scholarly journals Nutraceutical Supplementation Ameliorates Visual Function, Retinal Degeneration, and Redox Status in rd10 Mice

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1033
Author(s):  
Lorena Olivares-González ◽  
Sheyla Velasco ◽  
Isabel Campillo ◽  
David Salom ◽  
Emilio González-García ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Retinal Degeneration ◽  
Antioxidant Properties ◽  
Photoreceptor Cells ◽  
Redox Status ◽  
Inherited Retinal Dystrophies ◽  
Stress Markers ◽  
Retinal Dystrophies ◽  
Progressive Degeneration ◽  
Light Stimuli

Background: Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies characterized by progressive degeneration of photoreceptor cells. Ocular redox status is altered in RP suggesting oxidative stress could contribute to their progression. In this study, we investigated the effect of a mixture of nutraceuticals with antioxidant properties (NUT) on retinal degeneration in rd10 mice, a model of RP. Methods: NUT was orally administered to rd10 mice from postnatal day (PD) 9 to PD18. At PD18 retinal function and morphology were examined by electroretinography (ERG) and histology including TUNEL assay, immunolabeling of microglia, Müller cells, and poly ADP ribose polymers. Retinal redox status was determined by measuring the activity of antioxidant enzymes and some oxidative stress markers. Gene expression of the cytokines IL-6, TNFα, and IL-1β was assessed by real-time PCR. Results: NUT treatment delayed the loss of photoreceptors in rd10 mice partially preserving their electrical responses to light stimuli. Moreover, it ameliorated redox status and reduced inflammation including microglia activation, upregulation of cytokines, reactive gliosis, and PARP overactivation. Conclusions: NUT ameliorated retinal functionality and morphology at early stages of RP in rd10 mice. This formulation could be useful as a neuroprotective approach for patients with RP in the future.

scholarly journals On the Wrong Track: Alterations of Ciliary Transport in Inherited Retinal Dystrophies

2021 ◽  
Vol 9 ◽  
Author(s):  
Laura Sánchez-Bellver ◽  
Vasileios Toulis ◽  
Gemma Marfany
Keyword(s):  
Retinal Degeneration ◽  
Outer Segment ◽  
Molecular Mechanisms ◽  
Photoreceptor Cells ◽  
Cellular Functions ◽  
Inherited Disorders ◽  
Inherited Retinal Dystrophies ◽  
Retinal Dystrophies ◽  
Elevated Protein ◽  
And Function

Ciliopathies are a group of heterogeneous inherited disorders associated with dysfunction of the cilium, a ubiquitous microtubule-based organelle involved in a broad range of cellular functions. Most ciliopathies are syndromic, since several organs whose cells produce a cilium, such as the retina, cochlea or kidney, are affected by mutations in ciliary-related genes. In the retina, photoreceptor cells present a highly specialized neurosensory cilium, the outer segment, stacked with membranous disks where photoreception and phototransduction occurs. The daily renewal of the more distal disks is a unique characteristic of photoreceptor outer segments, resulting in an elevated protein demand. All components necessary for outer segment formation, maintenance and function have to be transported from the photoreceptor inner segment, where synthesis occurs, to the cilium. Therefore, efficient transport of selected proteins is critical for photoreceptor ciliogenesis and function, and any alteration in either cargo delivery to the cilium or intraciliary trafficking compromises photoreceptor survival and leads to retinal degeneration. To date, mutations in more than 100 ciliary genes have been associated with retinal dystrophies, accounting for almost 25% of these inherited rare diseases. Interestingly, not all mutations in ciliary genes that cause retinal degeneration are also involved in pleiotropic pathologies in other ciliated organs. Depending on the mutation, the same gene can cause syndromic or non-syndromic retinopathies, thus emphasizing the highly refined specialization of the photoreceptor neurosensory cilia, and raising the possibility of photoreceptor-specific molecular mechanisms underlying common ciliary functions such as ciliary transport. In this review, we will focus on ciliary transport in photoreceptor cells and discuss the molecular complexity underpinning retinal ciliopathies, with a special emphasis on ciliary genes that, when mutated, cause either syndromic or non-syndromic retinal ciliopathies.

scholarly journals Oxidative Stress and Marine Carotenoids: Application by Using Nanoformulations

