Swimming training and caffeine supplementation protects against metabolic syndrome-induced nuclear factor-κB activation and cognitive deficits in rats.

Metabolic syndrome (MS) is a disorder that increasingly affects the world population, mainly because of changes in lifestyle and dietary habits. In this regard, both physical exercise and caffeine are low-cost and easily accessible therapies that separately have shown positive effects against metabolic disorders. Therefore, we hypothesized that physical exercise combined with caffeine could have a synergistic effect in the treatment of MS, risk factors, and cognitive deficits. Animals were divided into 8 groups and received fructose (15% w/v) or vehicle for 10 weeks. Swimming training and caffeine (6 mg/kg) started 4 weeks after fructose administration. Trained animals presented decreased body weight and visceral fat mass and increased soleus weight compared with untrained fructose-treated animals. Caffeine supplementation also prevented the gain of visceral fat mass induced by fructose. Furthermore, both treatments reversed fructose-induced decrease in glucose clearance over time and fructose-induced increase in 4-hydroxynonenal and nuclear factor-κB immunoreactivity. Physical training also improved the lipidic profile in fructose-treated animals (high-density lipoprotein, low-density lipoprotein, and triglycerides), improved short-term, long-term, and localization memory, and reversed the fructose-induced deficit in short-term memory. Physical training also increased nuclear factor erythroid 2-related factor 2 immunoreactivity per se. Considering that physical training and caffeine reversed some of the damages induced by fructose it is plausible to consider these treatments as alternative, nonpharmacological, and low-cost therapies to help reduce MS-associated risk factors; however, combined treatments did not show additive effects as hypothesized.

Reprotoxicity induced by acute exposure to aqueous tuber extract of Peruvian Maca (Lepidium meyenii Walp.) in Caenorhabditis elegans.

Maca (Lepidium meyenii Walp.) has been used in folk medicine to treat fertility disturbances, a claim that has been evidenced in some studies. However, the clinical trials validating this use have shown paradoxical findings and then maca safety is not well known. This study investigated the effects and mechanisms by which maca affects the reproductive system using an in vivo model, the nematode Caenorhabditis elegans. Tuber maca powder, obtained from local commerce, was used to prepare the aqueous extract. Worms were acutely exposed to maca extracts (40, 120, 240, and 330 µg/µl), and 48 h after treatments, physiological and biochemical assays were conducted. Maca extract caused a significant decrease in total number of eggs and in the number of eggs per worm. These effects were associated to increased lipid peroxidation, reduced triacylglycerol levels, and also impaired vit-2 (vitellogenin) expression, besides increase in the number of apoptotic germline cells. We have found quantifiable levels of alkaloids in this maca extract, which presence could be related to this toxicity. Collectively, our data suggest that maca extract exposure causes reproductive toxicity to worms that could be, at least in part, associated to both an increase in apoptosis of germline cells and also to a decrease in vitellogenin expression, needed for egg yolk production and, consequently, successful reproduction.

In vivo effects of exposure to Golden trumpet Handroanthus chrysotrichus in mice.

The Golden trumpet Handroanthus chrysotrichus is a tree that presents beneficial health properties against various diseases. Thus, this study aims to verify the toxicity of H. chrysotrichus bark extract, observing the effects of exposure to this extract in mice. For this, mice were separated in groups: saline (sterile solution .9%); H. chrysotrichus crude extract (HCCE) 10; HCCE 50, and HCCE 100 mg. kg-1 (p.o.). We analyzed HCCE effects on acute (single exposure) and subchronic protocol (14 days exposure). After both exposures, acute, and subchronic, we collected samples from blood, brain, liver, and kidney tissues for biochemical evaluation. In addition, after subchronic exposure, we performed behavioral tests. Acute exposure caused an increase of lipid peroxidation in liver tissue. Moreover, we observed a significant carbonyl increase in liver and brain tissues from HCCE 50 mg. kg-1. Kidneys presented carbonyl increase in mice treated with the highest concentration. Besides, creatinine increased in the group of the acute exposure at HCCE 100 mg. kg-1. Total leukocyte count decreased in all concentrations tested. Sub-chronic exposure at HCCE 100 mg. kg-1 caused a decrease in the number of crossing and an increase in its self-grooming frequency in the open field test. In this exposure, the brain and liver had a significant increase in carbonyl levels in all concentrations. We concluded that H. chrysotrichus cause behavioral and biochemical alterations in mice. HCCE primary targets seem to be the liver, kidneys, and white cells.

