Lipoperoxidation Levels Research Articles

Gastroprotective potential of methanolic extract and dimethyl cardamonin from Campomanesia reitziana fruits in mice.

This study evaluated the gastroprotective potential of methanolic extract from fruits of Campomanesia reitziana (MECR) and its isolated chalcone dimethyl cardamonin (DMC). The phenolic compound in the extract, and the free radical scavenging activity of MECR and DMC, were quantified. The gastroprotective activity of MECR (30-300mg/kg, p.o) and DMC (1 and 3mg/kg, p.o) was determined by ethanol/HCl-induced gastric ulcers in mice. Histological, histochemical, and biochemical analyses were performed in the ulcerated tissue. MECR showed a high content of phenolic compounds, including DMC, and was able to scavenge DPPH radicals by 29.58% at 1000μg/mL. However, DCM (1-1000μg/mL) did not reduce DPPH radicals. Pre-treatment with MECR at doses of 100 and 300mg/kg reduced the gastric lesions by 35.07 and 79.47%, respectively (ulcerated-vehicle group 10.72±0.88mm2). Moreover, the extract increased the mucin content by 1044.44% and superoxide dismutase activity by 20.04%, and decreased the lipoperoxide levels by 39.39%, compared to the ulcerated-vehicle group (0.27±0.04pixels×103/field; 57.37±1.59USOD/mg of protein and 29.57±2.99mmolLOOH/mg of tissue, respectively). However, MECR did not prevent the depletion of reduced glutathione or the decrease in catalase activity. Pre-treatment with DMC, at 1 and 3mg/kg, also reduced the gastric ulcers by 53.83 and 52.64%, respectively. In summary, these findings confirm the gastroprotective activity of MECR and DMC, and open an interesting field concerning the gastroprotective potential of dimethyl cardamonin, given its potent antinociceptive and anti-inflammatory activity already described.

Hepatoprotective effect of Maytenus robusta Reiss extract on CCl4-induced hepatotoxicity in mice and HepG2 cells

We investigated the hepatoprotective effect of methanolic extract from Maytenus robusta leaves in mice and HepG2 cells. The administration of CCl4 in mice promoted a deep destruction of the histological lobular structure and increased the alanine aminotransferase (ALT) serum levels by 46.25% compared with the control group (p < 0.05). The M. robusta extract reduced the hepatic histological changes and normalization the ALT levels. The antioxidant effect of M. robusta in liver tissue promoted the reduction in 31.5% on lipoperoxides levels (p < 0.05), increased by 101.5% the reduced glutathione content (p < 0.05) and increased the activity of superoxide dismutase, catalase, and glutathione-S-transferase by 21.3% (p < 0.05), 49.3% (p < 0.05), and 27.6% (p < 0.05), respectively, compared with the vehicle group. Moreover, the extract reduced hepatic inflammation by diminishing myeloperoxidase activity, TNF and interleukin-6 levels by 29.4% (p < 0.05), 46.1% (p < 0.01), and 59.5% (p < 0.0001), respectively, compared with the vehicle group. The viability of HepG2 cells after incubation with CCl4 was 29.56± 3.07%, whereas the extract (300 μg/mL) restored the viability to 65.27± 8.75% and aspartate aminotransferase levels to 41.82 ± 4.41 U/L. The extract scavenged DPPH (IC50 = 14.44 μg/mL) and ABTS (IC50 = 3.00 μg/mL) radicals and did not produce acute toxicity in mice at 2000 mg/kg. In conclusion, was confirmed the hepatoprotective potential of M. robusta by its antioxidant effects.

Inhibition of aldose reductase ameliorates alcoholic liver disease by activating AMPK and modulating oxidative stress and inflammatory cytokines.

