scholarly journals The maternal effect in infantile autism: elevated DNA damage degree in patients and their mothers

2016 ◽  
Vol 62 (4) ◽  
pp. 466-470 ◽  
Author(s):  
L.N. Porokhovnik ◽  
S.V. Kostyuk ◽  
E.S. Ershova ◽  
S.M. Stukalov ◽  
N.N. Veiko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Maternal Effect ◽  
Infantile Autism ◽  
Reproductive Age ◽  
Control Group ◽  
Healthy Children ◽  
Tail Moment ◽  
Autistic Children ◽  
Comet Tail

Infantile autism is a common disorder of mental development, which is characterized by impairments in the communicative, cognitive and speech spheres and obsessional stereotyped behaviour. Although in most cases, pathogenic factors remain unclear, infantile autism has a significant hereditary component, however, its etiology is also under the influence of environmental factors, including the condition of the mother's body during pregnancy (“maternal effect”). Oxidative stress is assumed to play a key role in the pathogenesis of infantile autism. It is known that oxidative stress has a prominent genotoxic effect, which is realized through inducing single and double strand breaks of the nuclear DNA. We evaluated the degree of DNA damage in patients with infantile autism and their mothers using DNA comet assay. The comet tail moment and DNA per cent ratio in the tail were assessed for each individual. The two parameters appeared to be strongly correlated (r=0.90). Mean and median values of both parameters were considerably higher in the sample of autistic children, than in age-matching healthy controls. Interestingly, these parameters were also elevated in healthy mothers of autistic children, with no difference from the values in the group of autistic children. The control group of healthy women of reproductive age, who had no children with autism, differed by the DNA comet tail moment from the group of mothers of autistic children, but did not differ significantly from the control group of healthy children. The results suggest that there are genotoxic factors in mentally healthy mothers of autistic children, which can determine the pathological process in the foeti via environmental “maternal effect” during gestation.

scholarly journals Sulforaphane-Mediated Nrf2 Activation Prevents Radiation-Induced Skin Injury through Inhibiting the Oxidative-Stress-Activated DNA Damage and NLRP3 Inflammasome

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1850
Author(s):  
Jinlong Wei ◽  
Qin Zhao ◽  
Yuyu Zhang ◽  
Weiyan Shi ◽  
Huanhuan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Western Blotting ◽  
Nlrp3 Inflammasome ◽  
Fibrous Tissue ◽  
Mouse Skin ◽  
Control Group ◽  
Skin Injury ◽  
Antioxidant Genes ◽  
Radiation Induced

This article mainly observed the protective effect of sulforaphane (SFN) on radiation-induced skin injury (RISI). In addition, we will discuss the mechanism of SFN’s protection on RISI. The RISI model was established by the irradiation of the left thigh under intravenous anesthesia. Thirty-two C57/BL6 mice were randomly divided into control group (CON), SFN group, irradiation (IR) group, and IR plus SFN (IR/SFN) group. At eight weeks after irradiation, the morphological changes of mouse skin tissues were detected by H&E staining. Then, the oxidative stress and inflammatory response indexes in mouse skin tissues, as well as the expression of Nrf2 and its downstream antioxidant genes, were evaluated by ELISA, real-time PCR, and Western blotting. The H&E staining showed the hyperplasia of fibrous tissue in the mouse dermis and hypodermis of the IR group. Western blotting and ELISA results showed that the inflammasome of NLRP3, caspase-1, and IL-1β, as well as oxidative stress damage indicators ROS, 4-HNE, and 3-NT, in the skin tissues of mice in the IR group were significantly higher than those in the control group (p < 0.05). However, the above pathological changes declined sharply after SFN treatment (p < 0.05). In addition, the expressions of Nrf2 and its regulated antioxidant enzymes, including CAT and HO-1, were higher in the skin tissues of SFN and IR/SFN groups, but lower in the control and IR groups (p < 0.05). SFN may be able to suppress the oxidative stress by upregulating the expression and function of Nrf2, and subsequently inhibiting the activation of NLRP3 inflammasome and DNA damage, so as to prevent and alleviate the RISI.

scholarly journals Oxidative lipid, protein, and DNA damage as oxidative stress markers in vascular complications of diabetes mellitus