Marine Drugs ◽  
2020 ◽  
Vol 18 (8) ◽  
pp. 423 ◽  
Author(s):  
Yasin Genç ◽  
Hilal Bardakci ◽  
Çiğdem Yücel ◽  
Gökçe Şeker Karatoprak ◽  
Esra Küpeli Akkol ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Properties ◽  
Chemical Diversity ◽  
Biologically Active ◽  
Bioactive Molecules ◽  
Photosynthetic Organisms ◽  
Stress Markers ◽  
Potential Applications ◽  
Health Promoting ◽  
Cancer Types

Carotenoids are natural fat-soluble pigments synthesized by plants, algae, fungi and microorganisms. They are responsible for the coloration of different photosynthetic organisms. Although they play a role in photosynthesis, they are also present in non-photosynthetic plant tissues, fungi, and bacteria. These metabolites have mainly been used in food, cosmetics, and the pharmaceutical industry. In addition to their utilization as pigmentation, they have significant therapeutically applications, such as improving immune system and preventing neurodegenerative diseases. Primarily, they have attracted attention due to their antioxidant activity. Several statistical investigations indicated an association between the use of carotenoids in diets and a decreased incidence of cancer types, suggesting the antioxidant properties of these compounds as an important factor in the scope of the studies against oxidative stress. Unusual marine environments are associated with a great chemical diversity, resulting in novel bioactive molecules. Thus, marine organisms may represent an important source of novel biologically active substances for the development of therapeutics. Marine carotenoids (astaxanthin, fucoxanthin, β-carotene, lutein but also the rare siphonaxanthin, sioxanthin, and myxol) have recently shown antioxidant properties in reducing oxidative stress markers. Numerous of bioactive compounds such as marine carotenoids have low stability, are poorly absorbed, and own very limited bioavailability. The new technique is nanoencapsulation, which can be used to preserve marine carotenoids and their original properties during processing, storage, improve their physiochemical properties and increase their health-promoting effects. This review aims to describe the role of marine carotenoids, their potential applications and different types of advanced nanoformulations preventing and treating oxidative stress related disorders.

scholarly journals Sequential Analysis of Oxidative Stress Markers and Vitamin C Status in Acute Bacterial Osteomyelitis

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Rade Grbic ◽  
Dijana J Miric ◽  
Bojana Kisic ◽  
Ljiljana Popovic ◽  
Vojkan Nestorovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Sequential Analysis ◽  
Bone Cells ◽  
Redox Status ◽  
Oxidative Stress Markers ◽  
Total Vitamin ◽  
Baseline Serum ◽  
Stress Markers ◽  
Systemic Oxidative Stress

In bacterial bone infections, excessively formed oxidants may result in local and systemic oxidative stress. Vitamin C is the major extracellular nonenzymatic antioxidant, also implicated in bone cells metabolism and viability. The physiological functions of vitamin C largely depend on its redox status. We sequentially assessed oxidative stress markers, hydroperoxides and malondialdehyde (MDA), total antioxidant activity (AOA), total vitamin C, ascorbic acid (Asc), and oxidized/reduced vitamin C ratio in 137 patients with acute osteomyelitis (OM). Compared to 52 healthy controls, in OM group baseline serum hydroperoxides, MDA and oxidized/reduced vitamin C ratio were higher whilst Asc and AOA were lower (P < 0.05, resp.). On the other side, total vitamin C levels in patients and controls were similar(P > 0.05), thereby suggesting a relative rather than absolute vitamin C deficiency in OM. During the follow-up, oxidative stress markers, AOA, and oxidizedreduced vitamin C ratio were gradually returned to normal, while there was no apparent change of total vitamin C concentrations. Persistently high values of oxidized/reduced vitamin C ratio and serum MDA were found in subacute OM. In conclusion, acute OM was associated with enhanced systemic oxidative stress and the shift of vitamin C redox status towards oxidized forms.

scholarly journals The Tryptophan Pathway Targeting Antioxidant Capacity in the Placenta

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Kang Xu ◽  
Gang Liu ◽  
Chenxing Fu
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Fetal Development ◽  
Antioxidant Properties ◽  
Redox Status ◽  
Kynurenine Pathway ◽  
Vital Role ◽  
Tryptophan Metabolites ◽  
Antioxidant Proteins ◽  
Hydroxyanthranilic Acid