Aldose reductase (AR) expression is elevated in the livers of patients with alcoholic liver diseases. However, the role of AR in the development of alcoholic liver diseases remains unclear. The aim of the present study was to determine the effect of AR inhibition on ethanol‑induced hepatosteatosis invivo and invitro, and to identify possible underlying molecular mechanisms. Alcoholic fatty livers were induced in C57BL/6 mice by feeding the mice with Lieber‑DeCarli liquid diets. The expression of AR protein was elevated in the liver tissue of C57BL/6 mice fed with an ethanol diet and in mouse AML12 liver cells exposed to ethanol. In addition to the elevation in AR, hepatic steatosis was observed in ethanol diet‑fed mice, and this ethanol‑induced steatosis was significantly attenuated by inhibiting AR activity with a specific inhibitor, zopolrestat. The suppressive effect of AR inhibition was associated with decreased levels of hepatic lipoperoxides, decreased protein expression of hepatic cytochrome P450 2E1 (CYP2E1), increased phosphorylation of 5'‑AMP‑activated protein kinase (AMPK) and decreased mRNA expression of tumor necrosis factor‑α (TNF‑α). Treatment with the AR inhibitor attenuated the level of lipid accumulation and oxidative stress, activated AMPK, and suppressed the mRNA expression of TNF‑α, interleukin‑6 and transforming growth factor‑β1 in ethanol‑treated AML12 cells. The results of the present study demonstrated that inhibition of AR ameliorated alcoholic liver disease invivo and invitro, in part by activating AMPK, decreasing CYP2E1‑mediated oxidative stress and ameliorating the expression of pro‑inflammatory cytokines.

Effect of melatonin administration on cyclooxygenase-2 activity, serum levels of nitric oxide metabolites, lipoperoxides and glutathione peroxidase activity in patients with Parkinson’s disease

To determine the effect of melatonin (MEL) administration on ciclooxigenase 2 (COX-2) activity and serum concentration of nitric oxide metabolites, lipoperoxides and glutathione peroxidase (GPx) activity in patients with Parkinson's disease. Prospective double-blind randomized clinical pilot trial. 13 patients were included and two groups were formed: MEL at doses of 25 mg orally every 12 hours for 12 months and placebo with corn starch. Patients were assessed using the Unified Parkinson's Disease Scale. A blood sample was taken at baseline and every 3 months until 12 months. COX-2 activity decreased as did nitrates/nitrites (3, 6 and 9 months) and lipoperoxides (9 and 12 months); GPx exhibited no significant differences.

Involvement of the endocannabinoid system in the physiological response to transient common carotid artery occlusion and reperfusion

BackgroundThe transient global cerebral hypoperfusion/reperfusion achieved by induction of Bilateral Common Carotid Artery Occlusion followed by Reperfusion (BCCAO/R) may trigger a physiological response in an attempt to preserve tissue and function integrity. There are several candidate molecules among which the endocannabinoid system (ECS) and/or peroxisome-proliferator activated receptor-alpha (PPAR-alpha) may play a role in modulating oxidative stress and inflammation. The aims of the present study are to evaluate whether the ECS, the enzyme cyclooxygenase-2 (COX-2) and PPAR-alpha are involved during BCCAO/R in rat brain, and to identify possible markers of the ongoing BCCAO/R-induced challenge in plasma.MethodsAdult Wistar rats underwent BCCAO/R with 30 min hypoperfusion followed by 60 min reperfusion. The frontal and temporal-occipital cortices and plasma were analyzed by high performance liquid chromatography-mass spectrometry (HPLC-MS) to determine concentrations of endocannabinoids (eCBs) and related molecules behaving as ligands of PPAR-alpha, and of oxidative-stress markers such as lipoperoxides, while Western Blot and immunohistochemistry were used to study protein expression of cannabinoid receptors, COX-2 and PPAR-alpha. Unpaired Student’s t-test was used to evaluate statistical differences between groups.ResultsThe acute BCCAO/R procedure is followed by increased brain tissue levels of the eCBs 2-arachidonoylglycerol and anandamide, palmitoylethanolamide, an avid ligand of PPAR-alpha, lipoperoxides, type 1 (CB1) and type 2 (CB2) cannabinoid receptors, and COX-2, and decreased brain tissue concentrations of docosahexaenoic acid (DHA), one of the major targets of lipid peroxidation. In plasma, increased levels of anandamide and lipoperoxides were observed.ConclusionsThe BCCAO/R stimulated early molecular changes that can be easily traced in brain tissue and plasma, and that are indicative of the tissue physiological response to the reperfusion-induced oxidative stress and inflammation. The observed variations suggest that the positive modulation of the ECS and the increase of proinflammatory substances are directly correlated events. Increase of plasmatic levels of anandamide and lipoperoxides further suggests that dysregulation of these molecules may be taken as an indicator of an ongoing hypoperfusion/reperfusion challenge.