2011 ◽  
Vol 34 (3) ◽  
pp. 163 ◽  
Author(s):  
Omur Tabak ◽  
Remise Gelisgen ◽  
Hayriye Erman ◽  
Fusun Erdenen ◽  
Cüneyt Muderrisoglu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Vascular Complications ◽  
Diabetic Group ◽  
Control Group ◽  
Diabetic Patients ◽  
Serum Samples ◽  
Type 2 Diabetic Patients

Purpose: The purpose of this study was to determine the effects of diabetic complications on oxidation of proteins, lipids, and DNA and to investigate the relationship between oxidative damage markers and clinical parameters. Methods: The study group consisted of 69 type 2 diabetic patients (20 patients without complication, 49 patients with complication) who attended internal medicine outpatient clinics of Istanbul Education and Research Hospital and 19 healthy control subjects. In serum samples of both diabetic patients and healthy subjects, 8-hydroxy-2’deoxyguanosine (8-OHdG), as a marker of oxidative DNA damage, Nε-(hexanoyl)lysine (HEL) and 15-F2t-iso-prostaglandin (15-F2t-IsoP). as products of lipooxidative damage, advanced oxidation protein products (AOPP), as markers of protein damage, and paraoxonase1 (PON1) as antioxidant were studied. Results: 15-F2t-IsoP (p < 0.005) and AOPP (p < 0.001) levels were significantly higher in diabetic group than control group while there were no significant differences in levels of 8-OHdG and HEL between the two groups. AOPP (p < 0.001) and 8-OHdG (p < 0.001) were significantly higher in diabetic group with complications compared to diabetic group without complications. Conclusions: Increased formation of free radicals and oxidative stress, under conditions of hyperglycaemia, is one of the probable causes for evolution of complications in diabetes mellitus. Our study supports the hypothesis that oxidant/antioxidant balance is disturbed in diabetic patients.

scholarly journals Oxidative Stress, Folate Receptor Autoimmunity, and CSF Findings in Severe Infantile Autism

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Vincent T. Ramaekers ◽  
Jeffrey M. Sequeira ◽  
Beat Thöny ◽  
Edward V. Quadros
Keyword(s):  
Oxidative Stress ◽  
Folate Receptor ◽  
Regulation Of Gene Expression ◽  
Reactive Oxygen ◽  
Infantile Autism ◽  
Serum Folate ◽  
Controlled Study ◽  
Autistic Children ◽  
Serotonin Turnover ◽  
The Brain

Background. Biomarkers such as oxidative stress, folate receptor alpha (FRα) autoimmunity, and abnormal brain serotonin turnover are common in autism. Methods. Oxidative stress biomarkers with pro- and antioxidants were measured in the severe form of infantile autism (n = 38) and controls (n = 24). Children and parents had repeated testing for serum FR autoantibodies, spinal fluid dopamine and serotonin metabolites, pterins, and N5-methyltetrahydrofolate (MTHF). Statistical analysis assessed correlations between variables. Genetic analysis included the SLC6A4 and SLC29A4 genes encoding synaptic serotonin reuptake proteins. Results. Compared to controls, the autism group showed a significant increase in oxidative DNA damage in lymphocytes, plasma ceruloplasmin and copper levels with a high copper/zinc ratio, thiol proteins, and superoxide dismutase (SOD) activity. Vitamin C levels were significantly diminished. In most autistic patients, the vitamin A (64%) and D (70%) levels were low. Serum FR autoantibodies fluctuating over 5–7 week periods presented in 68% of all autistic children, 41% of parents vs. 3.3% of control children and their parents. CSF showed lowered serotonin 5-hydroxyindole acetic acid (5HIAA) metabolites in 13 (34%), a low 5HIAA to HVA (dopamine metabolite) ratio in 5 (13%), low 5HIAA and MTHF in 2 (5%), and low MTHF in 8 patients (21%). A known SLC6A4 mutation was identified only in 1 autistic child with low CSF 5HIAA and a novel SLC29A4 mutation was identified in identical twins. Low CSF MTHF levels among only 26% of subjects can be explained by the fluctuating FR antibody titers. Two or more aberrant pro-oxidant and/or antioxidant factors predisposed to low CSF serotonin metabolites. Three autistic children having low CSF 5HIAA and elevated oxidative stress received antioxidative supplements followed by CSF 5HIAA normalisation. Conclusion. In autism, we found diverse combinations for FR autoimmunity and/or oxidative stress, both amenable to treatment. Parental and postnatal FR autoantibodies tend to block folate passage to the brain affecting folate-dependent pathways restored by folinic acid treatment, while an abnormal redox status tends to induce reduced serotonin turnover, corrected by antioxidant therapy. Trial Registration. The case-controlled study was approved in 2008 by the IRB at Liège University (Belgian Number: B70720083916). Lay Summary. Children with severe infantile autism frequently have serum folate receptor autoantibodies that block the transport of the essential vitamin folate across the blood-brain barrier to the brain. Parents are often asymptomatic carriers of these serum folate receptor autoantibodies, which in mothers can block folate passage across the placenta to their unborn child. This folate deficiency during the child’s intrauterine development may predispose to neural tube defects and autism. Oxidative stress represents a condition with the presence of elevated toxic oxygen derivatives attributed to an imbalance between the formation and protection against these toxic reactive oxygen derivatives. Oxidative stress was found to be present in autistic children where these reactive oxygen derivatives can cause damage to DNA, which changes DNA function and regulation of gene expression. In addition, excessive amounts of these toxic oxygen derivatives are likely to damage the enzyme producing the neuromessenger serotonin in the brain, diminished in about 1/3 of the autistic children. Testing children with autism for oxidative stress and its origin, as well as testing for serum folate receptor autoantibodies, could open new approaches towards more effective treatments.