Protective effect of gamma-oryzanol against manganese-induced toxicity in Drosophila melanogaster.

Manganese (Mn) is an essential element that, in excess, seems to be involved in the development of different neurodegenerative conditions. Gamma-oryzanol (Ory) was previously reported to possess antioxidant and neuroprotective properties. Thus, we conducted this study to test the hypothesis that Ory can also protect flies in an Mn intoxication model. Adult wild-type flies were fed over 10 days with Mn (5 mM) and/or Ory (25 µM). Flies treated with Mn had a decrease in locomotor activity and a higher mortality rate compared to those in controls. Mn-treated flies also had a significant increase in acetylcholinesterase (AChE) activity, in Mn accumulation and in oxidative stress markers. Moreover, flies treated with Mn exhibited a significant decrease in dopamine levels and in tyrosine hydroxylase activity, as well as in mitochondrial and cellular viability. Particularly important, Ory protected against mortality and avoided locomotor and biochemical changes associated with Mn exposure. However, Ory did not prevent the accumulation of Mn. The present results support the notion that Ory effectively attenuates detrimental changes associated with Mn exposure in Drosophila melanogaster, reinforcing its neuroprotective action/potential.

Caffeic acid and caffeine attenuate toxicity associated with malonic or methylmalonic acid exposure in Drosophila melanogaster.

The deficiency in the activity of the mitochondrial enzyme methylmalonyl-CoA mutase (MCM, EC 5.4.99.2) leads to a condition called methylmalonic academia, which is characterised by the accumulation of methylmalonic (MMA), malonic (MA) or other organic acids. Importantly, we have recently found that supplementation with Ilex paraguariensis aqueous extract offered protection against toxicity associated with MMA or MA exposure to Drosophila melanogaster. Of note, caffeic acid (CA) and caffeine (CAF) were the major phytochemicals found in our Ilex paraguariensis crude extract. Therefore, here, we have exploited CA and/or CAF to test the hypothesis that supplementation with the isolated compounds (either alone or combined) could exert a protective effect against MMA or MA-induced toxicity in flies. Therefore, flies were exposed to MA (5 mM) or MMA (5 mM) and concomitantly treated with CA (1.39 µg/mL), CAF (1.27 µg/mL) or CA + CAF for 10 days for survival, and for 4 days for behavioural and biochemical assays. CA, CAF and CA + CAF treatments completely abolished the mortality associated with either MMA or MA exposure. Moreover, CA and CAF, either alone or combined, completely abolished behavioural changes, and completely protect against changes in thiobarbituric acid reactive substances (TBARS) levels, catalase (CAT) activity and MTT reduction ability, associated with MA or MMA exposure. In turn, CAF restored SOD activity in the head of flies exposed to MA or MMA. However, CA and CAF (either alone or combined) significantly decreased acetylcholinesterase (AChE) activity per se, while CAF alone protected from changes in AChE activity (in head tissue) associated with MA or MMA. Finally, CA and/or CAF were able to protect from a decrease in glucose and triglyceride levels associated with both MA and MMA exposures in haemolymph. Together, our data confirm the hypothesis that supplementation with CA and/or CAF offers protection against detrimental changes associated with MMA or MA exposure in flies, being responsible, at least in part, for the protective effect of I. paraguariensis crude extract which was reported previously.

Antidepressant-like effect of (3Z)-5-Chloro-3-(hydroxyimino)indolin-2-one in rats exposed to malathion: Involvement of BDNF-Trkß pathway and AChE.

