Antioxidant defences and oxidative damage in salt-treated olive plants under contrasting sunlight irradiance

Oxidative damage is present within the brains of patients with Alzheimer's disease (AD), and is observed within every class of biomolecule, including nucleic acids, proteins, lipids and carbohydrates. Oxidative injury may develop secondary to excessive oxidative stress resulting from β-amyloid-induced free radicals, mitochondrial abnormalities, inadequate energy supply, inflammation or altered antioxidant defences. Treatment with antioxidants is a promising approach for slowing disease progression to the extent that oxidative damage may be responsible for the cognitive and functional decline observed in AD. Although not a uniformly consistent observation, a number of epidemiological studies have found a link between antioxidant intake and a reduced incidence of dementia, AD and cognitive decline in elderly populations. In AD clinical trials molecules with antioxidant properties such as vitamin E andGinkgo bilobaextract have shown modest benefit. A clinical trial with vitamin E is currently ongoing to determine if it can delay progression to AD in individuals with mild cognitive impairment. Combinations of antioxidants might be of even greater potential benefit for AD, especially if the agents worked in different cellular compartments or had complementary activity (e.g. vitamins E, C and ubiquinone). Naturally-occurring compounds with antioxidant capacity are available and widely marketed (e.g. vitamin C, ubiquinone, lipoic acid, β-carotene, creatine, melatonin, curcumin) and synthetic compounds are under development by industry. Nevertheless, the clinical value of these agents for AD prevention and treatment is ambiguous, and will remain so until properly designed human trials have been performed.

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Increased lymphocyte antioxidant defences in response to exhaustive exercise do not prevent oxidative damage

The Journal of Nutritional Biochemistry ◽

10.1016/j.jnutbio.2005.10.013 ◽

2006 ◽

Vol 17 (10) ◽

pp. 665-671 ◽

Cited By ~ 48

Author(s):

P TAULER ◽

A SUREDA ◽

N CASES ◽

A AGUILO ◽

J RODRIGUEZMARROYO ◽

...

Keyword(s):

Oxidative Damage ◽

Exhaustive Exercise ◽

Antioxidant Defences

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Effect of Oxidative Stress on Lymphocytes from Elderly Subjects

Clinical Science ◽

10.1042/cs0940447 ◽

1998 ◽

Vol 94 (4) ◽

pp. 447-452 ◽

Cited By ~ 11

Author(s):

E. García-Arumí ◽

A. L. Andreu ◽

J. López-Hellín ◽

S. Schwartz

Keyword(s):

Oxidative Stress ◽

Enzyme Activity ◽

Oxidative Damage ◽

Antioxidant Enzyme ◽

Antioxidant Enzyme Activity ◽

Elderly Subjects ◽

Antioxidant Enzyme Activities ◽

Antioxidant Defences ◽

Protein Carbonyl Content ◽

Healthy Elderly

1. Oxidative damage has been associated with ageing, but there is no agreement as to whether or not it is produced by a decrease in antioxidant defences with the ageing process. In purified lymphocytes from 47 healthy elderly (75.27 ± 0.91 years) and 47 healthy young (29.87 ± 0.53 years) volunteers, we studied the levels of antioxidant enzyme activity (superoxide dismutase, catalase and glutathione peroxidase), protein oxidative damage (as protein carbonyl content) and lysosomal proteolytic activity (cathepsins B, H and L), with and without exposure to oxidative stress produced by 25 μmol/l H2O2. 2. There were no differences in antioxidant enzyme activities in the stressed and non-stressed samples between the young and elderly subjects, indicating that there was no relationship between age and antioxidant enzyme activity even in oxidative stress. However, a dissimilar response to oxidative stress was observed in protein oxidative damage and cathepsin B and L activities, depending on the age of the donor. 3. With these results we conclude that oxidative stress produces greater protein oxidative damage and increased protein degradation in elderly subjects than in young ones; this effect cannot be attributed to dissimilar antioxidant enzyme responses to oxidative stress, since these did not differ between the two age groups.