scholarly journals Bone Marrow Oxidative Stress and Acquired Lineage-Specific Genotoxicity in Hematopoietic Stem/Progenitor Cells Exposed to 1,4-Benzoquinone

2020 ◽  
Vol 17 (16) ◽  
pp. 5865
Author(s):  
Ramya Dewi Mathialagan ◽  
Zariyantey Abd Hamid ◽  
Qing Min Ng ◽  
Nor Fadilah Rajab ◽  
Salwati Shuib ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Marrow ◽  
Dna Damage ◽  
Progenitor Cells ◽  
Bone Marrow Cells ◽  
Protein Carbonyls ◽  
Mouse Bone Marrow ◽  
Tail Moment ◽  
Erythroid Progenitor ◽  
Hematopoietic Stem

Hematopoietic stem/progenitor cells (HSPCs) are susceptible to benzene-induced genotoxicity. However, little is known about the mechanism of DNA damage response affecting lineage-committed progenitors for myeloid, erythroid, and lymphoid. Here, we investigated the genotoxicity of a benzene metabolite, 1,4-benzoquinone (1,4-BQ), in HSPCs using oxidative stress and lineage-directed approaches. Mouse bone marrow cells (BMCs) were exposed to 1,4-BQ (1.25–12 μM) for 24 h, followed by oxidative stress and genotoxicity assessments. Then, the genotoxicity of 1,4-BQ in lineage-committed progenitors was evaluated using colony forming cell assay following 7–14 days of culture. 1,4-BQ exposure causes significant decreases (p < 0.05) in glutathione level and superoxide dismutase activity, along with significant increases (p < 0.05) in levels of malondialdehyde and protein carbonyls. 1,4-BQ exposure induces DNA damage in BMCs by significantly (p < 0.05) increased percentages of DNA in tail at 7 and 12 μM and tail moment at 12 μM. We found crucial differences in genotoxic susceptibility based on percentages of DNA in tail between lineage-committed progenitors. Myeloid and pre-B lymphoid progenitors appeared to acquire significant DNA damage as compared with the control starting from a low concentration of 1,4-BQ exposure (2.5 µM). In contrast, the erythroid progenitor showed significant damage as compared with the control starting at 5 µM 1,4-BQ. Meanwhile, a significant (p < 0.05) increase in tail moment was only notable at 7 µM and 12 µM 1,4-BQ exposure for all progenitors. Benzene could mediate hematological disorders by promoting bone marrow oxidative stress and lineage-specific genotoxicity targeting HSPCs.

scholarly journals Roles of Moringa oleifera Leaf Extract in Improving the Impact of High Dietary Intake of Monosodium Glutamate-Induced Liver Toxicity, Oxidative Stress, Genotoxicity, DNA Damage, and PCNA Alterations in Male Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Tarfa Albrahim ◽  
Manal Abdulaziz Binobead
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Leaf Extract ◽  
Liver Toxicity ◽  
Monosodium Glutamate ◽  
Male Rats ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Glutamyl Transferase ◽  
The Impact