BACKGROUND: Organophosphorus pesticides exert their toxic effects mainly by the inhibition of acetylcholinesterase (AChE), which is related to emotional disorders, such as depression. Atropine-oximes therapy is commonly used; however, the efficacy of oximes in the reactivation of AChE has been inconsistent. The objective of this study was to investigate the possible neuroprotective effect of (3Z)-5-Chloro-3-(hydroxyimino)indolin-2-one (Cℓ-HIN), a compound that combines the isatin and oxime functional groups, in rats exposed to malathion. The effect of Cℓ-HIN on the AChE activity and the BDNF-Trkß pathway in the prefrontal cortex of malathion-exposed rats were tested. METHODS: Wistar male rats were co-treated with Cℓ-HIN [50 mg/kg (p.o.) (3 mL/kg)] and/or malathion [250 mg/kg (i.p.) (5 mL/kg)] and performed behavioral tests twelve hours after these exposures. RESULTS: The Cℓ-HIN reversed the increased immobility time in the forced swimming test and the decreased grooming time in the splash test induced by malathion, but any significant difference was observed in locomotion analysis. These results demonstrate the antidepressant-like effect of Cℓ-HIN. The cortical AChE activity was reactivated by Cℓ-HIN in rats exposed to malathion. Malathion induced an increase in Trkß and a decrease in BDNF levels in the prefrontal cortex of rats, which were avoided by Cℓ-HIN. CONCLUSION: These findings support the hypothesis that Cℓ-HIN is an AChE reactivator with antidepressant-like properties, which is related to the improvement of BDNF-Trkß signaling after acute exposure to malathion in rats. Thus, the results allow suggesting the potential use of Cℓ-HIN as an oxime-based therapy against the neurotoxic effects of malathion.

Pre-clinical evidence of safety and protective effect of isatin and oxime derivatives against malathion-induced toxicity.

The inhibition of acetylcholinesterase (AChE) is a common outcome caused by organophosphorus (OPs) intoxication. Although inconsistent, the standard treatment consists of a muscarinic receptor antagonist (atropine) and AChE-reactivating molecules such as oximes. This study proposes to test unpublished compounds which contain the moieties of isatin and/or oxime have protective effects against the toxicity induced by malathion in two animal models: Artemia salina and Rattus norvegicus (Wistar rats). The lethality was assessed in A salina, and the calculated LD50 to (3Z)-5-chloro-3-(hydroxyimino) indolin-2-one oxime (Cℓ-HIN) and 2-(5-chloro-2-oxoindolin-3-ylidene)-hydrazinecarbothioamide (Cℓ-OXHS) was higher than 1000 µM while to 3-(phenylhydrazono) butan-2-one oxime (PHBO) was 38 µM. Our screening showed that Cℓ-HIN seems to be the most promising molecule, with low toxicity to A salina, protection against mortality (with or without atropine) and AChE inhibition induced by malathion. Similarly, the oral administration of 300 mg/kg of Cℓ-HIN induced low or no toxicity in rats. The plasma butyrylcholinesterase (BChE) and cortical AChE activities were reactivated by Cℓ-HIN (50 mg/kg, p.o.) in rats exposed to malathion (250 mg/kg, i.p). No difference was observed in paraoxonase-1 (PON-1) activity among groups treated. In conclusion, Cℓ-HIN restored the cholinesterase activities inhibited by malathion in A salina and rats with low toxicity in both. Thus, the data provide evidence that Cℓ-HIN, a compound that combines isatin and oxime functional groups, is safe and has important properties to reactivate the cholinesterases inhibited by malathion. In addition, we demonstrate the importance of a preliminary assessment in an alternative model in order to reduce the use of mammalians in drug discovery.

Antibacterial and antioxidant effects of Rosmarinus officinalis L. extract and its fractions.