The placenta plays a vital role in fetal development during pregnancy. Dysfunction of the placenta can be caused by oxidative stress and can lead to abnormal fetal development. Preventing oxidative stress of the placenta is thus an important measure to ensure positive birth outcomes. Research shows that tryptophan and its metabolites can efficiently clean free radicals (including the reactive oxygen species and activated chlorine). Consequently, tryptophan and its metabolites are suggested to act as potent antioxidants in the placenta. However, the mechanism of these antioxidant properties in the placenta is still unknown. In this review, we summarize research on the antioxidant properties of tryptophan, tryptophan metabolites, and metabolic enzymes. Two predicted mechanisms of tryptophan’s antioxidant properties are discussed. (1) Tryptophan could activate the phosphorylation of p62 after the activation of mTORC1; phosphorylated p62 then uncouples the interaction between Nrf2 and Keap1, and activated Nrf2 enters the nucleus to induce expressions of antioxidant proteins, thus improving cellular antioxidation. (2) 3-Hydroxyanthranilic acid, a tryptophan kynurenine pathway metabolite, changes conformation of Keap1, inducing the dissociation of Nrf2 and Keap1, activating Nrf2 to enter the nucleus and induce expressions of antioxidant proteins (such as HO-1), thereby enhancing cellular antioxidant capacity. These mechanisms may enrich the theory of how to apply tryptophan as an antioxidant during pregnancy, providing technical support for its use in regulating the pregnancy’s redox status and enriching our understanding of amino acids’ nutritional value.

scholarly journals Melatonin Modulation of Sirtuin-1 Attenuates Liver Injury in a Hypercholesterolemic Mouse Model

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Francesca Bonomini ◽  
Gaia Favero ◽  
Luigi Fabrizio Rodella ◽  
Mohammed H. Moghadasian ◽  
Rita Rezzani
Keyword(s):  
Oxidative Stress ◽  
Biochemical Markers ◽  
Antioxidant Properties ◽  
Sirtuin 1 ◽  
Oral Supplementation ◽  
Stress Markers ◽  
Serum Biochemical ◽  
Stress Signals

Hypercholesterolemia increases and exacerbates stress signals leading also to liver damage (LD) and failure. Sirtuin1 (SIRT1) is involved in lifespan extension and it plays an essential role in hepatic lipid metabolism. However, its involvement in liver hypercholesterolemic damage is not yet completely defined. This in vivo study evaluated the role of SIRT1 in the hypercholesterolemic-related LD and, then, investigated how oral supplementation of melatonin, pleiotropic indoleamine, may be protective. Control mice and apolipoprotein E-deficient mice (ApoE−/−) of 6 and 15 weeks of age were treated or not treated with melatonin at the dose of 10 mg/kg/day for 9 weeks. In this study, we evaluated serum biochemical markers, liver SIRT1 expression, and oxidative stress markers. We observed that hypercholesterolemia increased significantly serum cholesterol and triglycerides, reduced significantly liver SIRT1, and, in turn, induced hepatic oxidative stress in untreated ApoE−/− mice with respect to control mice. Interestingly, melatonin treatment improved serum biochemical markers and hepatic morphological impairment and inhibited oxidative stress through its antioxidant properties and also by SIRT1 upregulation. In summary, melatonin oral supplementation may represent a new protective approach to block hypercholesterolemic liver alterations involving also a SIRT1-dependent mechanism.

scholarly journals Sulphoraphane Supplementation Ameliorates Behavioural Impairments and Hippocampal Neurodegeneration Induced by Lead Exposure in Adult Wistar Rats

2020 ◽  
Vol 11 (2) ◽  
pp. 88-98
Author(s):  
Babatunde Ogunlade ◽  
◽  
Olasumbo Afolayan ◽  
Sunday Adelakun ◽  
◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Wistar Rats ◽  
Neurodegenerative Disorder ◽  
Antioxidant Properties ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Pb Exposure ◽  
Group B ◽  
Behavioural Tests