It is common for food to be made more palatable through the use of the flavour enhancer monosodium glutamate, also known as vetsin powder. The purpose of the study described in this paper was to explore how vetsin-induced hepatic toxicity, DNA fragmentation, damage, and oxidative stress modifications could be mitigated with moringa leaf extract (MLE). To that end, 40 male rats were separated into four groups: normal control, positive control or MLE, vetsin, and vetsin combined with MLE. Results indicated that, compared to the control group, the levels of serum alanine aminotransferase (ALT), aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), liver malondialdehyde (MDA), DNA damage, injury, PCNA, and P53 expressions were significantly enhanced by the administration of vetsin (P<0.05). However, the vetsin group had significantly reduced levels of albumin, globulin, total protein, liver glutathione (GSH), superoxide dismutase enzyme (SOD), catalase, and glutathione S-transferase (GST) enzyme activities (P<0.05) by comparison to control. Meanwhile, modifications in liver functions, oxidative stress, DNA damage, liver injury, and PCNA expression were alleviated when vetsin was administered alongside MLE. The authors conclude that vetsin may have many side effects and that MLE can ameliorate biochemical changes, oxidative stress, hepatic injury, PCNA, and P53 alterations induced by vetsin administration.

scholarly journals Modern possibilities of homeostatic reserves indication in bronchitis in children

2016 ◽  
Vol 97 (1) ◽  
pp. 41-47
Author(s):  
O I Pikuza ◽  
H M Vahitov ◽  
E V Generalova
Keyword(s):  
Oxidative Stress ◽  
Bacterial Infections ◽  
Acute Bronchitis ◽  
Main Group ◽  
Control Group ◽  
Healthy Children ◽  
Colonization Resistance ◽  
Non Invasive ◽  
Colonization Index ◽  
Buccal Epithelial Cells

Aim. To study the homeostatic reserves indicators in children with bronchitis by assessment of colonization resistance indicators and oxidative stress processes in the oral cavity.Methods. Clinical and instrumental examination of 115 children aged 5 to 14 years admitted to hospital with different variants of bronchitis was performed. The patients (main group) were divided into two subgroups according to the diagnosis: the first subgroup included 70 children with recurrent bronchitis, the second subgroup consisted of 45 children with acute bronchitis. The control group included 33 apparently healthy children of the same age. The examination complex included, in addition to conventional clinical and laboratory methods, special methods of examination - the oral cavity colonization resistance indicators identification (buccal epithelial cells colonization index and saliva anti-adhesive activity). In addition, oxidative stress indicators on oral neutrophils model - spontaneous and induced luminol-dependent chemiluminescence, were measured.Results. It was found that colonization index and saliva anti-adhesive activity was significantly lower in children of the main group than in control group. The lowest rates were characterstic for the first subgroup of patients. In children with acute bronchitis higher values of the induced and the spontaneous luminol-dependent chemiluminescence were registered as compared to control, whereas in recurrent bronchitis, by contrast, they were lower than in control (pConclusion. Patients with recurrent bronchitis extremely «vulnerable» in relation to recurrent bacterial infections (diseases) in connection with the mucosal protection system severe defects; they need to undergo aimed preventive and rehabilitation measures, the effectiveness control of which can be performed using the proposed non-invasive methods.

scholarly journals Evaluation of the state of the pro-oxidant/antioxidant system in children with hereditary spherocytosis

2021 ◽  
pp. 55-61
Author(s):  
E. F. Mitsura ◽  
I. A. Novikova ◽  
T. S. Petrenko ◽  
K. S. Makeeva ◽  
L. I. Volkova
Keyword(s):  
Oxidative Stress ◽  
Antioxidant System ◽  
Antioxidant Status ◽  
Hereditary Spherocytosis ◽  
The State ◽  
Control Group ◽  
Healthy Children ◽  
Gender And Age ◽  
Severity Of The Disease

