Antioxidant Defense In Rats Research Articles

Experimental study of the antioxidant and antidiabetic effects of a colloid nanosized selenium solution

Oxidative stress resulting from an imbalance of free radical oxidation (FRO) and antioxidant defense (AOD) is one of the main pathogenetic processes underlying the development of type 1 diabetes mellitus (DM1) and its complications. The purpose of the study was to reveal the ability of a colloidal nanosized selenium solution to correct the indices of FRO and AOD in rats when modeling alloxan DM1. Materials and methods. The experiment was carried out on male Wistar rats divided into groups: intact, control (healthy rats treated with selenium); DM1; DM1 treated with selenium. DM1 was simulated by intraperitoneal injection of an alloxan solution at a dose of 170 mg/kg. A solution of selenium was administered intragastrically to diabetic and control rats at a dose of 46.7 μg/kg three times a week (12 injections). A colloidal solution of nanosized selenium was obtained by laser ablation using radiation of two wavelengths. In blood plasma were determined: the content of glucose, urea, creatinine, total protein, reduced glutathione, and malondialdehyde; activity of aminotransferases (AST, ALT), α-amylase, alkaline phosphatase; in whole blood — the content of glycated hemoglobin (HbA1c); in hemolysate of erythrocytes — the activity of superoxide dismutase (SOD), catalase, glutathione peroxidase. Results and discussion. Modeling of alloxan diabetes mellitus is accompanied by the development of hyperglycemia and changes in biochemical parameters indicating damage to liver cells (ALT), kidneys (urea, creatinine), myocardium (AST), and the development of oxidative stress (accumulation of malondialdehyde), partially compensated by SOD activation. The antidiabetic effect of selenium solution is manifested in the correction of glucose and HbA1c levels, liver and kidney profile indicators. The antioxidant effect of selenium is manifested in the normalization of the level of malondialdehyde and in reducing the need for reduced glutathione. The administration of selenium to healthy animals is accompanied by an increase in indicators reflecting the stressful effect of intragastric administration procedures (glucose, SOD) and, possibly, the toxic effect of selenium nanoparticles, which requires a more detailed study. Conclusion. A colloidal solution of nanosized selenium, obtained by an original method, had an antioxidant and antidiabetic effect on rats with type 1 alloxan diabetes mellitus.

The protective effects of red beetroot (Beta vulgaris l.) against oxidative stress in rats induced by high fat and fructose diet

Background: One of consequence high-fat and fructose diet is oxidative stress. Consumption of antioxidants from red beetroot may increase antioxidant defense.
 Objectives: This study aimed to evaluate red beetroot administration on improving antioxidant defense in rats induced high fat and fructose diet.
 Methods: A total 20 male Wistar rats were divided into 4 groups: 1) normal control group (N), received standard diet; 2) High fat and fructose diet (HF), received high fat and fructose diet (HFFD); 8 weeks induction with HFFD and received 9g red beetroot (BA); and combination of HFFD and 9g of red beetroot from beginning of the study (HFBA). At the end of the study the levels of circulatory oxidized LDL (ox-LDL) were determined using enzyme-linked immunosorbent assay (ELISA) method. Superoxide dismutase 2 (SOD2) and catalase (CAT) gene expressions were determined by quantitative polymerase chain reaction (qPCR) method.
 Results: Induction HFFD increased the levels of circulatory ox-LDL levels compared to normal control (10.00±0.29 vs 12.69±0.57). Administration of red beetroot for 6 weeks and combination HFFD with red beetroot during the study significantly decreased ox-LDL levels compared to high fat and fructose group (12.69±0.57 vs 9.66±0.46) and (12.69±0.57 vs 8.59±0.18), respectively. The decreased circulatory ox-LDL levels were found negatively correlated with upregulation SOD2 (r=-0.548; P=0.012) and CAT (r=-0.460; P=0.041) gene expression in the liver tissues.
 Conclusion: Administration of red beetroot may ameliorate oxidative stress in rats induced high-fat and fructose diet through increasing antioxidant defense.

