scholarly journals New Markers of Oxidative Damage to Macromolecules

2008 ◽  
Vol 27 (1) ◽  
pp. 1-16 ◽  
Author(s):  
Emina Čolak
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Oxidative Damage ◽  
Protein Modification ◽  
Lipid Hydroperoxide ◽  
The Body ◽  
Oxidative Modification ◽  
Toxic Effects ◽  
Specific Marker

New Markers of Oxidative Damage to Macromolecules The presence of free radicals in biological material has been discovered some 50 years ago. In physiological conditions, free radicals, in the first place the ones of oxygen and nitrogen, are continuously synthesized and involved in the regulation of a series of physiological processes. The excess of free radicals is efficiently eliminated from the body in order to prevent their toxic effects. Toxic effects of free radicals may be classified into three groups: a) change of intracellular redox potential, b) oxidative modification of lipids, proteins and DNA, and c) gene activation. Lipid peroxidation involving cell membranes, lipoproteins and other molecules leads to the production of primary high-reactive intermediaries (alkyl radicals, conjugated dienes, peroxy- and alkoxyl radicals and lipid hydroperoxide), whose further breakdown generates the secondary products of lipid peroxidation: short-chain evaporable hydrocarbons, aldehydes and final products of lipid peroxidation: isoprostanes, MDA, 4-hydroxy-2, 3-transnonenal and 4,5-dihydroxydecenal which are important mediators of atherosclerosis, coronary disease, acute myocardial infarction, rheumatoid arthritis, systemic sclerosis and lupus erythematodes. Oxidative modification of proteins is manifested by changes in their primary, secondary and tertiary structures. Proteins have a specific biological function, and therefore their modification results in unique functional consequences. The nature of protein modification may provide valid information on the type of oxidants causing the damage. Chlorotyrosyl is a specific marker of oxidative damage to tyrosine caused by HOCl action, which most commonly reflects the involvement of neutrophils and monocytes in oxidative stress, while nitrotyrosyl indicates the presence of higher peroxy-nitrite synthesis. Methyonin and cysteine are the amino acids most sensitive to oxidative stress, carbonyl groups are markers of severe damage caused by free radicals, and di-tyrosyl is the most significant and sensitive marker of oxidative modification made by γ rays. >Carbonyl stress< is an important form of the secondary oxidation of proteins, where reducing sugars non-enzymatically react with amino groups of proteins and lipids and give rise to the production of covalent compounds known as advanced glycosylated end products (AGE-products). A hydroxyl radical damages the DNA, leading to a loss of base and the formation of abasic sites (AP sites), break of DNA chain and sugar modification. Final lipid peroxidation products (MDA) may covalently bind to DNA, producing the >DNA radicals< which are responsible for mutations. Measurement of an adequate oxidative stress biomarker may not only point to an early onset of disease, its progression and assessment of therapy effectiveness, but can also help in the clarification of the pathophysiological mechanisms of tissue damage caused by oxidative stress, prediction of disease prognosis and choice of appropriate treatment in the early stages of disease.

scholarly journals Oxidative stress in ageing

2017 ◽  
Vol 5 (11) ◽  
pp. 4826 ◽  
Author(s):  
Fasna K. A. ◽  
Geetha N. ◽  
Jean Maliekkal
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Free Radical ◽  
Age Groups ◽  
The Body ◽  
Antioxidant Systems ◽  
Lipid Peroxidation Product ◽  
Free Radical Theory ◽  
Radical Theory