Quality of life among post-menopausal women due to oxidative stress boosted by dysthymia and anxiety

BackgroundMenopause is the onset of aging in women. During this process, some women experience physical changes that may impact upon their psychological and social status, also affecting their quality of life. Furthermore, several psychological changes following menopause have been shown to act as pro-oxidant, but the association between the psychological status that modify the quality of life and oxidative stress in postmenopausal women is still unclear. The aim of this study was to determinate the relationship between oxidative stress with psychological disturbances, low self-esteem, depressive mood and anxiety, and quality of life in the postmenopausal women.MethodsWe carried out a cross-sectional study with101 premenopausal and 101 postmenopausal women from Mexico City. As markers of oxidative stress we measured plasma lipoperoxide levels, erythrocyte superoxide dismutase and glutathione peroxidase activities, and total antioxidant status. We calculate a stress score as global oxidative stress status, with cut-off values for each parameter; this score range from 0 to 6, representing the severity of markers modifications. All the women were rated using the Coopersmith Self-Esteem Inventory, the Zung Self-Rating Anxiety and the Zung Self-Rating Depression Scales, and the WHO Quality of Life-brief.ResultsThe postmenopausal women with low quality of life in the WHO Quality of Life-brief and their subscales had higher stress score compared with premenopausal women with high quality of life (p < 0.05). We found a positive correlation among lipoperoxide levels and Zung Self-Rating Anxiety and Zung Self-Rating Depression score (r = 0.226 and r = 0.173, respectively, p < 0.05), and a negative correlation with WHO Quality of Life-brief scores (r = −0.266, p < 0.01) in postmenopausal women. Multiple linear regression analysis revealed that average lipoperoxide levels increase by 0.0007 μmol/L for every 1-point increase in the Coopersmith Self-Esteem Inventory and by 0.001 μmol/L for every 1-point decrease in the WHO Quality of Life-brief, after adjusted for pro-oxidant factors. Zung Self-Rating Anxiety and Zung Self-Rating Depression Scales scores also contribute to increase lipoperoxides levels, but not significant.ConclusionOur findings suggest that oxidative stress is increased in postmenopausal women with psychological disturbances and low quality of life.

Enzymatic reduction of hydrogen peroxide on Polypogon australis plants grown in a copper mining liquid waste

This study was undertaken to characterize the status of H2O2-reducing enzyme activity in the metallophyte plant species Polypogon australis when treated with a mining liquid waste (MLW) derived from a copper mine. In order to determine the effect of the solubility of some metals present in the MLW the accumulation of the elements, the variation of H2O2 and lipoperoxidation levels, and their relationship with the H2O2 reduction activity was studied in P. australis plants at pH5.1 (acidic MLW) and at pH6.7 (neutral MLW) during two weeks. Plants treated with the acidic MLW showed an elevated copper and zinc accumulation in their tissues. Oxidation of lipids determined by the malondialdehyde (MDA) content increased during the first half hour in the roots of the treated plants, and remained constant to the end of the treatment. In leaves of the treated plants, MDA levels steadily increased throughout the treatment. H2O2 levels increased during the first 2h of the treatment, then decreased and reached values close to that observed in untreated control plants. The increase of copper in the roots of the plants treated with the acidic MLW and the H2O2 levels detected in the tissues was correlated with the activity of H2O2-reducing enzymes. The results show that the treatment of the plants with the MLW but not the solubility of metals provokes an increase of the H2O2 content in the tissues and triggers the enzymatic control of H2O2 levels.