The production of reactive species over physiological levels associated to pathogenic bacteria could represent a high risk for many diseases. The Rosmarinus officinalis L. is used around the world due its pharmacological proprieties. So, in this study our aim is to test for the first time if R. officinalis L. extract (eeRo) and its fractions (DCM, EA, ButOH) could have better or similar antioxidant action to standars and among themselves in vitro or ex vivo, in brain, stomach and liver of rats. Moreover, we intend to clarify their possible effects on pathogenic bacteria. The eeRo was obtained from the dried leaves subjected to an alcoholic extraction and fractioned. The quantification of the constituents of eeRo and fractions were done by HPLC. The antioxidant proprieties of R. officinalis was analyzed by DPPH•- radical scavenging, total antioxidant, dichlorofluorescein, lipid peroxidation and sodium nitroprusside -induced lipid peroxidation assays. The Minimum inhibitory concentrations of R. officinalis L. were tested with standard strains of danger bacteria. The eeRo, DCM, EA had significant total antioxidant and DPPH•- radical scavenging activities. The DCM and eeRo got significant effects against basal levels of reactive species in liver, stomach and brain. The eeRo and DCM protected the liver and brain against lipid peroxidation. The eeRo, DCM, EA and ButOH had inhibitory effect in the Gram-positive and Gram-negative bacteria. In general way, the DCM and eeRo had the best antioxidant and antibacterial effects among all tested fractions.

Ilex paraguariensis Attenuates Changes in Mortality, Behavioral and Biochemical Parameters Associated to Methyl Malonate or Malonate Exposure in Drosophila melanogaster.

Methylmalonic acidemia is a genetic disease characterized by accumulation of organic acids, such as methylmalonic (MMA) and malonic (MA) acids. Considering that the accumulation of MMA and MA causes several damages due to oxidative stress, antioxidants are thought to play a pivotal role in preventing deleterious effects associated with exposure to such compounds. Ilex paraguariensis (IP) was used here to test the hypothesis that supplementation with the aqueous extract of this plant could exert protective effect against MMA or MA induced mortality, behavioral and/or biochemical changes in Drosophila melanogaster (DM). Initially, a curve time- and dose-response to MMA (1-10 mM), MA (1-10 mM) and IP (63-500 µM) was performed. Thereafter, flies were concomitantly exposed to MA (5 mM), MMA (5 mM) and/or IP (250 µg/mL) during 15 days for survival assay, and for 48 hs to MA (1 or 5 mM), MMA (1 or 5 mM) and/or IP (250 µg/mL) for subsequent investigations. Both MMA and MA exposure resulted in higher incidence of mortality, a worse performance in the negative geotaxis assay and increased locomotion in open-field test as compared with control group. Furthermore, a marked increase in non-protein thiol (NPSH) and in thiobarbituric acid reactive substances (TBARS) levels, decrease in superoxide dismutase (SOD), catalase and acetylcholinesterase (AChE) activities, and decrease in MTT and resazurin reduction were noted in MMA or MA treated groups. IP treatment offered significant protection against all alterations associated to MMA or MA exposure. This study confirm the hypothesis that supplementation with IP offers protection against changes associated to MMA or MA exposure in DM, due, at least in part, to its antioxidant effect.

Salvia hispanica L. (chia) seeds oil extracts reduce lipid accumulation and produce stress resistance in Caenorhabditis elegans.

BACKGROUND: Salvia hispanica seeds have been commonly used by people that seek healthy habits through natural foods to reduce cholesterol and triacylglycerides levels, however, the evidences that support this assumption are still scarce in literature. Here, we aimed to evaluate the lipid lowering effects of chia by using Caenorhabditis elegans as animal model, a nematode that has proven its usefulness for lipid metabolism studies. METHODS: We prepared hexane (HE) and Bligh-Dyer (BDE) extracts, evaluated and compared their safety, antioxidant potential and their lipid-lowering activity in the worms. RESULTS: The characterization of both extracts demonstrated that there were no differences in their lipid composition; however, BDE depicted better antioxidant potential. Both extracts reduced worm's survival from 2%, and reproduction was reduced following treatment with both extracts, though a more notable effect was observed in HE-treated worms. In addition, the non-toxic concentration of both extracts (1%) increased stress resistance against paraquat toxicity in an antidote paradigm. Notably, this same concentration of both extracts reduced lipid accumulation in obese worms, which was not caused by food deprivation. CONCLUSIONS: Taken together, our data demonstrate that both extraction methods from chia seeds result in oils that are rich in mono and polyunsaturated fatty acids, which may modulate lipid accumulation and provide antioxidant resistance in C. elegans.