Background: Ageing is characterized by a gradual decline in body functions and decreased ability to maintain homeostasis. The free radical theory of ageing proposed by Harman D states that ageing is a result of cumulative damage incurred by free radical reactions. Free radicals are highly reactive molecular species with unpaired electrons; generated in the body by several physiological processes. Prime target to free radical attack are the polyunsaturated fatty acids of cell membranes causing lipid peroxidation. The free radicals are neutralized by the exogenous and endogenous antioxidant systems. Oxidative stress occurs when large number of free radicals are produced or the antioxidant activity is impaired. The present study is focused to find out the role of oxidative stress in ageing.Methods: A cross sectional observational study was undertaken to assess the oxidative stress in ageing; by determining the levels of lipid peroxidation product- malondialdehyde (MDA), the antioxidants- superoxide dismutase (SOD) and ceruloplasmin in various age groups. 150 healthy subjects were selected randomly and categorised into three different age groups of 20-30 years, 40-59 years and 60-90 years; with 50 subjects in each group. Results were expressed as mean ± standard deviation.Results: a significant elevation in serum MDA level and a decline in SOD were observed in 40-59 years and 60-90 years age groups. However, an elevated ceruloplasmin level was found in the above age groups.Conclusions: Aforementioned observations are suggestive of an association between oxidative stress and the progression of ageing process.

scholarly journals Oxidative stress in dogs

2016 ◽  
Vol 37 (3) ◽  
pp. 1431 ◽  
Author(s):  
Claudia Russo ◽  
Ana Paula F. Rodrigues Loureiro Bracarense
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Cell Membrane ◽  
The Body ◽  
Antioxidant Defenses ◽  
Cellular Respiration ◽  
Bodily Fluids ◽  
Cellular Components ◽  
Harmful Effects

Reactive oxygen species (ROS), also known as free radicals, are generated during cellular respiration. Under normal conditions, the body has the ability to neutralize the effects of free radicals by using its antioxidant defenses. In the case of an imbalance between oxidants and antioxidants, free radical production exceeds the capacity of organic combustion, resulting in oxidative stress. Of all the cellular components compromised by the harmful effects of ROS, the cell membrane is the most severely affected owing to lipid peroxidation, which invariably leads to changes in the membrane structure and permeability. With lipid peroxidation of the cell membrane, some by-products can be detected and measured in tissues, blood, and other bodily fluids. The measurement of biomarkers of oxidative stress is commonly used to quantify lipid peroxidation of the cell membrane in humans, a species in which ROS can be considered as a cause or consequence of oxidative stress-related diseases. In dogs, few studies have demonstrated this correlation. The present review aims to identify current literature knowledge relating to oxidative stress diseases and their detection in dogs.

scholarly journals PO-133 Effects of different concentrations of hydrogen on oxidative stress in rats with high intensity exercise

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Xue Geng ◽  
Zhihui Li ◽  
Lin Zhang ◽  
Chenggang Zhang
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Oxidative Damage ◽  
High Intensity ◽  
Statistical Difference ◽  
The Body ◽  
High Intensity Exercise ◽  
High Concentration ◽  
Significant Difference ◽  
Exercise Induced

Objective Exercise-induced oxidative stress is due to the massive increase in free radicals caused by strenuous exercise, which exceeds the ability of self-clearing. It is one of the main causes of sports injury and sports fatigue. Eliminating excessive production of free radicals is the key to alleviating exercise induced oxidative damage. Therefore, the purpose of this study is to study the effect of hydrogen on exercise-induced oxidative damage, to explore its possible mechanism and to explore the best dose of hydrogen with different concentrations. Methods 40 male SD rats (200±20g) were randomly divided into five groups(n=8):sedentary, exercise control, low concentration hydrogen with exercise(H1), medium concentration hydrogen with exercise(H2), high concentration hydrogen with exercise(H3). The rats performed high-intensity exercise for 4 weeks, except the sedentary. rats that with Low, medium and high concentration hydrogen were placed in a hydrogen atmosphere with a concentration of 0.5%, 1% and 1.5% for 1 h immediately after each exercise (keeping the concentration of oxygen and nitrogen in the environment the same as those in the air). The rats were weighed weekly during the experiment. The next day after 4 weeks of training, the samples were collected, and the contents of total superoxide dismutase (T-SOD), catalase (CAT), total antioxidant capacity (T- AOC) and malondialdehyde (MDA) were determined respectively. Results The weight of exercise control was significantly lower than sedentary in the third and fourth weeks of exercise (P<0.05). Compared to sedentary rats, there was no significant difference in the weight of rats between H1, H2 and H3 group. The contents of T-AOC, CAT and T-SOD in exercise control were significantly higher than those in sedentary (P<0.05). The content of CAT in H2 group was significantly decreased compared with exercise control (P<0.01). Compared with exercise control, the T-AOC and T-SOD in the H2 group showed a downward trend but no statistical difference (P>0.05), there was no significant difference between the above indexes, compared with sedentary. In addition, there was no difference in T-SOD and CAT content between H1 group and exercise control; Compared with exercise control, there was no significant difference in T-SOD, T-AOC and CAT in H3 group. At the MDA level, each exercise group increased significantly compared with the sedentary (P<0.05), and the MDA levels in the H1, H2, and H3 groups were decreased compared with the exercise control, but there was no statistical difference. Conclusions It can be seen from the above results that different concentrations of hydrogen intervention can improve the weight loss of rats after intensive exercise. More importantly, the dosage and effect of 1% concentration of hydrogen is easier to remove the excessive radicals produced by intense exercise in the body, avoid the aggravation of oxidative stress, and have very good therapeutic effect. It provides a theoretical basis for the further study of the application of hydrogen in exercise oxidative damage. 