Neuroprotective Effects of Guarana (Paullinia cupana Mart.) against Vincristine in Vitro Exposure.

Vincristine (VCR) is not a specific chemotherapeutic drug, responsible for cause several side effects. In this sense, many natural products have been studied to reduce this problem. Objetives: To examine the guarana neuroprotective effect in mice brain and cerebellum cells against vincristine (VCR) exposition. An in vitro study was performed using mice brain and cerebellum mice in monolayer culture. First, cells were exposed to VCR (0.009 µM for 24 hours and 0.0007 µM for 72 hours) to measure the cytotoxicity effect. Also, the cellular effect of hydroalcoholic extract of guarana (10; 30; 100 and 300 μg/mL) was evaluated in the same cells in 24 and 72 hours. After that, cells were exposed to VCR and guarana extract to evaluate the neuroprotective effect of guarana. Cell viability was analyzed by MTT, Free dsDNA and LHD Assays. Moreover, metabolism oxidative profile was evaluated by reactive oxygen species (ROS), lipoperoxidation (LPO) and catalase (CAT) levels through DCFH-DA, TBARS and Catalase Activity Assays, respectively. Our findings revealed that VCR caused neuronal cytotoxicity by reducing cell viability and increasing ROS and LPO levels. On the other hand, guarana did not cause cell damage in none of tested concentrations. In addition, guarana exhibited a notable protective effect on brain and cerebellum cells exposed to VCR by increasing cell viability, stimulating CAT activity, reducing levels of ROS and LPO. In this sense, guaraná is a remarkable antioxidant fruit that could be a target in new therapies development to reduce VCR neurotoxicity. .

Evaluation of Photosynthetic, Enzymatic Activities and Lipoperoxidation Level in Two Species of Bryophytes Exposed to Sencorate

To better understand the behavior of the plants towards xenobiotics, two species of bryophytes (<i>Orthotrichum affine</i> and <i>Scleropodium purum</i>), bioindicators of the region of Souk Ahras (Algeria) which have properties completely different (classification, reproductive cycle...) are treated under hydroponic conditions by 125, 250, 500, 1000 and 1500 mg / L of Sencorate herbicide (Metribuzin) for 3, 7, 14 and 21 days. A measure of some physiological, biochemical and enzymatic parameters characteristic of oxidative stress have allowed us to evaluate not only the effect of Sencorate herbicide but also the behavior of the two species with respect to pollution. Statistical analysis of the results showed significant differences between the treated and control samples for the majority of parameters studied, with lower levels of chlorophyll pigments (<i>a, b, a+b</i>) accompanied by increased levels of proline, total protein and soluble carbohydrates. Depletion of GSH at the beginning of treatment, accompanied by an increase in Malondialdehyde MDA levels were observed with low activity of the enzyme biomarkers Catalase and Ascorbat peroxydase (CAT and APX), which reflects the high tolerance of these species to pollutants.

Effect of Neonatal Exposure to Poly(Ethylene Glycol)-block-Poly(Lactic Acid) Nanoparticles on Oxidative State in Infantile and Adult Female Rats.

Our goal was to evaluate the potential health risk of the polymeric NP, poly(ethylene glycol)-block-poly(lactic acid) (PEG-b-PLA), from the view of redox imbalance of the organism in two different life stages. Female Wistar rats were neonatally administered intraperitoneally with PEG-b-PLA NPs [20 mg/kg of b.w. (PEG20) or 40 (PEG40) mg/kg of b.w.] from postnatal day 4 (PND4) to PND7. We measured antioxidant capacity (TEAC), level of protein carbonyls and lipoperoxides in plasma, activities of catalase, glutathione peroxidase (GPx), and superoxide dismutase (SOD) in hemolysates of infantile (sacrificed on PND17) and adult (sacrificed after PND176) rats. Compared to controls, neonatal PEG40 exposure induced a significant TEAC reduction in the infantile rats. Protein carbonyls and lipoperoxide levels were not affected after any dose of PEG-b-PLA NP administration. In adult rats, PEG20 administration caused a significant decrease of protein carbonyl levels compared to controls. In infantile rats, both doses of PEG-b-PLA NP administration increased catalase, Gpx, and SOD activities compared to controls. Surprisingly, in adult rats, the activities of Gpx and SOD decreased significantly after administration of both doses of PEG-b-PLA NPs. Obtained data indicate a possible age-related association between the oxidative status and neonatal PEG-b-PLA NP administration in female rats.