Dietary hydrogenated vegetable fat exacerbates the activation of kynurenine pathway caused by peripheral lipopolysaccharide immune challenge in aged mice.

Sickness behavior is a normal immune response of body to fight infection, accompanied by endocrine and behavioral alterations. Lipopolysaccharide (LPS) causes sickness behavior in rodents through the increase of proinflammatory cytokines, generating peripheral inflammation and thus overactivation of kynurenine pathway (KP). In the present study we investigated the effects of dietary hydrogenated vegetable fat (HVF) in sickness behavior induced by LPS in aged mice. Male C57BJ/6 aged mice received a supplementation with HVF for six months. After HVF supplementation mice were treated with LPS (0.15 mg/kg; i. p. injection). Twenty-four hours post LPS injection mice were submitted to behavioral tests and then, the hippocampus, striatum and prefrontal cortex were removed for neurochemical determinations. Our results showed that dietary HVF did not exacerbate the behavioral alterations induced by LPS. Although HVF did not modulate the proinflammatory cytokines analyzed, it caused a potentiation in the increase of brain tumor necrosis factor-alpha levels induced by LPS. Moreover, dietary HVF aggravated LPS-induced KP activation in the brain of mice, mainly by further increase of neurotoxic metabolite quinolinic acid and further decrease of kynurenic acid/kynurenine ratio, a marker of neuroprotective branch of KP. Overall, our study demonstrated that dietary HVF did not worsen the sickness behavioral induced by LPS administration. However, HVF aggravated the activation of KP and exacerbated the shift of KP metabolism towards the neurotoxic branch.

Fish oil ameliorates sickness behavior induced by lipopolysaccharide in aged mice through the modulation of kynurenine pathway.

Sickness behavior is an expression of a central motivational state triggered by activation of the immune system, being considered a strategy of the organism to fight infection. Sickness behavior is induced by peripheral administration of lipopolysaccharide (LPS). LPS can increase the levels of proinflammatory cytokines, which induce the activation of the kynurenine pathway (KP) and behavioral alterations. Previous studies have shown that omega-3 (n-3) polyunsaturated fatty acid (PUFA) has anti-inflammatory properties. Because of this, the purpose of the present study was to evaluate the protective effect of fish oil (FO) supplementation against LPS-induced sickness behavior in aged mice with respect to anhedonia, locomotor activity and body weight. Moreover, we evaluated the ability of FO treatment on the regulation of neuroinflammation (levels of interleukin-1ß, interleukin-6, tumor factor necrosis-α and interferon-γ), KP biomarkers (levels of tryptophan, kynurenine, kynurenic acid, 3-hydroxykynurenine and quinolinic acid and activities of indoleamine-2,3-dioxygenase, kynurenine monooxygenase and kynurenine aminotransferase) and serotonergic system (levels of serotonin and 5-hydroxyindoleactic acid) in the hippocampus, striatum and prefrontal cortex of LPS-treated mice. We found that FO prevented the LPS-mediated body weight loss, anhedonic behavior, reduction of locomotor activity, up-regulation of the proinflammatory cytokines and serotoninergic alterations. We also found that FO was effective in modulating the KP biomarkers, inhibiting or attenuating KP dysregulation induced by LPS. Together, our results indicated that FO may have beneficial effects on LPS induced sickness-behavior in aged mice either by modulating central inflammation, KP and serotonergic signaling (indirectly effect) or by fatty acids incorporation into neuronal membranes (direct effect).

The phytoremediation potential of Plectranthus neochilus on 2,4-dichlorophenoxyacetic acid and the role of antioxidant capacity in herbicide tolerance.