scholarly journals STUDI PRELIMINARI TENTANG PENGARUH D-GALAKTOSA DALAM MENGINDUKSI STRES OKSIDATIF PADA MENCIT JANTAN GALUR OUTBRED FK USU

2019 ◽  
Vol 2 (1) ◽  
pp. 1-5
Author(s):  
Siti Sarah Bintang Sarah Bintang ◽  
Yahwardiah Siregar ◽  
Muhammad Ichwan
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
The Body ◽  
Blood Collection ◽  
Male Mice ◽  
North Sumatra

Abstract Oxidative stress occurs due to imbalance of free radicals over antioxidant level in the body. This condition causes lipid peroxidation and DNA damage. D-Galaktosa is The mechanism of oxidative stress induced by d-galactose occurs in the subcellular, especially in the brain's mitochondria. Increasing the concentration of d-galaktosa is oxidized by galaktosa oxidase to form hydrogen peroxide (H202) which causes a decrease in superoxide dismutase (SOD). H202 reacts with reduced iron and forms hydroxide ions (OH-). Objective: The aim of this study was to determine the effect of d-galaktosa induction on oxidative stress levels (MDA) in male mice. Methods: Methods of samples of mice given d-galaktosa and blood collection from the heart were carried out at the Pharmacology Laboratory of the Faculty of Medicine, University of North Sumatra. Results: The results showed that administration of d-galaktosa, through intraperitonial injection every day for 6 weeks, had an effect on the levels of oxidative stress in male mice. Conclusion: The results of this study indicate that administration of d-galaktosa, through intraperitonial injection every day for 6 weeks, has an effect on levels of oxidative stress in male mice.

Toxicity of carbon tetrachloride, free radicals and role of antioxidants

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Velid Unsal ◽  
Mustafa Cicek ◽  
İlhan Sabancilar
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Endoplasmic Reticulum ◽  
Free Radicals ◽  
Carbon Tetrachloride ◽  
Side Effects ◽  
Oxidative Damage ◽  
Cytochrome P450 Enzyme ◽  
Pathological Conditions

