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Results for “Antioxidant defense system”

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At least 19 recordsLinked to original sources

PubMed1998

Impaired antioxidant defense system in the kidney tissues from rabbits treated with cyclosporine. Protective effects of vitamins E and C.

Enzymatic antioxidant defense system and antioxidant defense potential (AOP) were studied in kidney tissue from rabbits treated with cyclosporine (CsA, 25 mg/kg/day), antioxidant vitamins (E, 100 mg/kg/day plus C, 200 mg/ kg/day), and CsA plus antioxidant vitamins, and in kidney tissue from control animals. Although no change was observed in superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) and catalase (CAT) activities were found decreased in kidney tissue exposed to CsA for 10 days compared with control tissue. The level of thiobarbituric acid-reagent substances (TBARS) was higher and antioxidant defense potential (AOP) lower in the CsA-treated group compared with the other groups. Histopathological examination reveals important subcellular damage in the renal tissue from the animals treated with CsA. Antioxidant vitamin therapy caused full improvement in the enzyme activities, TBARS levels and AOP, but the subcellular damage was partly ameliorated in the CsA plus vitamin group. Results suggest that CsA impairs the antioxidant defense system and reduces the antioxidant defense potential in the renal tissue. Antioxidant vitamin treatment protects the tissue in part against toxic effects of the drug.

Animals↗

PubMed1991

[Effects of ethanol and limontar in the antenatal period of development on lipid peroxidation process and antioxidant defense system in the brain and liver tissue of fetal and newborn rats].

The process of lipid peroxidation and the system of antioxidant defense in brain and liver of fetuses on the 20th day of gestation and 1 day old rats after antenatal exposure to ethanol and limontar were studied. It was shown that antenatal exposure to ethanol led to activation of the process of lipid peroxidation in brain and to inhibition of of the enzyme system of antioxidant defense in liver of fetal and newborn rats. Limontar promoted the normalization of both the process of lipid peroxidation and the system of antioxidant defense.

Animals↗

PubMed2000

Defective antioxidant defense system in patients with a human leptin gene mutation.

Antioxidant defense system prevents the organism from the detrimental effects of free radicals via scavenging or inhibiting their formation. Changes in the antioxidant defense mechanisms and alterations of several essential trace elements in both plasma and various tissues of ob/ob mice have been reported previously. Recent finding of the restoration of the defective antioxidant enzyme activity after leptin treatment in ob/ob mice suggests a putative role of leptin in modulation of antioxidant enzyme activity. Therefore, the aim of this study was to investigate whether antioxidant enzymes and trace elements could also be altered in patients with leptin gene mutation. Seven patients (five men and two women, two of them are homozygous and 5 are heterozygous) with leptin gene mutation and 31 healthy, sex- and age-matched and non-related to the patients (24 male and 9 female), control volunteers were enrolled in the study. Plasma and erythrocyte glutathione peroxidase (GSH-Px) and erythrocyte copper-zinc superoxide dismutase (CuZn-SOD) activities were measured spectrophotometrically. Plasma selenium (Se), manganese (Mn), zinc (Zn), copper (Cu), and iron (Fe) levels were measured by atomic absorption spectrophotometry. Mean Cu and Fe levels in patients were not significantly different than those in controls whereas mean Se, Zn and Mn levels were significantly lower in patients than those of controls (P=0.007, P=0.001, and P=0.001, respectively). Erythrocyte GSH-Px (39%), plasma GSH-Px (24%) and erythrocyte CuZn-SOD activities (32%) were significantly lower than those of the control group (P=0.001, P=0.002, P=0.001, respectively). In conclusion, our results demonstrate that the activity of antioxidant enzymes and plasma levels of Se, Zn and Mn levels were decreased in both homozygous and heterozygous subjects with leptin gene mutation. We suggest that both leptin and trace elements might be involved in the modulation of antioxidant defense system.

Adult↗

PubMed1997

Oxidative injury of synapse and alteration of antioxidative defense systems in rats, and its prevention by vitamin E.