Stigmasterol alleviates cerebral ischemia/reperfusion injury by attenuating inflammation and improving antioxidant defenses in rats.

Background/aims: The paper aimed to investigate the effects of Stigmasterol on inflammatory factors, antioxidant capacity, and apoptotic signaling pathways in brain tissue of rats with cerebral ischemia/reperfusion (I/R) injury. Methods: The neurological deficits of the rats were analyzed and HE staining was performed. The cerebral infarct volume was calculated by means of TTC staining, and neuronal apoptosis was detected by TUNEL staining. At the same time, the contents of glutathione peroxidase, glutathione, superoxide dismutase (SOD), nitric oxide, and malondialdehyde in brain tissue were measured. The expression of the relevant protein was detected by means of Western blotting. Results: The results showed that the neurological deficit score and infarct area of the I/R rats in the soy sterol treatment group were significantly lower than those in the I/R group. Moreover, the levels of carbon monoxide and malondialdehyde in the soysterol group were significantly lower than those in the I/R group, and the expressions of cyclooxygenase-2 (Cox-2) and NF-κB (p65) in the soysterol group were also significantly lower than those in the I/R group. The expression of Nrf2 (nucleus) and heme oxygenase-1 (HO-1) increased significantly, and the activities of antioxidant enzymes and SOD were increased. In addition, the stigmasterol treatment can inhibit apoptosis, down-regulate Bax and cleaved caspase-3 expression, and up-regulate Bcl-Xl expression. Conclusion: Stigmasterol protects the brain from brain I/R damage by reducing oxidative stress and inflammation.

ANTIOXIDANT EFFECTS OF ADEMETIONINE UNDER ADMINISTRATION OF ANTITUBERCULOSIS DRUGS IN TOXIC DOSES TO RATS

The article presents the results of the experimental toxicological study on the use of ademetionine as an antioxidant defense in rats under administration of anti-tuberculosis drugs.

A4073 Sodium acetate and androgen receptor blockade improve gestational androgen excess-induced deteriorated glucose homeostasis and antioxidant defenses in rats

A4073 Sodium acetate and androgen receptor blockade improve gestational androgen excess-induced deteriorated glucose homeostasis and antioxidant defenses in rats

Sodium acetate and androgen receptor blockade improve gestational androgen excess-induced deteriorated glucose homeostasis and antioxidant defenses in rats: roles of adenosine deaminase and xanthine oxidase activities

Nutritional challenges and androgen excess have been implicated in the development of gestational diabetes and poor fetal outcome, but the mechanisms are not well delineated. The effects of short chain fatty acid (SCFA) on glucose dysmetabolism and poor fetal outcome induced by gestational androgen excess is also not known. We tested the hypothesis that blockade of androgen receptor (AR) and suppression of late gestational androgen excess prevents glucose dysmetabolism and poor fetal outcome through suppression of adenosine deaminase (ADA)/xanthine oxidase (XO) pathway. Twenty-four pregnant Wistar rats were treated (sc) with olive oil, testosterone propionate (0.5 mg/kg) singly or in combination with SCFA (sodium acetate; 200 mg/kg; p.o.) or AR blocker (flutamide; 7.5 mg/kg; p.o.) between gestational days 14 and 19. The results showed that late gestational androgen excess led to glucose deregulation, poor fetal outcome, increased plasma and hepatic free fatty acid and lactate dehydrogenase, liver function marker enzymes, malondialdehyde, uric acid, ADA and XO activities. Conversely, gestational androgen excess resulted in reduced body weight gain, visceral adiposity, plasma and hepatic anti-oxidant defenses (glutathione peroxidase, reduced glutathione/glutathione disulphide ratio, glucose-6-phosphate dehydrogenase, adenosine and nitric oxide). However, all these effects were ameliorated by either sodium acetate or flutamide treatment. The study demonstrates that suppression of testosterone by SCFA or AR blockade protects against glucose deregulation and poor fetal outcome by improvement of anti-oxidant defenses and replenishment of hepatic oxidative capacity through suppression of ADA/XO pathway. Hence, utility of SCFA should be encouraged for prevention of glucose dysmetabolism and poor fetal outcome.