AbstractSeveral chemicals, including environmental toxicants and clinically useful drugs, cause severe cellular damage to different organs of our body through metabolic activation to highly reactive substances such as free radicals. Carbon tetrachloride is an organic compound of which chemical formula is CCl₄. CCl4 is strong toxic in the kidney, testicle, brain, heart, lung, other tissues, and particularly in the liver. CCl4 is a powerful hepatoxic, nephrotoxic and prooxidant agent which is widely used to induce hepatotoxicity in experimental animals and to create hepatocellular carcinoma, hepatic fibrosis/cirrhosis and liver injury, chemical hepatitis model, renal failure model, and nephrotoxicity model in recent years. The damage-causing mechanism of CCl4 in tissues can be explained as oxidative damage caused by lipid peroxidation which starts after the conversion of CCl4 to free radicals of highly toxic trichloromethyl radicals (•CCl₃) and trichloromethyl peroxyl radical (•CCl₃O2) via cytochrome P450 enzyme. Complete disruption of lipids (i.e., peroxidation) is the hallmark of oxidative damage. Free radicals are structures that contain one or more unpaired electrons in atomic or molecular orbitals. These toxic free radicals induce a chain reaction and lipid peroxidation in membrane-like structures rich in phospholipids, such as mitochondria and endoplasmic reticulum. CCl4-induced lipid peroxidation is the cause of oxidative stress, mitochondrial stress, endoplasmic reticulum stress. Free radicals trigger many biological processes, such as apoptosis, necrosis, ferroptosis and autophagy. Recent researches state that the way to reduce or eliminate these CCl4-induced negative effects is the antioxidants originated from natural sources. For normal physiological function, there must be a balance between free radicals and antioxidants. If this balance is in favor of free radicals, various pathological conditions occur. Free radicals play a role in various pathological conditions including Pulmonary disease, ischemia / reperfusion rheumatological diseases, autoimmune disorders, cardiovascular diseases, cancer, kidney diseases, hypertension, eye diseases, neurological disorders, diabetes and aging. Free radicals are antagonized by antioxidants and quenched. Antioxidants do not only remove free radicals, but they also have anti-inflammatory, anti-allergic, antithrombotic, antiviral, and anti-carcinogenic activities. Antioxidants contain high phenol compounds and antioxidants have relatively low side effects compared to synthetic drugs. The antioxidants investigated in CCI4 toxicity are usually antioxidants from plants and are promising because of their rich resources and low side effects. Data were investigated using PubMed, EBSCO, Embase, Web of Science, DOAJ, Scopus and Google Scholar, Carbon tetrachloride, carbon tetrachloride-induced toxicity, oxidative stress, and free radical keywords. This study aims to enlighten the damage-causing mechanism created by free radicals which are produced by CCl4 on tissues/cells and to discuss the role of antioxidants in the prevention of tissue/cell damage. In the future, Antioxidants can be used as a therapeutic strategy to strengthen effective treatment against substances with high toxicity such as CCl4 and increase the antioxidant capacity of cells.

scholarly journals Study of prooxidant activity and some indicators of the pituitary-gonadal system in patients suffering from chronic endometritis

2020 ◽  
Vol 22 (1) ◽  
pp. 66-69
Author(s):  
N V Kirillova ◽  
O M Spasenkova ◽  
A G Platonova
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Modification ◽  
Aliphatic Aldehyde ◽  
Oxidative Modification ◽  
Control Group ◽  
Diene Conjugates ◽  
Oxidative Modification Of Proteins ◽  
Chronic Endometritis ◽  
Oxidative Protein Modification

The state of lipid peroxidation and the oxidative modification of proteins in the blood of 29 women with chronic endometritis aged 27 to 40 years were studied. The control group consisted of 19 healthy women aged 27 to 44 years. The intensity of lipid peroxidation was estimated by the level of diene conjugates and malondialdehyde, the oxidative modification of proteins - by the level of carbonyl derivatives. It was shown that in the blood of women with chronic endometritis, the concentration of aliphatic aldehyde groups and 1,9 times the carbonyl groups in protein molecules increases by 3,3 times compared with the control group. A significant increase in diene conjugates by 34% and malondialdehyde in blood plasma and red blood cells by 47 and 43%, respectively, was established. The increase in lipid peroxidation products and oxidative protein modification in the blood indicates the development of oxidative stress in women suffering from chronic endometritis. Compared with healthy patients with chronic endometritis, a convincing tendency toward an increase in prolactin and anti- Muller hormone against a decrease in progesterone was revealed in the group compared to healthy ones. To predict possible complications in patients with chronic endometritis, it is advisable to study the indicators of protein and lipid peroxidation as markers of oxidative stress and the severity of the inflammatory process. In addition, such patients should be advised to take antioxidant drugs in combination with the basic therapy.