In order to define whether active oxygen species actually induce oxidative damage to the nervous system, and how antioxidative defense systems are changed by oxidative stress, morphological and functional changes in the nervous system and antioxidant status were investigated. When rats were exposed to 100% oxygen in a chamber, many morphological changes, e.g. swollen astrocytes around vessels, deformed nuclei in nerve cells, pigmentation, swollen mitochondria, and abnormal accumulation of synaptic vesicles in swollen nerve terminals, were observed by electron microscopy. When synaptosomes isolated from oxygen-exposed rats were stimulated by KCl, acetylcholine release from the terminal was decreased more significantly than in synaptosomes from unexposed rats (P < 0.01). Synaptic plasma membrane fluidity decreased in response to oxygen exposure, and plasma membrane permeability to sucrose was increased significantly (P < 0.05). The cholesterol/phospholipid ratio of the plasma membranes was increased by oxidative stress and the content of unsaturated fatty acids, especially arachidonic acid and docosahexaenoic acid, decreased. The levels of thiobarbituric-acid-reactive substances in the plasma membranes of oxygen-exposed rats were significantly higher than in unexposed rats (P < 0.01). These results suggest that free radicals derived from oxygen may attack nerve terminals and peroxidize the plasma membrane. It was found that in response to the oxidative stress, the status of the defense system in synapse, i.e. the concentration of vitamin E, activities of superoxide dismutase and glutathione peroxidase changed, and that many of the changes observed were reduced remarkably by the intraperitoneal administration of vitamin E prior to stress. Data support the idea that vitamin E contributes to the protection against nerve dysfunction caused by oxidative stress.

Acetylcholine↗

PubMed2000

[Use of soluble ozone in combined treatment of pulmonary tuberculosis: lipid peroxidation and blood antioxidative defense systems].

Changes in lipid peroxidation and blood antioxidative defense systems and red blood cell function were studied in 16 patients with prolonged progressive pulmonary tuberculosis in response to intravenous soluble ozone (SO) administration. There was a drastic rise in the activity of intraerythrocytic superoxide dismutase (SOD) and a reduction in intracellular malonic dialdehyde (MDA) levels. In the remaining patients, there was a decrease in the activity of SOD and an increase in intraerythrocytic MDA concentrations. Plasma catalase activity increased in all patients and MDA levels lowered. It is proposed that initial SO doses for patients with chronic pulmonary tuberculosis should be chosen on an individual basis by taking into account intraerythrocytic SOD-MDA changes due to SO initiation.

Adolescent↗

PubMed2001

Effects of multinutrient supplementation on antioxidant defense systems in healthy human beings.

Oxidative damage involved in the pathogenesis of many diseases, such as cardiovascular disease, cancer and diabetics. The antioxidant defense system plays an important role in protecting body from oxidative damage. Numerous studies have been shown that a single vitamin or mineral supplementation has the beneficial effect on the antioxidant defense system. However, the overall combined effect of multinutrient supplementation on antioxidant defense system remains to be clarified. In the present double blind, placebo-controlled study, the antioxidative defense system was measured in 34 healthy subjects before and after multinutrient supplementation. Plasma vitamin C, E and beta-carotene, erythrocyte vitamin E, as well as whole blood selenium all showed increase at 5 weeks of supplementation. The activities of catalase (CAT) and glutathione peroxidase (GPX), but not superoxide dismutase (SOD), as well as GSH level were significantly increased at 16 weeks of supplementation. Moreover, the resistance of erythrocytes to 2,2'-Azobis(2-amidinopropane) dihydrochloride (AAPH)-induced oxidation was elevated at 5 weeks after supplementation. These results clearly demonstrated that short-term supplementation (16 weeks) with multinutrient could markedly improve antioxidative vitamin status and enzymatic activities. These improvements also led to the reduction of RBC susceptibility to free radial peroxidation.

Journal Article↗

PubMed1997

Effects of acrolein on rat liver antioxidant defense system.

Effect of acrolein (2.5 mg/kg body wt/day) on the rat liver antioxidant defense system was investigated. Following 45 days of acrolein exposure, the levels of glutathione, ascorbic acid and the activity of catalase were decreased whereas the activities of superoxide dismutase and glutathione peroxidase were increased. The increase in the level of thiobarbituric acid reactive substances in the acrolein treated rats showed oxidative damage. The results indicate that acrolein interferes with the antioxidant defense system of rat liver.

Acrolein↗

PubMed1995

Impact of nutrients on cellular lipid peroxidation and antioxidant defense system.

A symposium entitled Impact of Nutrients on Cellular Lipid Peroxidation and Antioxidant Defense System was held at the 33rd Annual Meeting of the Society of Toxicology (SOT) at the Loews Anatole Hotel in Dallas, Texas. The symposium was sponsored by the Food Safety Specialty Section and focused on the role of particular nutrients in cellular lipid peroxidation and antioxidant defense system. Emphasis was placed on defining underlying mechanisms for damage and protection, as well as potential ramification in human health issues. The following are extractions of some of the highlights from each presentation.

Antioxidants↗

PubMed1999

Change in hepatic antioxidant defense system with liver injury development in rats with a single alpha-naphthylisothiocyanate intoxication.