The possible phytoremediation capacity of Plectranthus neochilus (boldo) exposed to the commercial pesticide (Aminol) in soil and water through consecutive extractions (days interval) was evaluated. After the exposure period, tea leaves from the plant were analyzed in terms of the presence of 2,4-D, total antioxidant capacity (DPPH), concentration of total polyphenols and flavonoids for plants exposed to soil and water. In water, 2,4-D remained up to 67% in the 60 days of experiment in the control group, which provided the use of two treatment groups with the plant (one group of plants for 30 days and another group in the remaining 30 days in the same system), thus, a decontamination up to 49% of the 2,4-D was obtained in this system with water. In both experiments (soil and water) the 2,4-D was not detected in tea leaves, the reduction of the antioxidant activity, polyphenols and flavonoids of plants exposed to the herbicide was also observed when compared to the non-exposed plants. In tea - plants in water - it was also possible to quantify the phenolic compounds and it was observed that in the group of plants of the first 30 days there was a decrease in caffeic acid and an increase in coumaric and ferulic acids, compared to the group of plants that were not exposed to 2,4-D. In the remaining 30 days with the new seedlings there was a decrease of the coumaric acid and an increase of the caffeic and ferulic acids.

Effects of Bauhinia forficata Tea on Oxidative Stress and Liver Damage in Diabetic Mice.

This study was designed to evaluate the effects of Bauhinia forficata Link subsp. pruinosa (BF) tea on oxidative stress and liver damage in streptozotocin (STZ)-induced diabetic mice. Diabetic male mice have remained 30 days without any treatment. BF treatment started on day 31 and continued for 21 days as a drinking-water substitute. We evaluated (1) BF chemical composition; (2) glucose levels; (3) liver/body weight ratio and liver transaminases; (4) reactive oxygen species (ROS), lipid peroxidation, and protein carbonylation in liver; (5) superoxide dismutase (SOD) and catalase (CAT) activities in liver; (6) δ-aminolevulinate dehydratase (δ-ALA-D) and nonprotein thiols (NPSH) in liver; (7) Nrf2, NQO-1, and HSP70 levels in liver and pancreas. Phytochemical analyses identified four phenols compounds. Diabetic mice present high levels of NQO-1 in pancreas, increased levels of ROS and lipid peroxidation in liver, and decrease in CAT activity. BF treatment normalized all these parameters. BF did not normalize hyperglycemia, liver/body weight ratio, aspartate aminotransferase, protein carbonyl, NPSH levels, and δ-ALA-D activity. The raised oxidative stress seems to be a potential mechanism involved in liver damage in hyperglycemic conditions. Our results indicated that BF protective effect could be attributed to its antioxidant capacity, more than a hypoglycemic potential.

Protective Effects of Aqueous Extract of Luehea divaricata against Behavioral and Oxidative Changes Induced by 3-Nitropropionic Acid in Rats.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disease. Accordingly, 3-nitropropionic acid (3-NP) has been found to effectively produce HD-like symptoms. Luehea divaricata (L. divaricata), popularly known in Brazil as "açoita-cavalo," may act as a neuroprotective agent in vitro and in vivo. We evaluated the hypothesis that the aqueous extract of L. divaricata could prevent behavioral and oxidative alterations induced by 3-NP in rats. 25 adult Wistar male rats were divided into 5 groups: (1) control, (2) L. divaricata (1000 mg/kg), (3) 3-NP, (4) L. divaricata (500 mg/kg) + 3-NP, and (5) L. divaricata (1000 mg/kg) + 3-NP. Groups 2, 4, and 5 received L. divaricata via intragastric gavage daily for 10 days. Animals in groups 3, 4, and 5 received 20 mg/kg 3-NP daily from days 8-10. At day 10, parameters of locomotor activity and biochemical evaluations were performed. Indeed, rats treated with 3-NP showed decreased locomotor activity compared to controls. Additionally, 3-NP increased levels of reactive oxygen species and lipid peroxidation and decreased ratio of GSH/GSSG and acetylcholinesterase activity in cortex and/or striatum. Our results suggest that rats pretreated with L. divaricata prior to 3-NP treatment showed neuroprotective effects when compared to 3-NP treated controls, which may be due to its antioxidant properties.