Roles of dietary supplementation with arginine or N-carbamylglutamate in modulating the inflammation, antioxidant property, and mRNA expression of antioxidant-relative signaling molecules in the spleen of rats under oxidative stress

This study evaluated the effects of arginine (Arg) or N-carbamylglutamate (NCG) on inflammation, antioxidant property, and antioxidant-related gene expression in rat spleen under oxidative stress. A total of 52 rats were randomly distributed into 4 treatment groups with 13 replicates per group. Rats were fed a basal diet (BD) or BD supplemented with Arg or NCG for 30 days. On day 28, half of the BD-fed rats were intraperitoneally injected with sterile saline (control group), and the other half with 12 mg/kg body weight of diquat (DT; DT group). The other 2 diet groups were intraperitoneally injected with 12 mg/kg body weight of DT with either Arg (1%) (DT + Arg) or NCG (0.1%) (DT + NCG). Rat spleen samples were collected for analysis at 48 h after DT injection. Results showed that DT damaged the antioxidant defense in rats compared with the control group (P < 0.05). Compared with the DT group, the DT + Arg and DT + NCG groups manifested improved anti-hydroxyl radical, catalase, and total superoxide dismutase (T-SOD) activities, increased glutathione content (P < 0.05), and decreased malondialdehyde content (P < 0.05). Moreover, compared with the DT group, the DT + Arg and DT + NCG groups enhanced mRNA expression of superoxide dismutase (SOD), glutathione peroxidase 1 (GPx1), glutathione reductase (GR), nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH-associated protein 1(Keap-1), and mammalian target of rapamycin (mTOR) (P < 0.05). Both NCG and Arg significantly increased anti-inflammatory cytokine mRNA level but suppressed the pro-inflammatory cytokine mRNA expression under oxidative stress (P < 0.05). In summary, NCG and Arg effectively alleviated oxidative stress, improved the antioxidant capacity and regulated the antioxidant-related signaling molecular expression in rat spleen. N-carbamylglutamate and Arg reduced the inflammation in the spleen by mediating the gene expression of anti-inflammatory and pro-inflammatory cytokines and transforming growth factor-β (TGF-β).

Research of indicators of the endogenous antioxidant system in rats affected with sodium nitrite on the background of tobacco intoxication

Under conditions of progression of environmental pollution, the one of priority directions of toxicology and medicine is the study of features and mechanisms of the combined effect of xenobiotics – risk factors of many ecologically depending diseases. In last years there is widely studied the influence of tobacco smoking on the human organism. The numerous researches proved that the wide use of mineral fertilizers in agriculture resulted in environmental pollution, especially pollution of atmospheric air, drinking water and food and created the real threat for life of both human and other living beings. All these anthropogenic toxicants penetrate the human organism and lead to the oxidative stress and activation of free radical processes in the organism and imbalance in functioning of pro- and antioxidant systems.The aim of the research is to establish the level of the oxidative stress and activity of indicators of the system of antioxidant defense in rats, injured with sodium nitrite on the background of 45 days tobacco intoxication for choosing adequate schemes of correction of detected disorders.Experiments were realized on non-linear white male rats of different age groups, who underwent the effect of tobacco smoke during 45 days. Two groups of animals, injured by smoke, received sodium nitrite in dose 45 mg / kg of body mass for 24 hours and 72 hours before the end of experiment. Euthanasia was realized under thiopental anesthesia. Blood, blood serum liver and kidneys were taken for the study.For determining AOF, there was realized extraction of blood neutrophils by the method of gradient centrifugation. For measuring AOF level in neutrophils, dichlofluorescein diacetate was used. The level of AOF production was analyzed by the intensity of dye stuff lighting on the current cytometer. Catalase activity in the reaction with ammonium molybdate, superoxide dismutase activity with nitrotetrazolium blue, the content of restored glutathione at interaction of Ellman reagent with free SH-groups were determined in blood serum and tissues. The content of ceruloplasmin in blood serum was determined by the reaction of para-phenylendiamine oxidation.The studies were realized observing general principles of experiments on animals, coordinated with statements of the European convention about protection of vertebral animals, used for experimental and other scientific aims.Rats of all age groups, injured by tobacco smoke demonstrated the increase of AOF level in blood that resulted in the oxidative process development in the organism. The synchronous intoxication of rats with tobacco smoke and sodium nitrite deepened even more all detected disorders that testify to the reliable (p≤0,05) increase of AOF that acquired the maximal values in immature animals. The oxidative stress, observed in the organism of rats of all age groups, caused inhibition of antioxidant enzymes activity: superoxide dismutase, catalase and decrease of the non-enzyme component of the antioxidant system – restored glutathione. The synchronous injure of animals by sodium nitrite and tobacco smoke resulted in the decrease of catalase activity in lungs of mature rats in 2,4times compared with intact animals in the final term of the study. After sodium nitrite intoxication of rats, toxicated by smoke, the content of restored glutathione was maximally decreased in the liver of mature rats (in 4,5 times). Most expressed changes of indicators of the antioxidant system were observed in blood serum and organs of mature rats