Aging modifies daily variation of antioxidant enzymes and oxidative status in the hippocampus

BackgroundAging is a complex and multifactorial biological process that leads to the progressive deterioration of physiological systems, including the circadian system. In addition, oxidative stress has been associated with the aging of the normal brain and the development of late-onset neurodegenerative diseases. Even though, functional weakening of circadian rhythms and antioxidant function has been observed during aging, the mechanisms by which the circadian system signaling and oxidative stress are interrelated have not yet been elucidated. The objectives of this study were to evaluate the consequences of aging on the temporal organization of the antioxidant defense system and oxidative status as well as to analyze the endogenous clock activity, in the hippocampus of aged rats. MethodsYoung adults (3-month-old) or older (22-month-old) male Holtzman rats were maintained under constant darkness conditions, during 15days before the sacrifice. Levels of catalase (CAT) and glutathione peroxidase (GPx) mRNA and activity, reduced glutathione (GSH), lipoperoxidation (LPO) and BMAL1 protein were analyzed in hippocampus samples isolated every 4h during a 24-h period. Locomotor activity was recorded during 20days before the experiment. ResultsOur results show that aging modifies temporal patterns of CAT and GPx expression and activity in the hippocampus in a different way. On the one hand, it abolishes the oscillating CAT expression and specific enzymatic activity while, on the other, it increases the mesor of circadian GPx activity rhythm (p<0.01). Additionally, we observed increased GSH (p<0.05) and reduced LPO (p<0.01) levels in the hippocampus of aged rats. Moreover, the nocturnal locomotor activity was reduced in the older animals in comparison to the young adult rats (p<0.01). Interestingly, the 22month-old animals became arrhythmic and showed a marked fragmentation as well as a significant decline in daily locomotor activity when they were maintained under constant darkness conditions (p<0.05). Aging also abolished circadian rhythms of the core clock BMAL1 protein. ConclusionThe loss of temporal organization of the antioxidant enzymes activity, the oxidative status and the cellular clock machinery could result in a temporally altered antioxidant defense system in the aging brain. Learning about how aging affects the circadian system and the expression of genes involved in the antioxidant defense system could contribute to the design of new strategies to improve the quality of life of older people and also to promote a healthy aging.

177 - Non-Enzymatic Antioxidant Response in Postmenopausal Women with Decreased Muscle Strength

Background Menopause is the beginning of aging in woman due to loss of ovarian follicular function that produces an abrupt drop in estrogen levels as well as body and biochemical changes like muscle strength loss and oxidative stress (OS). Objective To determinate OS biomarkers in postmenopausal women with low muscle strength. Methods We carried out a cross-sectional study with 42 premenopausal [PRE] (47.8±1.9 years) and 48 postmenopausal [POS] women (53.9±2.3 years) from Mexico City. We measured as OS biomarkers: plasma lipoperoxides (LPO) by the TBARS assay, serum uric acid (UA) using a Cobas© C111 analyzer, erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx), and total plasma antioxidant status (TAS) with Randox kits, and we calculated SOD/GPx ratio and antioxidant gap. Handgrip strength was measured with a dynamometer; also we measured weight and height and we calculated the body mass index (BMI). An alternative cut-off value of handgrip strength <20 kg was defined according the Sarcopenia European consensus. Results We found that PRE women had good strength and 20 (42%) of the POS women had low handgrip strength; 83 (92%) of the all women were obese (BMI >25 kg/m2). LPO levels were higher, and SOD and GPx activities were lower in POS women with low muscle strength compared with PRE women (control group), although only GPx had low activity statistically significant (58.6±2.9 vs. 69.2±.1 U/gHb, p<0.05). Non-enzymatic antioxidants were statistically higher (p<0.05) in POS women with low muscle strength than control group: TAS 1262±48.2 vs. 1147±29.9 μmol/L, UA 296±21.8 vs. 265±9.5 μmol/L, and GAP 502±46.1 vs. 395±28.4 μmol/L. Conclusion Our findings suggest that there is a non-enzymatic antioxidant response in postmenopausal women with decreased muscle strength. This work was supported by grant UNAM-IN224115.