Lead (Pb) exposure induces oxidative stress causing imbalance in antioxidant enzymes, cognitive impairments and neurodegeneration. This study investigated the neuroprotective and antioxidant properties of sulphoraphane (SFN) on Pb-induced neurotoxicity of adult Wistar rats. Forty animals (150 ± 20 g) were divided into four groups (n=10): Group A received normal saline as placebo; Group B received 50 mg/kg body weight (bw) of Lead only; Group C received a combination of 50 mg/kg bw of Lead and 50 mg/kg bw of SFN; Group D received 50 mg/kg bw of SFN only. All administration was through oral gavages for 28 days; animals underwent behavioural tests (Morris water and Y- mazes); and thereafter sacrificed and brains extracted. Biochemical estimations of antioxidants (superoxide dismutase, reduced glutathione, and catalase), oxidative stress markers (malondialdehyde, nitric oxide, and hydrogen peroxide), neurotransmitters (dopamine, serotonin, and norepinephrine) and hippocampal histology were done. The results showed significant increase in escape latency, norepinephrine and oxidative stress markers with concomitant decrease percentage correct alternation, serotonin, dopamine and antioxidant enzymes in Pb exposed rats compared with the control. However, the co-administration of SFN and Pb significantly attenuated Pb neurotoxicity. Sulphoraphane is capable of ameliorating oxidative stress induced neurobehavioural deficits and hippocampal neurochemistry caused by Pb exposure in Alzheimer’s type animal model of neurodegenerative disorder.

scholarly journals Significance of Elevated Blood Metal Ion Levels in Patients with Metal-on-Metal Prostheses: An Evaluation of Oxidative Stress Markers

2010 ◽  
Vol 4 (1) ◽  
pp. 221-227 ◽  
Author(s):  
Cathy Tkaczyk ◽  
Alain Petit ◽  
John Antoniou ◽  
David J Zukor ◽  
Maryam Tabrizian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metal Ion ◽  
Biological Effects ◽  
Redox Status ◽  
Heme Oxygenase 1 ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Systemic Oxidative Stress ◽  
Metal On Metal ◽  
Significant Difference

It is widely known that cobalt and chromium ions can enhance the production of reactive oxygen species, known to be damaging to cells by disturbing their redox status and then generating oxidative stress. The aim of the present study was to determine if increased metal ion levels induce a state of oxidative stress in patients with metal-on-metal (MM) hip arthroplasty. Results indicated that there was no significant difference in the concentration of oxidative stress markers (total antioxidants, peroxides, and nitrated proteins) in the patients with MM bearings compared to patients without prostheses. The activity antioxidant enzymes was stable (catalase and glutathione peroxidase) or slightly decreased (superoxide dismutase and heme oxygenase-1) over time. This work is the first to determine the biological effects of metal ions released from MM hip implants with regards to mid-term systemic oxidative stress and showed that the increased levels of Co and Cr ions are not associated with significant oxidative stress damage in the plasma of patients with these implants.

scholarly journals Effects of estrogens on oxidative protein damage in plasma and tissues in ovariectomised rats

2009 ◽  
Vol 32 (2) ◽  
pp. 133 ◽  
Author(s):  
A Topçuoglu ◽  
H Uzun ◽  
H Balci ◽  
M Karakus ◽  
I Çoban ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hormone Replacement ◽  
Redox Status ◽  
The Other ◽  
Protein Damage ◽  
Stress Markers ◽  
Ovx Rats ◽  
Oxidative Protein Damage ◽  
Norethisterone Acetate ◽  
Oxidation Parameters

Purpose: To assess estrogen-related changes in the redox status of the brain and liver proteins as well as the systemic oxidative stress in ovarectomised (OVX) rats Methods: Twelve-week-old, sexually mature female Sprague–Dawley rats (200-250g) were randomly divided into four groups: The following treatment combinations were administrated daily to all in 0.05 ml 96% ethanol solution by gastric gavage. (1) Sham operation (2) OVX rats (3) OVX rats [0.02 mg/kg/day of 17?-estradiol (E2) and 0.01 mg/kg/day of norethisterone acetate] (4) OVX rats [E2 (0.01 mg/kg/day) and drospirenon (0.02 mg/kg/day)]. Estrogen levels were determined using routine clinical-chemistry methods. We also measured protein oxidation parameters such as protein carbonyl (PCO), total thiol (T-SH) and the other oxidative stress markers malondialdehyde (MDA) and glutathione (GSH). Results: Ovariectomy resulted in abnormal elevation of plasma and tissue oxidative stress markers and changes in redox status of the proteins in tissue dependent manner. Supplementation of various estrogens combinations partially alleviated these abnormalities and restored redox homeostasis of proteins after the ovariectomy. Among the studied protein oxidation parameters, plasma and tissue PCO levels of the OVX rats were higher than those of the control groups (P < 0.01). Hormone replacement therapies (HRT) caused a decrease in PCO and MDA in both plasma and tissue of the OVX rats (P < 0.01). HRT in OVX rats decreased plasma MDA and increased liver and brain GSH (P < 0.01). Liver MDA levels of the Drospirenon-treated rats were lower than in the norethisterone acetate group (P < 0.01). On the other hand, Drospirenon increases brain GSH s more effectively than norethisterone acetate (P < 0.01). After bilateral oopherectomy, plasma and tissue T-SH levels decreased in the OVX group compared with control (P < 0.01). Norethisterone acetate increased plasma T-SH more effectively than Drospirenon (P < 0.05) Conclusions: The study showed the extent of oxidative protein damage (OPD) in this model of estrogen deficiency. The protective effect of estrogens against tissue specific OPD suggests that estrogens play an important role within the antioxidant defense systems in plasma, liver and brain. The exact molecular mechanisms leading to these findings are not yet completely known. Meanwhile, hormone replacement therapy for the prevention of OPD in a tissue specific manner may be required.