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Metals as a cause of oxidative stress in fish: a review

Veterinární Medicína ◽

10.17221/4272-vetmed ◽

2011 ◽

Vol 56 (No. 11) ◽

pp. 537-546 ◽

Cited By ~ 139

Author(s):

M. Sevcikova ◽

H. Modra ◽

A. Slaninova ◽

Z. Svobodova

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Oxidative Damage ◽

Metal Binding ◽

Special Functions ◽

Current Knowledge ◽

Reactive Oxygen ◽

Enzyme Inactivation ◽

Oxygen Species ◽

Antioxidant Defences

This review summarizes the current knowledge on the contribution of metals to the development of oxidative stress in fish. Metals are important inducers of oxidative stress in aquatic organisms, promoting formation of reactive oxygen species through two mechanisms. Redox active metals generate reactive oxygen species through redox cycling, while metals without redox potential impair antioxidant defences, especially that of thiol-containing antioxidants and enzymes. Elevated levels of reactive oxygen species lead to oxidative damage including lipid peroxidation, protein and DNA oxidation, and enzyme inactivation. Antioxidant defences include the enzyme system and low molecular weight antioxidants. Metal-binding proteins, such as ferritin, ceruloplasmin and metallothioneins, have special functions in the detoxification of toxic metals and also play a role in the metabolism and homeostasis of essential metals. Recent studies of metallothioneins as biomarkers indicate that quantitative analysis of mRNA expression of metallothionein genes can be appropriate in cases with elevated levels of metals and no evidence of oxidative damage in fish tissue. Components of the antioxidant defence are used as biochemical markers of oxidative stress. These markers may be manifested differently in the field than in results found in laboratory studies. A complex approach should be taken in field studies of metal contamination of the aquatic environment.  

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Protective effects of oestradiol against cadmium-induced changes in blood parameters and oxidative damage in rats

Archives of Industrial Hygiene and Toxicology ◽

10.2478/10004-1254-65-2014-2405 ◽

2014 ◽

Vol 65 (1) ◽

pp. 37-46 ◽

Cited By ~ 20

Author(s):

Jelena Mladenović ◽

Branka Ognjanović ◽

Nataša Đorđević ◽

Miloš Matić ◽

Veroljub Knežević ◽

...

Keyword(s):

Oxidative Damage ◽

Oxygen Free Radicals ◽

Redox Balance ◽

Blood Parameters ◽

Enzymatic Antioxidants ◽

Protective Effects ◽

Antioxidant Defences ◽

Biochemical Effects ◽

Endogenous Antioxidants ◽

Induced Changes

Summary The aim of this study was to investigate the protective effects of oestradiol (E2, 4 mg kg-1 b.w. i.p.) against cadmium-induced (Cd, 2 mg kg-1 b.w. i.p.) blood changes in rats. Cadmium induced a significant decline in haemoglobin, haematocrit, and total erythrocyte, lymphocyte, and thrombocyte count, whereas total leukocytes and granulocytes increased. A significant increase was also observed in serum cholesterol, triglycerides, glucose, AST, and ALT activities, whereas total protein and albumin levels dropped significantly. Administration of E2 in combination with Cd alleviated most of these adverse effects. In terms of oxidative stress, Cd significantly increased oxygen-free radicals (O2 •- and H2O2) in neutrophils and lipid peroxidation in erythrocytes, whereas E2 treatment reversed these changes to control values. Acute Cd poisoning significantly lowered antioxidant enzyme (SOD and CAT) activity and the level of non-enzymatic antioxidants (GSH and vitamin E), while increasing in GSSG. Treatments with E2 reversed Cd-induced effects on the antioxidant defences and significantly lowered Cd-induced oxidative damage in erythrocytes. This study suggests that exogenous E2 effectively restores redox balance in rat erythrocytes and counters adverse haematological and biochemical effects of Cd poisoning. It also improves the antioxidant capacity of erythrocytes, acting in synergy with endogenous antioxidants.

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The effects of temperature and dissolved oxygen on antioxidant defences and oxidative damage in the fathead minnow Pimephales promelas

Journal of Fish Biology ◽

10.1111/jfb.12050 ◽

2013 ◽

Vol 82 (3) ◽

pp. 1086-1092 ◽

Cited By ~ 8

Author(s):

E. D. Clotfelter ◽

S. J. H. Lapidus ◽

A. C. Brown

Keyword(s):

Oxidative Damage ◽

Dissolved Oxygen ◽

Fathead Minnow ◽

Pimephales Promelas ◽

Antioxidant Defences ◽

Effects Of Temperature

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Yolk testosterone reduces oxidative damages during postnatal development

Biology Letters ◽

10.1098/rsbl.2010.0421 ◽

2010 ◽

Vol 7 (1) ◽

pp. 93-95 ◽

Cited By ~ 25

Author(s):