Moderate aerobic exercise on the recovery phase of gentamicin-induced acute kidney injury in rats

IntroductionAcute kidney injury is a serious public health problem, especially in intensive care units, where patients may require dialysis support, resulting in 50% mortality. AimTo evaluate the effects of moderate aerobic exercise on the recovery phase of acute kidney injury induced by gentamicin in rats. Main methodsMale adult Wistar rats were allocated into 4 groups: W10+R30, G10+R30, W10+EX30 and G10+EX30; W10 received water (gentamicin vehicle) and G10 received gentamicin for 10days; R30 remained resting and EX30 made exercise for 30days after gentamicin suspension. Training was performed on treadmill. Blood, 24h urine and kidneys were collected for renal function and oxidative stress, antioxidant, TGF-β and histological analysis. Key findingsGentamicin treatment caused decreased renal function significant oxidative stress, reduced urinary nitric oxide and increased TGF-β. G10+R30 presented partial recovery of metabolic data, renal function and lipoperoxidation levels, although they were still altered compared to W10+R30. Besides, we observed the presence of lymphomononuclear infiltrate in the kidneys of G10+R30. G10+EX30 vs G10+R30 showed additional improvement of all the mentioned parameters, showing at histology, regeneration of the tubule epithelium. SignificanceOur data suggest that moderate exercises could help in the recovery of metabolic parameters, renal function and structure on gentamicin-induced AKI, perhaps due to restoration of redox balance. This could protect the kidneys from further insults like challenges with nephrotoxic drugs or the aging per se.

Multibiomarker responses in aquatic insect Belostoma elegans (Hemiptera) to organic pollution in freshwater system.

The present study analyzes a battery of biomarkers in the water bug Belostoma elegans from a stream polluted with organic matter (OMS), and another one considered as reference site (RS) during spring-summer season (December to March). Biochemical parameters of glucidic, lipidic and oxidative metabolic pathways were analyzed in males and females of this insect. In general, no significant differences were observed in all biomarkers assayed between both sexes, except lactate concentration which was higher in males than in females (p<0.0006) in the first three months. About carbohydrate metabolism parameters, only pyruvate-kinase showed significant differences between insects collected in both streams (p<0.05) during December. However, the total lipid content, saturated fatty acid, and mainly triacylglycerol were higher in insects from RS compared to those from OMS (p<0.002) in all sampled months. Levels of lipoperoxidation, protein oxidation, reduced glutathione and glutathione-S-transferase activity showed no differences between insects collected from both streams. Nevertheless, the significant increase observed in superoxide dismutase and catalase activities (p<0.004) could be due to the elevated oxidative metabolism in insects from RS compared to those from OMS with lower dissolved oxygen. Regarding those responding parameters, males accounted for the differences between the two sites during the study period. In conclusion, our results support that lipidic energetic reserves and antioxidant enzyme activities in B. elegans could be used as biomarkers of environmental pollution by organic matter.

Fructose during pregnancy provokes fetal oxidative stress: The key role of the placental heme oxygenase-1.