ХАРАКТЕРИСТИКА ПРОЦЕСІВ ПЕРЕКИСНОГО ОКИСНЕННЯ ЛІПІДІВ ТА АНТИОКСИДАНТНОГО ЗАХИСТУ В ОРГАНІЗМІ ЩУРІВ ПРИ ВПЛИВІ МІКРО- І НАНОЧАСТИНОК НЕОРГАНІЧНИХ СПОЛУК СВИНЦЮ НА НЕПОШКОДЖЕНУ ШКІРУ

ХАРАКТЕРИСТИКА ПРОЦЕСІВ ПЕРЕКИСНОГО ОКИСНЕННЯ ЛІПІДІВ ТА АНТИОКСИДАНТНОГО ЗАХИСТУ В ОРГАНІЗМІ ЩУРІВ ПРИ ВПЛИВІ МІКРО- І НАНОЧАСТИНОК НЕОРГАНІЧНИХ СПОЛУК СВИНЦЮ НА НЕПОШКОДЖЕНУ ШКІРУ

Changes in Processes of Free Radical Oxidation of Lipids and Proteins, Antioxidant Defense in Rats with Thyroid Hypofunction against Iodine and Copper Deficiency

Changes in Processes of Free Radical Oxidation of Lipids and Proteins, Antioxidant Defense in Rats with Thyroid Hypofunction against Iodine and Copper Deficiency

Dosakaya Juice Assuages Development of Sucrose Induced Impaired Glucose Tolerance and Imbalance in Antioxidant Defense.

Objective:The objective was to explore the effect of Dosakaya (DK) (Cucumis melo var. chito) juice on sucrose induced dysglycemia and disturbances in antioxidant defense in rats.Materials and Methods:Rats were preconditioned with DK juice before administration of sucrose beverage continuously for 1-month. Blood glucose tolerance test and glutathione (GSH) homeostasis pathways in kidney were analyzed in different group of animals at the end of the study.Results:DK juice diffused (P < 0.001) hypertriglyceridemia inducing effect of sucrose and arrested sucrose induced weight gain. It improved glucose tolerance ability by significantly reducing (P < 0.05) first-hour glycemic excursion and decreasing 2 h glycemic load (P < 0.05) following oral glucose tolerance test in sucrose fed animals. Furthermore, disturbances in antioxidant defense mechanisms in terms of GSH homeostasis in kidney were restored due to juice feeding. DK juice administration checked reduction in GSH-S-transferase and glyoxalase-I activity, thus, significantly mitigated lipid peroxidation (P < 0.05), and formation of advanced glycation end-products (P < 0.001) in kidney and serum (P < 0.01). Quantitative analysis of juice found it a rich source of protein and polyphenols. Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) analysis revealed the presence of multiple protein bands in whole fruit juice. Therefore, SDS-PAGE protein fingerprint of DK juice may serve as a quality control tool for standardization of juice.Conclusion:The whole fruit juice of DK may become cost-effective, affordable health beverage in extenuating ill-health effects of sugar consumption. This is the first report identifying DK juice in preventing development dysglycemia, dyslipidemia, and oxidative stress induced due to chronic sucrose feeding in rats.SUMMARY Chronic sucrose consumption induced development of dysglycemia and also impaired antioxidant defense mechanism in rats. The oral administration of Dosakaya juice prior to sucrose feeding however, mitigated the development of dysglycemia and impairment in antioxidant defense in rats.