Changes in lipid peroxidation during pregnancy and after delivery in rats: effect of pinealectomy

Reproduction ◽  
2000 ◽  
pp. 143-149 ◽  
Author(s):  
RM Sainz ◽  
RJ Reiter ◽  
JC Mayo ◽  
J Cabrera ◽  
DX Tan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Energy Demand ◽  
Physiological State ◽  
High Energy ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Oxygen Requirement ◽  
Pregnant Rats

Pregnancy is a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement. Because of the increased intake and utilization of oxygen, increased levels of oxidative stress would be expected. In the present study, the degree of lipid peroxidation was examined in different tissues from non-pregnant and pregnant rats after the delivery of their young. Melatonin and other indole metabolites are known to be direct free radical scavengers and indirect antioxidants. Thus the effect of pinealectomy at 1 month before pregnancy on the accumulation of lipid damage was investigated in non-pregnant and pregnant rats after the delivery of their young. Malonaldehyde and 4-hydroxyalkenal concentrations were measured in the lung, uterus, liver, brain, kidney, thymus and spleen from intact and pinealectomized pregnant rats soon after birth of their young and at 14 and 21 days after delivery. The same parameters were also evaluated in intact and pinealectomized non-pregnant rats. Shortly after delivery, lipid oxidative damage was increased in lung, uterus, brain, kidney and thymus of the mothers. No differences were detected in liver and spleen. Pinealectomy enhanced this effect in the uterus and lung. It is concluded that during pregnancy high levels of oxidative stress induce an increase in oxidative damage to lipids, which in some cases is inhibited by the antioxidative actions of pineal indoles.

Evaluation of Salivary Antioxidants and Oxidative Stress Markers in Male Smokers

2019 ◽  
Vol 22 (7) ◽  
pp. 496-501
Author(s):  
Fatemeh Ahmadi-Motamayel ◽  
Parisa Falsafi ◽  
Hamidreza Abolsamadi ◽  
Mohammad T. Goodarzi ◽  
Jalal Poorolajal
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Free Radicals ◽  
Antioxidant Capacity ◽  
Cigarette Smoke ◽  
Total Antioxidant Capacity ◽  
The Body ◽  
Total Antioxidant ◽  
The Mean ◽  
And Oxidative Stress

Background: Cigarette smoke free radicals can cause cellular damage and different diseases. All the body fluids have antioxidants which protect against free radicals. Objective: The aim of this study was to evaluate salivary total antioxidant capacity and peroxidase, uric acid and malondialdehyde levels in smokers and a nonsmoking control group. Methods: Unstimulated saliva was collected from 510 males. A total of 259 subjects were current smokers and 251 were non-smokers. The levels of salivary total antioxidant capacity, uric acid, peroxidase and malondialdehyde were measured using standard procedures. Data were analyzed with t test and ANOVA. Results: The smokers were younger and dental hygiene index was higher than healthy nonsmoking controls. The mean total antioxidant capacity in smokers and nonsmokers was 0.13±0.07 and 0.21±011, respectively (P=0.001). Smokers had significantly lower peroxidase and uric acid levels than healthy controls. In addition, the mean malondialdehyde levels in the smokers and nonsmokers were 4.55 ±2.61 and 2.79 ±2.21, respectively (P=0.001). Conclusion: Cigarette smoke produces free radical and oxidative stress, causing many side effects. Salivary antioxidant levels decreased and malondialdehyde levels increased in smokers, indicating the high oxidative stress among smokers compared to nonsmokers. Cigarette smoke had deleterious effects on main salivary antioxidants levels.

