Caffeine alters oxidative homeostasis in the body of BALB/c mice

Pohanka, Miroslav

doi:10.4149/bll_2014_135

Cited by 5 publications

(3 citation statements)

References 45 publications

(31 reference statements)

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“…Caffeine also reduced hydrogen levels in lung cells in vitro [ 62 ]. In mice, caffeine reduces lipid peroxidation [ 63 ]. Cytokine and anti-oxidative enzyme over expression in normoxic exposure could be protective in oxidative stress models [ 64 , 65 ].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotection by Caffeine in Hyperoxia-Induced Neonatal Brain Injury

Endesfelder

Weichelt

Strauss

et al. 2017

IJMS

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Sequelae of prematurity triggered by oxidative stress and free radical-mediated tissue damage have coined the term “oxygen radical disease of prematurity”. Caffeine, a potent free radical scavenger and adenosine receptor antagonist, reduces rates of brain damage in preterm infants. In the present study, we investigated the effects of caffeine on oxidative stress markers, anti-oxidative response, inflammation, redox-sensitive transcription factors, apoptosis, and extracellular matrix following the induction of hyperoxia in neonatal rats. The brain of a rat pups at postnatal Day 6 (P6) corresponds to that of a human fetal brain at 28–32 weeks gestation and the neonatal rat is an ideal model in which to investigate effects of oxidative stress and neuroprotection of caffeine on the developing brain. Six-day-old Wistar rats were pre-treated with caffeine and exposed to 80% oxygen for 24 and 48 h. Caffeine reduced oxidative stress marker (heme oxygenase-1, lipid peroxidation, hydrogen peroxide, and glutamate-cysteine ligase catalytic subunit (GCLC)), promoted anti-oxidative response (superoxide dismutase, peroxiredoxin 1, and sulfiredoxin 1), down-regulated pro-inflammatory cytokines, modulated redox-sensitive transcription factor expression (Nrf2/Keap1, and NFκB), reduced pro-apoptotic effectors (poly (ADP-ribose) polymerase-1 (PARP-1), apoptosis inducing factor (AIF), and caspase-3), and diminished extracellular matrix degeneration (matrix metalloproteinases (MMP) 2, and inhibitor of metalloproteinase (TIMP) 1/2). Our study affirms that caffeine is a pleiotropic neuroprotective drug in the developing brain due to its anti-oxidant, anti-inflammatory, and anti-apoptotic properties.

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Section: Discussionmentioning

confidence: 99%

Neuroprotection by Caffeine in Hyperoxia-Induced Neonatal Brain Injury

Endesfelder

Weichelt

Strauss

et al. 2017

IJMS

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“…The assay was performed using instructions by manufacturer. Total level of antioxidants by Ferric Reducing Antioxidant Power (FRAP), reduced glutathione (GSH) and malondialdehyde by Thiobarbituric Acid Reactive Substances (TBARS) assay were done using earlier written protocols (12)(13)(14).…”

Section: Determining Of Markersmentioning

confidence: 99%

Freund´s complete adjuvant effect on BALB/c mice: an insight into inflammation and oxidative stress after immunity challenge

Pohanka¹,

Vobornikova²,

Fusek³

2016

BLL

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Freund´s complete adjuvant (FCA) is a mean used for improving immunization effi cacy in experiments and veterinary medicine. Despite high effi cacy, it is not used in human vaccination due to number of adverse effects. Arthritis can be an example of a typical adverse consequence. In this work, we decided to investigate the link between oxidative stress and infl ammation in animals exposed to FCA. BALB/c mice received either saline or FCA in doses 10-50 μl and were euthanized from one to three days after infection. Interleukins (IL) IL-2, IL-4 and tumor necrosis factor α (TNF-α) were determined in plasma. Ferric reducing antioxidant power (FRAP), malondialdehyde by thiobarbituric acid reactive substances assay (TBARS), reduced glutathione (GSH) and caspase-3 were measured in livers, muscles and other organs. We determined signifi cant effect of FCA on TBARS and GSH in the livers. Beside this, TBARS were altered in muscles as well. Infl ammation was confi rmed by increased level of TNF-α. Taking the results into account, we infer that the harmful effect of FCA is mediated not only by infl ammation but also by oxidative. This should be considered when pathological consequences of FCA are scored (Fig. 4, Ref. 21). Text in PDF www.elis.sk.

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“…The marker malondialdehyde, a product of membrane oxidative degradation was determined by assessing contents of thiobarbituric acid reactive substances (TBARS), using the spectrophotometric procedure (absorbance 532 nm) of Pohanka (2014). Glutathione reductase (GR) is an antioxidant enzyme that produces reduced glutathione in its oxidised form.…”

Section: Methodsmentioning

confidence: 99%

Oxidative stress response of rainbow trout (Oncorhynchus mykiss) to multiple stressors

et al. 2018

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Fish can be exposed to multiple stressors at the same time, including natural toxins, environmental pollutants or feed contamination. In this study, we report on the effects of controlled exposure of rainbow trout (Oncorhynchus mykiss) to multiple stressors. In doing so, we test the hypothesis that cyanobacterial biomass and arsenic in feed combine to enhance negative effects on fish, including modulation of antioxidant response. The trout (mean weight 288 ± 59 g) were divided into six experimental groups of 25 fish each (C -control group; B -3% lyophilised toxic cyanobacterial biomass; As5 -arsenic at 5 mg·kg -1 ; As50 -arsenic at 50 mg·kg -1 ; and two combinations of cyanobacterial biomass and arsenic (B+As5 and B+As50). All indicators of oxidative stress were determined using standard methods, showing significant changes. Overall antioxidant capacity (ferric reducing antioxidant power) decreased significantly in the liver, gills and heart after 10-days, while lipid peroxidation (thiobarbituric acid reactive substances) increased in the liver of groups exposed to cyanobacterial biomass, and in the heart of groups exposed to increased concentrations of arsenic and those under combined exposure. Levels of glutathione reductase showed a significant reduction following exposure, especially in the gills and liver. Our results indicate that the antioxidant system plays an important role in the protective response of tissues to stressors, and especially arsenic.

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Caffeine alters oxidative homeostasis in the body of BALB/c mice

Cited by 5 publications

References 45 publications

Neuroprotection by Caffeine in Hyperoxia-Induced Neonatal Brain Injury

Neuroprotection by Caffeine in Hyperoxia-Induced Neonatal Brain Injury

Freund´s complete adjuvant effect on BALB/c mice: an insight into inflammation and oxidative stress after immunity challenge

Oxidative stress response of rainbow trout (Oncorhynchus mykiss) to multiple stressors

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