Polyols accumulated in ribose-5-phosphate isomerase deficiency increase mitochondrial superoxide production and improve antioxidant defenses in rats’ prefrontal cortex

The ribose-5-phosphate isomerase deficiency is an inherited condition, which results in cerebral d-arabitol and ribitol accumulation. Patients present leukoencephalopathy, mental retardation, and psychomotor impairment. Considering that the pathophysiology of this disorder is still unclear, and literature are sparse and contradictory, reporting pro and antioxidant activities of polyols, the main objective of this study was to investigate some parameters of oxidative homeostasis of prefrontal cortex of rats incubated with d-arabitol and ribitol. We found evidences that ribitol promoted an increase in antioxidant enzymes activity (superoxide dismutase, catalase, and glutathione peroxidase), probably secondary to enhanced production of superoxide radical, measured by flow cytometry. Oxidation of proteins and lipids was not induced by polyols. Our data allow us to conclude that, at least in our methodological conditions, arabitol and ribitol probably have a secondary effect on the pathophysiology of ribose-5-phosphate isomerase deficiency.

Milk lipids and sardine oil intake modulate differently enzymatic antioxidant defense in rats fed an atherogenic diet

Objective: The effect of milk lipids compared to sardine oil on antioxidant enzymes activities was evaluated in rats fed an atherogenic diet. Methods: Male Wistar rats were divided into three groups (n = 8 for each). Two experimental groups received a 20% casein diet combined with 5% milk lipids or sardine oil and 1% cholesterol for 4 weeks. The control group was fed a standard diet without cholesterol. Results: In red blood cells, superoxide dismutase (SOD) activity was 1.4- and 1.3-fold higher in the milk lipids group compared to the sardine oil and control groups, respectively. In tissues, SOD activity was respectively 2.5- and 1.8-fold lower in heart and aorta, but 1.2- fold higher in liver of rats fed milk lipids compared to those fed sardine oil. In milk lipids group, liver glutathione reductase (GR) and catalase (CAT) activities were respectively 2.5- and 1.2- fold lower compared to sardine oil group. In contrast, liver and heart glutathione peroxidase (GSH-Px) activities were respectively 1.2- and 2.3-fold higher. In aorta, milk lipids decreased SOD, GR, GSH-Px, and CAT activities and the values were respectively 1.8-, 1.7-, 1.2- and 1.5-fold lower than those found in the sardine oil group. Brain GSH-Px and CAT activities were respectively increased by 1.2- and 1.9-fold in the milk lipids group compared with the sardine oil. Milk lipids improved lecithin:cholesterol acyltransferase (LCAT) activity (2.5-fold) when compared with sardine oil. However, serum paraoxonase (PON)1 activity was 2-fold lower in milk lipids group vs control whereas, compared with the sardine oil group, PON1 activity had a tendency to decrease, but not significantly. Conclusion: This study shows that milk lipids and sardine oil intake modulate differently enzymatic antioxidant defense in hypercholesterolemic rats. Milk lipids improve reverse cholesterol transport from peripheral tissues to the liver by enhancing LCAT activity, leading to anti-atherogenic effects.

Protective effects of dietary ginger (Zingiber officinales Rosc.) on lindane-induced oxidative stress in rats.