José Carlos Noguera ◽

Carlos Alonso-Alvarez ◽

Sin-Yeon Kim ◽

Judith Morales ◽

Alberto Velando

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Postnatal Development ◽

Early Development ◽

Early Life ◽

Antioxidant Defences ◽

Oxidative Damages ◽

Plasma Antioxidant ◽

Yolk Testosterone

Conditions experienced during early life can influence the development of an organism and several physiological traits, even in adulthood. An important factor is the level of oxidative stress experienced during early life. In birds, extra-genomic egg substances, such as the testosterone hormone, may exert a widespread influence over the offspring phenotype. Interestingly, testosterone can also upregulate the bioavailability of certain antioxidants but simultaneously increases the susceptibility to oxidative stress in adulthood. However, little is known about the effects of maternally derived yolk testosterone on oxidative stress in developing birds. Here, we investigated the role of yolk testosterone on oxidative stress of yellow-legged gull chicks during their early development by experimentally increasing yolk testosterone levels. Levels of antioxidants, reactive oxygen species and lipid oxidative damage were determined in plasma during nestlings' growth. Our results revealed that, contrary to control chicks, birds hatched from testosterone-treated eggs did not show an increase in the levels of oxidative damage during postnatal development. Moreover, the same birds showed a transient increase in plasma antioxidant levels. Our results suggest that yolk testosterone may shape the oxidative stress-resistance phenotype of the chicks during early development owing to an increase in antioxidant defences and repair processes.

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Effect of overexpression of wild-type and mutant Cu/Zn-superoxide dismutases on oxidative damage and antioxidant defences: relevance to Down's syndrome and familial amyotrophic lateral sclerosis

Journal of Neurochemistry ◽

10.1046/j.1471-4159.2001.00107.x ◽

2001 ◽

Vol 76 (4) ◽

pp. 957-965 ◽

Cited By ~ 56

Author(s):

MoonHee Lee ◽

Dong-Hoon Hyun ◽

Peter Jenner ◽

Barry Halliwell

Keyword(s):

Amyotrophic Lateral Sclerosis ◽

Oxidative Damage ◽

Down's Syndrome ◽

Down’S Syndrome ◽

Superoxide Dismutases ◽

Familial Amyotrophic Lateral Sclerosis ◽

Wild Type ◽

Antioxidant Defences ◽

Lateral Sclerosis

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Interacting effects of early dietary conditions and reproductive effort on the oxidative costs of reproduction

PeerJ ◽

10.7717/peerj.3094 ◽

2017 ◽

Vol 5 ◽

pp. e3094 ◽

Cited By ~ 6

Author(s):

Jose Carlos Noguera

Keyword(s):

Oxidative Damage ◽

Damage Accumulation ◽

Diet Composition ◽

Oxidative Dna Damage ◽

Cost Of Reproduction ◽

Postnatal Period ◽

Easy Access ◽

Zebra Finches ◽

Costs Of Reproduction ◽

Antioxidant Defences

The hypothesis that oxidative damage accumulation can mediate the trade-off between reproduction and lifespan has recently been questioned. However, in captive conditions, studies reporting no evidence in support of this hypothesis have usually provided easy access to food which may have mitigated the cost of reproduction. Here, I test the hypothesis that greater investment in reproduction should lead to oxidative damage accumulation and telomere loss in domestic zebra finchesTaeniopygia guttata. Moreover, since the change or fluctuation in diet composition between early and late postnatal period can impair the ability to produce antioxidant defences in zebra finches, I also tested if early nutritional conditions (constant vs fluctuating early diet) influenced the magnitude of any subsequent costs of reproduction (e.g., oxidative damage and/or telomere shortening). In comparison to pairs with reduced broods, the birds that had to feed enlarged broods showed a higher level of oxidative DNA damage (8-OHdG), but brood size had no effect on telomeres. Fluctuating early diet composition reduced the capacity to maintain the activity of endogenous antioxidants (GPx), particularly when reproductive costs were increased (enlarged brood). The decline in GPx in birds feeding enlarged broods was accompanied by a change in bill colouration. This suggests that birds with lower endogenous antioxidant defences might have strategically increased the mobilization of antioxidants previously stored in other tissues (i.e., bill and liver) and thus, preventing an excessive accumulation of damage during reproduction.

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