One of the features of metabolic syndrome caused by liquid fructose intake is an impairment of redox status. We have investigated whether maternal fructose ingestion modifies the redox status in pregnant rats and their fetuses. Fructose (10% wt/vol) in the drinking water of rats throughout gestation, leads to maternal hepatic oxidative stress. However, this change was also observed in glucose-fed rats and, in fact, both carbohydrates produced a decrease in antioxidant enzyme activity. Surprisingly, mothers fed carbohydrates displayed low plasma lipid oxidation. In contrast, fetuses from fructose-fed mothers showed elevated levels of plasma lipoperoxides versus fetuses from control or glucose-fed mothers. Interestingly, a clearly augmented oxidative stress was observed in placenta of fructose-fed mothers, accompanied by a lower expression of the transcription factor Nuclear factor-erythroid 2-related factor-2 (Nrf2) and its target gene, heme oxygenase-1 (HO-1), a potent antioxidant molecule. Moreover, histone deacetylase 3 (HDAC3) that has been proposed to upregulate HO-1 expression by stabilizing Nrf2, exhibited a diminished expression in placenta of fructose-supplemented mothers. Maternal fructose intake provoked an imbalanced redox status in placenta and a clear diminution of HO-1 expression, which could be responsible for the augmented oxidative stress found in their fetuses.

Fighting Oxidative Stress: Increased Resistance of Male Rat Cerebellum at Weaning Induced by Low Omega 6/Omega 3 Ratio in a Protein-Deficient Diet

The cerebellum is vulnerable to malnutrition effects. Notwithstanding, it is able to incorporate higher amount of docosahexaenoic acid (DHA) than the cerebral cortex (Cx) when low n-6/n-3 fatty acid ratio is present in a multideficient diet. Considering importance of DHA for brain redox balance, we hypothesize that this cerebellum feature improves its antioxidant status compared to the Cx. A chronic malnutrition status was induced on dams before mating and kept until weaning or adulthood (offspring). A group nutritionally rehabilitated from weaning was also analyzed. Morphometric parameters, total-superoxide dismutase (t-SOD) and catalase activities, lipoperoxidation (LP), nitric oxide (NO), reduced (GSH) and oxidized (GSSG) glutathione, reactive oxygen species (ROS), and reduced nicotinamide adenine dinucleotide/phosphate levels were assessed. Both ROS and LP levels were increased (∼53 %) in the Cx of malnourished young animals while the opposite was seen in the cerebellum (72 and 20% of the control, respectively). Consistently, lower (∼35%) and higher t-SOD (∼153%) and catalase (CAT) (∼38%) activities were respectively detected in the Cx and cerebellum compared to the control. In malnourished adult animals, redox balance was maintained in the cerebellum and recovered in the Cx (lower ROS and LP levels and higher GSH/GSSG ratio). NO production was impaired by malnutrition at either age, mainly in the cerebellum. The findings suggest that despite a multinutrient deficiency and a modified structural development, a low dietary n-6/n-3 ratio favors early antioxidant resources in the male cerebellum and indicates an important role of astrocytes in the redox balance recovery of Cx in adulthood.

Oxidative stress influence on renal dysfunction in patients with obstructive jaundice: A case and control prospective study

Background: Obstructive Jaundice (OJ) is associated with a significant risk of developing acute renal failure (ARF). The involvement of oxidative stress in the development of cholestasis has been demonstrated in different experimental models. However, its role in the morbidity of human cholestasis is far to be elucidated. The aim of the study was the evaluation of oxidative stress markers in blood from patients with OJ and its relation to complications and benign/malignant evolution of cholestasis. Methods: A prospective cross-sectional study of 105 patients with OJ and 34 control subjects were included. Several markers of liver function and oxidative stress, such as lipoperoxides (LPO), as well as reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were assessed. Results: The patients with OJ showed a marked increase in plasma levels of LPO, SOD and GSH, while GSH-Px levels were decreased. The increase in lipid peroxidation products and the depletion of SOD activity in blood were also related to renal dysfunction. The highest level of LPO was associated with malignant etiology of the disease. The logistic regression analysis showed that the age of the patient and the levels of LPO in blood were predictors of renal dysfunction in OJ patients. Conclusions: This study demonstrates a correlation between oxidative stress and renal dysfunction patients with OJ.