The protective effect of dietary feeding of Zingiber officinales Rosc. (ginger) against lindane-induced oxidative stress was investigated in male albino rats. Oxidative stress was monitored by estimating the extent of lipid peroxidation, activities of the oxygen free radical (OFR) scavenging enzymes superoxide dismutase (SOD) and catalase (CAT) and the status of the glutathione redox cycle antioxidants. Lindane administration (30 mg/kg bw orally for 4 weeks) was associated with enhanced lipid peroxidation and compromised antioxidant defenses in rats fed a normal diet. Concomitant dietary feeding of ginger (1%w/w) significantly attenuated lindane-induced lipid peroxidation, accompanied by modulation of OFR scavenging enzymes as well as reduced glutathione (GSH) and the GSH dependent enzymes glutathione peroxidase (Gpx), glutathione reductase (GR) and glutathione-S-transferase (GST) in these rats. These findings suggest that a diet containing naturally occurring compounds is effective in exerting protective effects by modulating oxidative stress.

24-Hour rhythms in oxidative stress during hepatocarcinogenesis in rats: effect of melatonin or α-ketoglutarate

To compare the effects of α-ketoglutarate (α-KG) and melatonin on 24-h rhythmicity of oxidative stress in N-nitrosodiethylamine (NDEA)-injected Wistar male rats, melatonin (5 mg/kg i.p.) or α-KG (2 g/kg through an intragastric tube) was given daily for 20 weeks. In blood collected at 6 time points during a 24-h period, serum activity of aspartate transaminase (AST) and alanine transaminase (ALT) and the levels of α-fetoprotein (α-FP) were measured as markers of liver function. To assess lipid peroxidation and the antioxidant status, plasma levels of thiobarbituric acid reactive substances (TBARS) and of reduced glutathione (GSH) were measured, together with the activity of erythrocyte superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST). NDEA augmented mesor and amplitude of rhythms in AST and ALT activity and plasma α-FP levels and mesor values of plasma TBARS, while decreasing mesor values of plasma GSH and erythrocyte SOD, CAT, GPx and GST. Acrophases were delayed by NDEA in all cases except for α-FP rhythm, which became phase-advanced. Co-administration of melatonin or α-KG partially counteracted the effects of NDEA. Melatonin decreased mesor of plasma TBARS and augmented mesor of SOD activity. The results indicate that melatonin and α-KG are effective in protecting from NDEA-induced perturbation of 24-h rhythms in oxidative stress. Melatonin augmented antioxidant defense in rats.

Beneficial effects of diclofenac therapy on serum lipids, oxidized low-density lipoprotein and antioxidant defenses in rats

To study the effects of diclofenac, a nonselective nonsteroidal anti-inflammatory drug (NSAID), on lipid profile, oxidized low-density-lipoprotein (Ox-LDL), serum antioxidant defenses and markers of oxidative stress, male Wistar rats were divided into two groups ( n = 10): (C) receiving intramuscularly a single daily dose of saline (NaCl 0.9%), and (AI) receiving intramuscularly a single daily dose of 10 mg/kg diclofenac sodium (C 14H 10Cl 2NNaO 2). After 28 days diclofenac-treated rats had lower Ox-LDL, apoprotein B (apo-B), apo-B/LDL-cholesterol and lipid hydroperoxide than C. Total antioxidant substances and superoxide dismutase were increased in diclofenac-treated rats, while no significant changes were observed in catalase, glutathione peroxidase and nitric oxide. A perincubation test done to examine the possibility of mechanism-based activation showed that diclofenac had no effect on maximal superoxide dismutase velocity, but significantly reduced the Michaelis–Menten ( K M) constant, indicating that diclofenac induced SOD activation increasing substrate linkage affinity to the enzyme-catalytic site. In conclusion, diclofenac had beneficial effects decreasing Ox-LDL and improving antioxidant defense. It appears that the application of this agent may be feasible and beneficial for serum antioxidant protection, which certainly would bring new insights on dyslipidemia control.

