NF-κB activation, FOXO3 and eNOS regulation, as well as chromatin remodeling/histone modifications during inflammaging are discussed. Furthermore, we also discussed various novel ways to activate SIRT1 either directly or indirectly, which may have therapeutic potential in attenuating inflammation and premature senescence involved in chronic lung diseases.

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“…More recently, some authors believe that it is not only an imbalance or a single entity, since redox of plasma GSH/GSSG is not equilibrated with the larger plasma cysteine/cystine (Cys/CySS) pool. Thus, from a mechanistic standpoint, oxidative stress may be better defined as a disruption of redox signaling and control [16,17]. …”

Section: Introductionmentioning

confidence: 99%

Antioxidant intake among Brazilian adults - The Brazilian Osteoporosis Study (BRAZOS): a cross-sectional study

Pinheiro

Ciconelli²,

Chaves

et al. 2011

Nutr J

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BackgroundAntioxidant nutrient intake and the lesser formation of free radicals seem to contribute to chronic diseases. The aim of the present study was to evaluate the intake profile of the main dietary antioxidants in a representative sample of the adult Brazilian population and discuss the main consequences of a low intake of these micronutrients on overall health.MethodsThe sample comprised 2344 individuals aged 40 years or older from 150 cities and was based on a probabilistic sample from official data. The research was conducted through in-home interviews administered by a team trained for this purpose. Dietary intake information was obtained through 24-h recall. The Nutrition Data System for Research software program was used to analyze data on the intake of vitamins A, C and E, selenium and zinc, which was compared to Dietary Reference Intakes (DRIs). Differences in intake according to sex, anthropometrics, socioeconomic status and region were also evaluated. The SPSS statistical package (version 13) was used for the statistical analysis. P-values < 0.05 were considered significant.ResultsHigher proportions of low intake in relation to recommended values were found for vitamin E (99.7%), vitamin A (92.4%) and vitamin C (85.1%) in both genders. Intake variations were found between different regions, which may reflect cultural habits.ConclusionThese results should lead to the development of public health policies that encourage educational strategies for improving the intake of micronutrients, which are essential to overall health and prevention of non-communicable diseases.

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Biological Redox Systems and Oxidative Stress

Cited by 45 publications

References 24 publications

AMP-activated protein kinase, stress responses and cardiovascular diseases

AMP-activated protein kinase, stress responses and cardiovascular diseases

Redox regulation of SIRT1 in inflammation and cellular senescence

Antioxidant intake among Brazilian adults - The Brazilian Osteoporosis Study (BRAZOS): a cross-sectional study

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