The change in hepatic antioxidant defense system with the development of alpha-naphthylisothiocyanate (ANIT)-induced liver injury was examined in rats injected once with the toxicant (75 mg/kg body weight). Liver injury with cholestasis did not occur 12 h after ANIT injection, but appeared at 24 h, progressed at 48 h, and recovered at 72 h, judging from the serum levels of marker enzymes and components. Liver lipid peroxide content increased 12 h after ANIT injection and further increased 24 and 48 h, but this increase was attenuated at 72 h. Liver superoxide dismutase and catalase activities decreased 24 and 48 h, respectively, after ANIT injection, although the catalase activity increased at 12 h, but these decreases were attenuated at 72 h. Liver Se-glutathione peroxidase activity remained unchanged 24, 48, and 72 h after ANIT injection, although the activity increased at 12 h. Liver reduced glutathione content increased 24 h after ANIT injection, but the increase was reduced time dependently thereafter. Liver ascorbic acid content increased 12 h after ANIT injection and further increased at 24 h, but the increase was reduced time dependently thereafter. These results indicate that the change in hepatic antioxidant defense system occurs before and with the development of ANIT-induced liver injury in rats, and suggest that the reduction of hepatic antioxidant defense system mediated by SOD and catalase could contribute to the liver injury development through an enhancement of hepatic lipid peroxidation.

1-Naphthylisothiocyanate↗

PubMedDate not supplied

[Lipid peroxidation and antioxidant defense system in rats after a 14-day space flight in the "Space-2044" spacecraft].

After 14-day space flight of rats onboard Cosmos 2044 in their blood plasma, homogenates of liver, skeletal muscles and myocardium there were determined the parameters of peroxide oxidation of lipids (POL) and system of antioxidant defense: content of dienic conjugates (DC), malonic dialdehyde (MDA), schiff bases (SB), tocopherol (TF), total antioxidative activity (AOA, only in plasma), activity of antioxidative enzymes (only in tissues) superoxide (SOD), catalase, glutathione-peroxidase (GP), glutathione-reductase (GR). In the animal liver there was a decrease in SB content and an increase of SOD, catalase and GP activities. Skeletal muscles exhibited a reduced SB concentration. In myocardium there was a reduction of DC and SB levels, activity of GR with an increase of TF concentration, activity of SOD and catalase. In the blood plasma there occurred a decline of SB and TF contents and an elevation of MDA and total AOA concentrations. The authors drew a conclusion about a compensated process of POL in the tested animals and about the relation of the observed changes with body response to the final phase of the space mission and acute gravitational stress during a readaptation to the Earth environments. On the basis of the analysis of similar data from shorter-duration space experiments, the noted changes in the parameters of the system of POL and antioxidant defense are considered a universal response which does not directly depend on duration of the orbital phase of a space mission.

Adaptation, Physiological↗

PubMed2000

Chronic diarrhea impairs intestinal antioxidant defense system in rats at weaning.

The aim of the present study was to evaluate the influence of severe protein-energy malnutrition on the antioxidant defense system in the small and large intestine in rats at weaning. Chronic diarrhea and the subsequent malnutrition were induced by oral intake of a lactose-enriched diet. Twenty rats were weaned at 21 days of age, and the control group was fed a semipurified synthetic diet for two weeks. The malnourished group was fed the same diet but carbohydrates were replaced by lactose, and they developed diarrhea one day after. Rats were killed, and macroscopic and histological features were analyzed, DNA content was measured, and alkaline phosphatase, myeloperoxidase, and gamma-glutamyltranspeptidase activities were determined to assess the degree of intestinal injury. Glutathione levels as well as the activities of intestinal glutathione transferase, glutathione reductase, total glutathione peroxidase, selenium-dependent glutathione peroxidase, superoxide dismutase, and catalase were measured to study the antioxidant defense system. Malnourished rats showed loss of body weight and an increase in length and weight in jejunum and ileum, while no significant changes were observed in colon. Epithelial cells showed fewer and shorter microvilli, larger mitochondria with low inner density and loss of cristae, dilated endoplasmic reticulum, and Golgi apparatus. The protein-to-DNA ratio was higher in the jejunum, ileum, and colon of malnourished rats. Glutathione levels decreased 40% in jejunum and 50% in colon of malnourished rats. A 40-50% decrease in the activity of all the enzymes of the antioxidant defense system was observed in the jejunum and ileum of malnourished rats, while only catalase and glutathione transferase activities decreased 50% in colon. These results suggest that early chronic diarrhea and severe protein-energy malnutrition impair the antioxidant defense system in both the small and large intestine, which may have a role in the pathogenesis and maintenance of the vicious circle of malabsorption-diarrhea-malnutrition in infancy.