Objective: to assess the state of the pro-oxidant/antioxidant system in children with hereditary spherocytosis (HS) depending on its severity.Material and methods. The study involved 44 HS patients at the age from 1 to 17 who were divided into 2 groups depending on the disease severity: mild course (n = 24) and moderate or severe course (n = 20). The control group included 23 practically healthy children who were comparable with the main group by gender and age. The state of the pro-oxidant/antioxidant balance of blood plasma was assessed by the method of luminol-dependent chemiluminescence (LDCL) with the determination of the maximum luminescence intensity (Imax, %) and the light sum of chemiluminescence (S, %). The activity of superoxide dismutase (SOD) and catalase was determined in the erythrocytes of the examined children.Results. On average, the parameters of the pro-oxidant/antioxidant status in the HS patients significantly differed from those of the control group (p <0.05), which corresponded to moderately pronounced oxidative stress. The activity of SOD and catalase in the erythrocytes of the patients was higher as compared with that of the control group (p = 0.0001 and p <0.0001, respectively). The comparison of the severity of oxidative stress depending on HS severity has determined that the degree of stress was more pronounced in patients with moderate or severe course of the disease (p <0.05).Conclusion. HS patients develop oxidative stress (decreased activity of the antioxidant system associated with increased accumulation of prooxidant substances), the degree of which is higher in patients with a severe course of the disease. This allows of considering plasma LDCL indicators as an additional marker for the assessment of the severity of the disease and of justifying the necessity to include antioxidants in the HS treatment regimen.

scholarly journals EVALUATION OF THE RELATIONSHIP BETWEEN DENTAL CARIES AND OXIDATIVE STRESS AND ANTIOXIDANT CAPACITY

2021 ◽  
Author(s):  
Ahmet Güzelçiçek ◽  
Mahmut Demir ◽  
Adnan Kirmit ◽  
MEHMET DOGAN
Keyword(s):  
Oxidative Stress ◽  
Dental Caries ◽  
Patient Group ◽  
Total Antioxidant Status ◽  
Stress Index ◽  
Control Group ◽  
Healthy Children ◽  
Markers Of Oxidative Stress ◽  
The Relationship ◽  
And Oxidative Stress

Background Dental caries can be affected or altered by the body’s oxidant / antioxidant balance and oxidative stress. Aim/Hypothesis To examine the relationship between dental caries and Total Oxidant Status (TOS), Total Antioxidant Status (TAS), and Oxidative Stress Index (OSI). Design The study group consisted of 52 children with dental caries (DMFS/dfs ≥ 5), and the control group consisted of 42 healthy children (DMFS/dfs = 0). The saliva samples, unstimulated and mid-morning, were collected from all children. Participants’ saliva samples were acquired by spitting for 5 minutes, after which the samples were frozen and stored at 4 ° C and kept at -80 ° C until analysis. NCSS (Number Cruncher Statistical System) 2007 (Kaysville, Utah, USA) was used for the statistical analysis. Results TOS of the patient group cases were statistically significantly higher than those of the control group (p=0,004; p<0,01). OSI values of the patient group cases were statistically significantly higher than those of the control group (p=0,008; p<0,01). Conclusion OSI and TOS as markers of oxidative stress levels were found to be significantly higher in the group of patients with dental caries than in the healthy group.

145 STAGE-SPECIFIC EFFECT OF OXIDATIVE STRESS ON DEVELOPMENTAL COMPETENCE, ROS GENERATION AND DNA DAMAGE OF PORCINE PARTHENOGENETIC EMBRYOS

2006 ◽  
Vol 18 (2) ◽  
pp. 180
Author(s):  
M. Takahashi ◽  
M. Sakatani ◽  
S. Kobayashi ◽  
S. Kobayashi ◽  
H. Nagashima
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Fluorescent Dyes ◽  
Specific Effect ◽  
Ros Generation ◽  
Blastocyst Formation ◽  
Comet Tail ◽  
Intracellular Ros ◽  
O2 Concentration ◽  
High O2