Retinitis Pigmentosa: Clinical Features, Imaging, and Diagnosis

2021 ◽  
pp. 107-112
Keyword(s):  
Retinitis Pigmentosa ◽  
Vision Loss ◽  
Fundus Autofluorescence ◽  
Visual Field Loss ◽  
Clinical Findings ◽  
Autofluorescence Imaging ◽  
Inherited Retinal Dystrophies ◽  
Retinal Dystrophies ◽  
Central Vision Loss ◽  
Progressive Degeneration

Retinitis pigmentosa (RP) is a heterogeneous group of inherited retinal dystrophies characterized by progressive degeneration of rod and cone photoreceptors. The worldwide prevalence of the disease is 1/4000. The earliest symptom in RP is most commonly night blindness, followed by concentric visual field loss. Central vision loss occurs later in life due to cone dysfunction. Photoreceptor responses measured with an electroretinogram are reduced or undetectable. Optical coherence tomography shows a progressive loss of outer retinal layers and fundus autofluorescence imaging reveals alteration autofluorescence in a characteristic pattern. Mutations in more than 80 different genes have been associated with non-syndromic RP. The heterogeneity of RP makes it challenging to describe the clinical findings. The objective of this review is to provide an overview of the clinical characteristics and diagnosis of RP.

The benefit of a supplement with the antioxidant melatonin on redox status and muscle damage in resistance-trained athletes

2017 ◽  
Vol 42 (7) ◽  
pp. 700-707 ◽  
Author(s):  
Roberto C. Leonardo-Mendonça ◽  
Javier Ocaña-Wilhelmi ◽  
Tomás de Haro ◽  
Carlos de Teresa-Galván ◽  
Eduardo Guerra-Hernández ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Muscle Damage ◽  
Antioxidant Properties ◽  
Redox Status ◽  
Absorption Capacity ◽  
Double Blind ◽  
Beneficial Effects ◽  
Before And After ◽  
High Doses ◽  
Exercise Induced

Previous data showed that the administration of high doses of melatonin improved the circadian system in athletes. Here, we investigated in the same experimental paradigm whether the antioxidant properties of melatonin has also beneficial effects against exercise-induced oxidative stress and muscle damage in athletes. Twenty-four athletes were treated with 100 mg·day−1 of melatonin or placebo 30 min before bedtime during 4 weeks in a randomized double-blind scheme. Exercise intensity was higher during the study that before starting it. Blood samples were collected before and after treatment, and plasma was used for oxygen radical absorption capacity (ORAC), lipid peroxidation (LPO), nitrite plus nitrate (NOx), and advanced oxidation protein products (AOPP) determinations. Glutathione (GSH), glutathione disulphide (GSSG) levels, and glutathione peroxidase (GPx) and reductase (GRd) activities, were measured in erythrocytes. Melatonin intake increased ORAC, reduced LPO and NOx levels, and prevented the increase of AOPP, compared to placebo group. Melatonin was also more efficient than placebo in reducing GSSG·GSH−1 and GPx·GRd−1 ratios. Melatonin, but not placebo, reduced creatine kinase, lactate dehydrogenase, creatinine, and total cholesterol levels. Overall, the data reflect a beneficial effect of melatonin treatment in resistance-training athletes, preventing extra- and intracellular oxidative stress induced by exercise, and yielding further skeletal muscle protection against exercise-induced oxidative damage.

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