Specificity of antioxidant defense in rats with fluorine intoxication treated by intermittent hypoxic training and amaranth oil

Specificity of antioxidant defense in rats with fluorine intoxication treated by intermittent hypoxic training and amaranth oil

Beneficial Effect of Caffeic Acid on Alcohol-Induced Alterations in Lipid Peroxidation and Antioxidant Defense in Rats

ABSTRACTWe studied the effect of caffeic acid on alcohol-induced oxidative stress in alcohol-induced toxicity in rats. The elevation in the levels of lipid peroxidation in alcohol administration was accompanied by a significant decrease in the levels of vitamins C and E, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), and glutathione S-transferase (GST) in the liver and kidney. Oral administration of caffeic acid at a dose of 12 mg/kg/body weight for 45 days significantly reduced the severe oxidative stress in alcohol toxicity as evidenced by the decrease in the levels of lipid peroxidation with a simultaneous increase in the level of enzymic and nonenzymic antioxidants in liver and kidney. Histological studies in the liver and kidney also showed that administration of caffeic acid to alcohol-treated rats resulted in a marked reduction in alcohol-induced pathological changes. These results suggest that administration of caffeic acid to alcohol-supplemented rats alleviates the alcohol-induced oxidative damage in the liver and kidney.

Beneficial Effects of Dietary Copper Supplementation on Serum Lipids and Antioxidant Defenses in Rats

Background: A nutrition experiment was utilized to investigate the effects of two levels of dietary copper (Cu) supplementation on lipid profile and antioxidant defenses in serum of rats. Methods: Male Wistarrats (180–200 g; n = 10) were divided into three groups: control group (A), fed a basal diet with 6 µg Cu/g, and rats fed a basal diet with Cu (CuSO₄) supplementation from aqueous solutions, for 4 weeks at the final concentrations of 2 mg Cu/rat (B) and 3 mg Cu/rat (C). Results: No significant changes were observed in final body weight, body weight gain, food consumption, total serum protein and high-density lipoprotein. Cu supplementation reduced the triacylglycerol (TG), total cholesterol and low-density lipoprotein (LDL-C). The LDL-C/TG ratio and total antioxidant substances (TAS) were higher in (B) and (C) groups than in (A) group. There was a positive correlation between Cu supplementation and ceruloplasmin levels. The markers of oxidative stress, lipid hydroperoxide and lipoperoxide were decreased with Cu supplementation. No alterations were observed in superoxide dismutase, indicating saturation of Cu enzyme site. The glutathione peroxidase activities (GSH-Px) were increased in both Cu-supplemented groups. Considering that a copper-selenium interaction can affect mineral availability of both elements, the effects of Cu on TAS and GSH-Px activities were associated with increased selenium disposal. Conclusions: Dietary Cu supplementation had beneficial effects on lipid profile by improving endogenous antioxidant defenses and decreasing the oxidative stress in vivo.

Protective effects of L-arginine on pulmonary oxidative stress and anti-oxidant defenses during exhaustive exercise in rats1

To assess the effects of L-arginine (L-Arg) supplementation on pulmonary oxidative stress and antioxidant defenses in rats after exhaustive exercise. Rats were randomly divided into four groups: sedentary control (SC), sedentary control with L-Arg treatment (SC+Arg), exhaustive exercise with control diet (E) and exhaustive exercise with L-Arg treatment (E+Arg). Rats in groups SC+Arg and E+Arg received a 2% L-Arg diet. Rats in groups E and E+Arg underwent an exhaustive running test on a motorized treadmill. Pulmonary oxidative stress indices [xanthine oxidase (XO), myeloperoxidase (MPO), and malondialdehyde (MDA)] and antioxidant defense systems [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), and glutathione (GSH)] were investigated in this study. L-Arg supplementation significantly reduced exercise-induced elevations of XO and MPO activities in lung. L-Arg reversed the exercise-induced increase in SOD and GR activities, but increased CAT and GPX activities. L-Arg administration also significantly increased the GSH levels in plasma. L-Arg supplementation can prevent elevations of XO and MPO activities in the lung and favorably influence pulmonary antioxidant defense systems after exhaustive exercise.