We investigated the effect of oxidative stress on stage specific developmental ability, reactive oxygen species (ROS) generation and DNA damage of parthenogenetically activated porcine embryos. Cumulus-oocyte complexes (COCs) were aspirated from follicles on the surface of ovaries. The COCs were matured in NCSU-23 containing 10% (vol/vol) porcine follicular fluid and 10 IU/mL hCG during the first 22 h followed by an extra 22 h of culture in the hormone free NCSU-23. After 44 h of maturation, oocytes were denuded of cumulus cells and used for activation. Oocytes were activated by a 100-�sec pulse of 1.5 kV/cm DC with 1-mm electrodes in 0.3 m mannitol, 0.1 mm MgSO4, and 0.05 mm CaCl2. Activated oocytes were then cultured for 5 h in NCSU-23 containing 5 mg/mL BSA, 10 �g/mL EGF and 7.5 �g/mL cytochalasin B. Embryos were then cultured for 6 days in PZM-5. In Experiment 1, after parthenogenetic activation, embryos were cultured at 38.5�C under 5% O2, 5% CO2 and 90% N2 (defined as 5% O2) or 5% CO2 in air (20% O2). The oxygen concentration for embryo culture was changed from 5% to 20% on day 1, 2, 3, 4, and 5 post-activation, respectively. Embryos were also cultured throughout 6 days in 5 and 20% O2. About 100 embryos were used in each experiment. The number of embryos cleaved and developed to blastocyst stage was observed on day 2 and 6, respectively. In Experiment 2, 10 to 20 embryos cultured in 5 and 20% O2 were collected on Days 2, 4, and 6 for the detection of ROS, intracellular glutathione (GSH) levels and DNA damage. Intracellular ROS and GSH levels, were measured with fluorescent dyes (22,72-dichlorodihydrofluorescein diacetate for ROS and Cell Tracker" Blue for GSH). DNA damage of individual embryos was detected with a comet assay. DNA damage was quantified by measuring the length of the streak of DNA comet tail between the edge of the zona pellucida and the end of the visible comet tail by image analysis software. The rate of migrated DNA area per total DNA was also quantified. In Exp. 1, the rate of blastocyst formation was significantly decreased (P < 0.001) when embryos were cultured for 6 days under 20% O2 (17.8 � 4%) than 5% O2 (38.5 � 5%). The rates of blastocyst formation were significantly decreased (P < 0.05) when O2 concentration was changed from 5 to 20% before Day 3. After Day 4, high O2 concentration did not affect the development. In Exp. 2, relative ROS levels were significantly higher (P < 0.05) on Day 2 (1.5 � 0.03) and Day 4 (1.4 � 0.06) in embryos cultured under 20% O2 than in those cultured under 5% O2 (1.0). No difference was observed in GSH level. DNA damage was significantly increased (P < 0.05) in Day 2 embryos cultured under 20% O2 (161 � 54 �m) than 5% O2 (65 � 8.8 �m). These results indicate that the oxidative stress to embryo development by high O2 concentration is stage specific, that embryos are more sensitive in early stages, and that the oxidative stress has correlation with the increase of intracellular ROS and DNA damage.

scholarly journals Fish Oil Supplementation Reduces Markers of Oxidative Stress But Not Muscle Soreness After Eccentric Exercise

2014 ◽  
Vol 24 (2) ◽  
pp. 206-214 ◽  
Author(s):  
Patrick Gray ◽  
Andrew Chappell ◽  
Alison McE Jenkinson ◽  
Frank Thies ◽  
Stuart R. Gray
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Fish Oil ◽  
Eccentric Exercise ◽  
Muscle Soreness ◽  
Protein Carbonyls ◽  
Fish Oils ◽  
Control Group ◽  
Markers Of Oxidative Stress ◽  
Fish Oil Supplementation

Due to the potential anti-inflammatory properties of fish-derived long chain n-3 fatty acids, it has been suggested that athletes should regularly consume fish oils—although evidence in support of this recommendation is not clear. While fish oils can positively modulate immune function, it remains possible that, due to their high number of double bonds, there may be concurrent increases in lipid peroxidation. The current study aims to investigate the effect of fish oil supplementation on exercise-induced markers of oxidative stress and muscle damage. Twenty males underwent a 6-week double-blind randomized placebo-controlled supplementation trial involving two groups (fish oil or placebo). After supplementation, participants undertook 200 repetitions of eccentric knee contractions. Blood samples were taken presupplementation, postsupplementation, immediately, 24, 48, and 72 hr postexercise and muscle soreness/maximal voluntary contraction (MVC) assessed. There were no differences in creatine kinase, protein carbonyls, endogenous DNA damage, muscle soreness or MVC between groups. Plasma thiobarbituric acid reactive substances (TBARS) were lower (p < .05) at 48 and 72 hr post exercise and H2O2 stimulated DNA damage was lower (p < .05) immediately postexercise in the fish oil, compared with the control group. The current study demonstrates that fish oil supplementation reduces selected markers of oxidative stress after a single bout of eccentric exercise.

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