Mechanisms of Nickel-Induced Cell Damage in Allergic Contact Dermatitis and Nutritional Intervention Strategies

2020 ◽  
Vol 20 (7) ◽  
pp. 1010-1014 ◽  
Author(s):  
Dana Filatova ◽  
Christine Cherpak
Keyword(s):  
Lipid Peroxidation ◽  
Contact Dermatitis ◽  
Oxidative Damage ◽  
Allergic Contact Dermatitis ◽  
Cell Damage ◽  
Consumer Products ◽  
The Body ◽  
Cellular Damage ◽  
Nutritional Interventions ◽  
Allergic Contact

Background: Hypersensitivity to nickel is a very common cause of allergic contact dermatitis since this metal is largely present in industrial and consumer products as well as in some commonly consumed foods, air, soil, and water. In nickel-sensitized individuals, a cell-mediated delayed hypersensitivity response results in contact to dermatitis due to mucous membranes coming in long-term contact with nickel-containing objects. This process involves the generation of reactive oxidative species and lipid peroxidation-induced oxidative damage. Immunologically, the involvement of T helper (h)-1 and Th-2 cells, as well as the reduced function of T regulatory cells, are of importance. The toxicity, mutagenicity, and carcinogenicity of nickel are attributed to the generation of reactive oxygen species and induction of oxidative damage via lipid peroxidation, which results in DNA damage. Objective: The aim of this research is to identify nutritionally actionable interventions that can intercept nickel-induced cell damage due to their antioxidant capacities. Conclusion: Nutritional interventions may be used to modulate immune dysregulation, thereby intercepting nickel-induced cellular damage. Among these nutritional interventions are a low-nickel diet and an antioxidant-rich diet that is sufficient in iron needed to minimize nickel absorption. These dietary approaches not only reduce the likelihood of nickel toxicity by minimizing nickel exposure but also help prevent oxidative damage by supplying the body with antioxidants that neutralize free radicals.

scholarly journals Antioxidants, lysosomes and elements status during the life cycle of sea trout Salmo trutta m. trutta L.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Natalia Kurhaluk ◽  
Halyna Tkachenko
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Muscle Tissue ◽  
Salmo Trutta ◽  
Protein Carbonyl ◽  
Oxidative Modification ◽  
Oxidative Stress Biomarkers ◽  
Development Stages ◽  
Stress Biomarkers ◽  
Element Contents

AbstractThe aim of our study was to elucidate the effects of both development stages (parr, smolt, adult, spawner), and kelt as a survival form and sex (male, female) on the functional stability of the lysosomal complex, biomarkers of oxidative stress, and element contents in the muscle tissue of the sea trout (Salmo trutta m. trutta L.) sampled in the Pomerania region (northern Poland). We have evaluated the maximal activities of lysosomal enzymes (alanyl aminopeptidase, leucyl aminopeptidase, β-N-acetylglucosaminidase, and acid phosphatase), lipid peroxidation level, and protein carbonyl derivatives as indices of muscle tissue degradation. The relationship between lysosomal activity and oxidative stress biomarkers estimated by the lipid peroxidation level and protein carbonyl derivatives was also assessed, as well as the relationships between element levels and oxidative stress biomarkers. Trends of the main effects (i.e., the development stages and sex alone, the interaction of the sex and development stage simultaneously) on oxidative stress biomarkers, lysosomal functioning, and element contents in the muscle tissue were evaluated. The study has shown sex-related relationships between the pro- and antioxidant balance and the tissue type in the adult stage as well as modifications in the lysosomal functioning induced by long-term environmental stress associated with changing the habitats from freshwater to seawater and intense migrations. The highest level of toxic products generated in oxidative reactions and oxidative modification of proteins was noted in both the spawner stage and the kelt form. The holistic model of analysis of all parameters of antioxidant defense in all development stages and sex demonstrated the following dependencies for the level of lipid peroxidation, oxidative modification of proteins, lysosomal activities, and element contents: TBARS > OMP KD > OMP AD > TAC, AcP > NAG > LAP > AAP and Cu > Fe > Ca > Mn > Zn > Mg, respectively.

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