Animals↗

PubMed1999

Dose response of ethanol ingestion on antioxidant defense system in rat brain subcellular fractions.

This study investigated the response of the antioxidant defense system in brain subcellular fractions after oral graded doses of ethanol to rat. Four groups of male Fischer-344 rats were orally administered saline, ethanol 2 g, 4 g, and 6 g/kg, respectively, and sacrificed 1 hour post treatment. Brain cytosol, synaptosomes, microsomes and mitochondria were separated by density gradient differential centrifugation and assayed for antioxidant system. A significant and dose-dependent-decrease in superoxide dismutase (SOD) activity was observed in all brain subcellular fractions. Catalase (CAT) activity was significantly decreased in brain mitochondria (67% and 80% of control) at higher doses of ethanol; whereas, CAT activity was significantly increased in cytosol, synaptosomes and microsomes. Glutathione peroxidase (GSH-Px) activity was significantly increased in all brain subcellular fractions except in cytosol at higher dose of ethanol. Malondialdehyde (MDA) content was significantly increased in all brain subcellular fractions showing dose response of ethanol-induced oxidative stress. The increase in MDA levels in the brain synaptosomes and microsomes were higher at 6 g dose of ethanol (155% and 163% of control) when compared to mitochondria and cytosol. Glutathione (GSH) levels were significantly increased in brain cytosol and microsomes at higher dose of ethanol (164% and 159% of control); whereas, the GSH concentration was significantly decreased in brain synaptosomes and mitochondria. The antioxidant enzyme (AOE) activity ratios (GSH-Px/SOD and GSH-Px + CAT/SOD) were dose dependently increased in all brain subcellular fractions, particularly in synaptosomes. The GSH/GSSG ratio was dose dependently increased in brain microsomes. The perturbations in the antioxidant defense system and enhanced lipid peroxidation following graded doses of ethanol ingestion indicate a dose-dependent-oxidative 2133stress response in brain subcellular compartments of rats.

Animals↗

PubMed2003

Chronic cold exposure affects the antioxidant defense system in various rat tissues.

BACKGROUND: Chronic exposure to stress alters the normal body homeostasis and, hence, leads to the development of various human pathologies, which might involve alterations in the antioxidant defense system. We studied the effect of chronic cold exposure on oxidative stress and antioxidant defense system in various rat tissues. METHODS: Male albino rats (Wistar strain), 2-3 months old, were exposed to 3 weeks of cold treatment. Antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) were measured in addition to the antioxidants, ascorbic acid (AsA) and glutathione (GSH), and the prooxidants, lipid peroxides (LPO) and xanthine oxidase (XOD), in brain, heart, kidney, liver and small intestine using standard protocols. RESULTS: Chronic cold exposure resulted in a significant increase in LPO in all the tissues studied while XOD was increased in the brain and intestine. Total SOD activity was significantly decreased in all the tissues, whereas CAT activity was significantly increased in the kidney and decreased in heart, liver and intestine in the animals exposed to cold. GPx activity was increased only in the brain and intestine of stressed rats. Chronic cold exposure resulted in significant decrease in GR activity in heart, liver and intestine. GST activity was increased (except heart) and GSH was significantly decreased in all the tissues in treated rats. AsA was increased in kidney and intestine but decreased in heart of stressed animals. CONCLUSIONS: The observed changes in the antioxidant defense system are tissue specific, but it is evident that chronic exposure to cold leads to oxidative stress by displacing the prooxidant-antioxidant balance of this defense system by increasing the prooxidants while depleting the antioxidant capacities.

Animals↗

PubMed2000

[Indices of lipid peroxidation and antioxidant defense system and prostanoid level in patients with uterine cancer].

The state of peroxydal oxidation of lipids, system of antioxidant defense and content of prostanoids in patients with cancer of the corpus uteri were investigated. Syndrome of endogenous intoxication with lowering of antioxidant potential and dysbalance of cyclic nucleotides and prostaglandines was established. The severity of above-cited disorders increased significantly after operation and during conduction of radiotherapy. This demanded administration of antioxidant and detoxicational therapy in complex of preoperative preparation.

Adult↗

PubMed2003

Protective influence of vitamin E on antioxidant defense system in the blood of rats treated with cadmium.