Training Status as a Marker of the Relationship between Nitric Oxide, Oxidative Stress, and Blood Pressure in Older Adult Women.

The purpose of this study was to evaluate the influence of functional fitness and oxidative capacity on the nitric oxide concentration associated with hemodynamic control in older adult women. The sample consisted of 134 women (65.73 ± 6.14 years old). All subjects underwent a physical examination to assess body mass index, waist-hip ratio, body fat measurement by dual energy X-ray absorptiometry, and blood pressure (BP). Training status (TS) was evaluated by indirect determination of maximal oxygen uptake by a treadmill test using Balke protocol modified for older adults. Functional fitness was also evaluated through a “Functional Fitness Battery Test” to determine the general fitness functional index (GFFI). All participants were separated according to the functional fitness (TS1, very weak and weak; TS2, regular; TS3, good and very good). Plasma blood samples were used to evaluate prooxidant and antioxidant activity and nitrite and nitrate concentrations. The general results of this study showed that good levels of TS were related to lower levels of lipoperoxidation and protein damage, higher levels of antioxidant, and higher concentration of nitrite and nitrate. This combination may be responsible for the lower levels of BP in subjects with better TS.

Physical exercise prevents motor disorders and striatal oxidative imbalance after cerebral ischemia-reperfusion.

Stroke is the third most common cause of death worldwide, and most stroke survivors present some functional impairment. We assessed the striatal oxidative balance and motor alterations resulting from stroke in a rat model to investigate the neuroprotective role of physical exercise. Forty male Wistar rats were assigned to 4 groups: a) control, b) ischemia, c) physical exercise, and d) physical exercise and ischemia. Physical exercise was conducted using a treadmill for 8 weeks. Ischemia-reperfusion surgery involved transient bilateral occlusion of the common carotid arteries for 30 min. Neuromotor performance (open-field and rotarod performance tests) and pain sensitivity were evaluated beginning at 24 h after the surgery. Rats were euthanized and the corpora striata was removed for assay of reactive oxygen species, lipoperoxidation activity, and antioxidant markers. Ischemia-reperfusion caused changes in motor activity. The ischemia-induced alterations observed in the open-field test were fully reversed, and those observed in the rotarod test were partially reversed, by physical exercise. Pain sensitivity was similar among all groups. Levels of reactive oxygen species and lipoperoxidation increased after ischemia; physical exercise decreased reactive oxygen species levels. None of the treatments altered the levels of antioxidant markers. In summary, ischemia-reperfusion resulted in motor impairment and altered striatal oxidative balance in this animal model, but those changes were moderated by physical exercise.

Characterization of an alcoholic hepatic steatosis model induced by ethanol and high-fat diet in rats

Alcoholic liver disease is characterized by a wide spectrum of liver damage, which increases when ethanol is associated with high-fat diets (HFD). This work aimed to establish a model of alcoholic hepatic steatosis (AHS) by using a combination of 10% ethanol and sunflower seeds as the source of HFD. Male rats received water or 10% ethanol and regular chow diet and/or HFD, which consisted of sunflower seeds. The food consumption, liquid intake and body weight of the rats were monitored for 30 days. After this period, blood was collected for biochemical evaluation, and liver samples were collected for histological, mitochondrial enzyme activity and oxidative stress analyses. Our results indicated that the combination of 10% ethanol and HFD induced micro- and macrosteatosis and hepatocyte tumefaction, decreased the levels of reduced glutathione and glutathione S-transferase activity and increased the level of lipoperoxidation and superoxide dismutase activity. The mitochondrial oxidation of NADH and succinate were partially inhibited. Complexes I and II were the main inhibition sites. Hepatic steatosis was successfully induced after 4 weeks of the diet, and the liver function was modified. The combination of 10% ethanol and sunflower seeds as an HFD produced an inexpensive model to study AHS in rats.