The effects of acute exposure to cadmium (Cd) on the blood antioxidant defense system, lipid peroxide concentration and hematological parameters, as well as the possible protective role of vitamin E were studied. Male Wistar albino rats (3 months old) were treated with cadmium (0.4 mg Cd/kg b.m., i.p., 24 h before the experiment) or with vitamin E + Cd (20 IU Vit E/kg b.m., i.m., 48 h + 0.4 mg Cd/kg b.m., i.p., 24 h before the experiment). The hematological parameters were assessed: red blood cell counts, hematocrit value and hemoglobin concentration were significantly decreased in the blood of Cd-treated rats. Intoxication with cadmium was also followed by significantly increased lipid peroxide concentrations. We also observed increased activity of antioxidant defense enzymes: copper zinc containing superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase as well as concentrations of non-enzymatic components of antioxidant defense system: reduced glutathione, vitamin C and vitamin E. Pretreatment with vitamin E exhibited a protective role on the toxic effects of cadmium on the hematological values, lipid peroxide concentration as well as on enzymatic and non-enzymatic components of antioxidant defense system.

Animals↗

PubMed1990

Red blood cells and serum antioxidant defense systems of galactosaemic children.

Many reports have pointed out that oxidative damage and disturbances in antioxidant defense systems of the lenses may play an important role in the development of cataract. In the present study the activities of glutathione peroxidase, glutathione reductase, glutathione-S-transferase, glucose-6-phosphate dehydrogenase, catalase and the level of glutathione and lipid peroxides were measured in red blood cells of galactosaemic children with cataract and without cataract. Furthermore the serum antioxidant activity and the level of uric acid. ceruloplasmin and transferrin in serum were estimated. It was found that in red blood cells of galactosaemic children with cataract the activity of glutathione reductase was slightly lower than in a control age-matched group of children and in galactosaemic children without cataract. The increase of serum antioxidant activity in both groups of galactosaemic children was also observed. Probably it could be due to the increase of the level of ceruloplasmin. Except glutathione reductase activity no other differences were found in the investigated components of the antioxidant defense systems of red blood cells and serum between galactosaemic children with cataract and those without cataract. Therefore it seems that red blood cells and serum metabolism are no good reflections of disturbances in antioxidant defense mechanisms which may be involved in the cataract development in galactosaemic children.

Antioxidants↗

PubMed1987

Age-related development profiles of the antioxidative defense system and the peroxidative status of the pig heart.

The developmental profiles of the antioxidative defense system and the peroxidative status of the heart during growth and development were studied in pigs of three different age groups. A unique age-specific myocardial lipid peroxidation expressed in terms of malonaldehyde formation occurred after incubation of neonatal and adult pig heart homogenates in the absence of any added factors. Very little malonaldehyde release was noticed in the 0- to 2-day age group, while considerably higher activity was found in the 8- to 10-day-old animals. The 2-month-old pig heart again formed very little malonaldehyde. Myocardial injury from lipid peroxidation was highest in the 0- to 2-day age group, as evidenced by the release of oxidized glutathione, lactate dehydrogenase (LDH) and creatine kinase (CK) activities. Release of glutathione, LDH and CK decreased with age and was minimal in the adult group. The antioxidative enzymes, superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, increased during the first 10 days of neonatal growth and then levelled off. Glucose-6-phosphate dehydrogenase was present in appreciably lower amounts in adult hearts compared to neonatal hearts. Heart weight increased with aging, but myocardial water content decreased. Protein and DNA contents of hearts increased with age, such that the protein/DNA ratio almost doubled from the newborn to adult age. The results indicate that the newborn pig hearts are equipped with the antioxidative defense system, which undergoes significant development during the initial phase of neonatal growth and does not change appreciably thereafter. The results further suggest that the change in activity profile with aging is different for different enzymes, and the peroxidative status of the myocardium is not a function of these enzyme activities.

Aging↗

PubMed1988

Effects of gossypol on the antioxidant defense system of the rat testis.

This study examined the effects of gossypol acetic acid on the antioxidant defense system of the rat testis. In gossypol-treated animals testis catalase and glutathione peroxidase activities were decreased. Catalase and glutathione peroxidase are the two enzymes that protect against oxidative damage by hydrogen peroxide. Other antioxidants that were reduced in treated animals were glucose-6-phosphate dehydrogenase, superoxide dismutase, glutathione reductase, alpha-tocopherol, and ascorbate. Gossypol, a pigment of cottonseed and cottonseed products, causes infertility in humans and many animal species, but its mechanism of action is unknown. Gossypol is known to produce reactive oxygen species in vitro. Oxidative injury caused by the generation of reactive oxygen species and a compromised antioxidant defense system may be responsible for the antifertility effects of gossypol.

Administration, Oral↗