Oxidative stress and labile plasmatic iron in anemic patients following blood therapy.

AIM: To determine the plasmatic iron content and evaluate the oxidative stress (OS) markers in subjects receiving blood therapy. METHODS: Thirty-nine individuals with unspecified anemia receiving blood transfusions and 15 healthy subjects were included in the study. Anemic subjects were divided into three subgrouP: (1) those that received up to five blood transfusions (n = 14); (2) those that received from five to ten transfusions (n = 11); and (3) those that received more than ten transfusions (n = 14). Blood samples were collected by venous arm puncture and stored in tubes containing heparin. The plasma and cells were separated by centrifugation and subsequently used for analyses. Statistical analyses were performed using Kruskal-Wallis analysis of variance followed by Dunn's multiple comparison tests when appropriate. RESULTS: The eletrophoretic hemoglobin profiles of the subjects included in this study indicated that no patients presented with hemoglobinopathy. Labile plasmatic iron, ferritin, protein carbonyl, thiobarbituric acid-reactive substances (TBARS) and dichlorofluorescein diacetate oxidation were significantly higher (P < 0.05), whereas total thiol levels were significantly lower (P < 0.05) in transfused subjects compared to controls. Additionally, the activity of catalase, superoxide dismutase and glutathione peroxidase were significantly lower in the transfused subjects (P < 0.05). Antioxidant enzyme activities and total thiol levels were positively correlated (P < 0.05), and negatively correlated with the levels of protein carbonyl and TBARS (P < 0.05). In contrast, protein carbonyl and TBARS were positively correlated (P < 0.05). Altogether, these data confirm the involvement of OS in patients following therapy with repeated blood transfusions. CONCLUSION: Our data reveal that changes in OS markers are correlated with levels of labile plasmatic iron and ferritin and the number of transfusions.

Manganese in health and disease.

Manganese is an important metal for human health, being absolutely necessary for development, metabolism, and the antioxidant system. Nevertheless, excessive exposure or intake may lead to a condition known as manganism, a neurodegenerative disorder that causes dopaminergic neuronal death and parkinsonian-like symptoms. Hence, Mn has a paradoxal effect in animals, a Janus-faced metal. Extensive work has been carried out to understand Mn-induced neurotoxicity and to find an effective treatment. This review focuses on the requirement for Mn in human health as well as the diseases associated with excessive exposure to this metal.

Organochalcogens inhibit mitochondrial complexes I and II in rat brain: possible implications for neurotoxicity.

Organochalcogens, such as organoselenium and organotellurium compounds, can be neurotoxic to rodents. Since mitochondrial dysfunction plays a pivotal role in neurological disorders, the present study was designed to test the hypothesis that rat brain mitochondrial complexes (I, II, I-III, II-III and IV) could be molecular targets of organochalcogens. The results show that organochalcogens caused statistically significant inhibition of mitochondrial complex I activity, which was prevented by preincubation with NADH and fully blunted by reduced glutathione (GSH). Mitochondrial complex II activity remained unchanged in response to (PhSe)2 treatment. Ebs and (PhTe)2 caused a significant concentration-dependent inhibition of complex II that was also blunted by GSH. Mitochondrial complex IV activity was not modified by organochalcogens. Collectively, Ebs, (PhSe)2 and (PhTe)2 were more effective inhibitors of brain mitochondrial complex I than of complex II, whereas they did not affect complex IV. These observations are consistent with organochalcogens inducing mitochondrial complex I and II inhibition via their thiol-oxidase-like activity, with Ebs, (PhSe)2 and (PhTe)2 effectively oxidising critical thiol groups of these complexes.

Prevalência de comportamentos de risco em adolescentes / Risk behaviors prevalence in adolescents

Este estudo visou analisar a prevalência de comportamentos de risco à saúde, tais como: sedentarismo, má alimentação, etilismo, adição em drogas, envolvimento em brigas e relações sexuais sem proteção, em adolescentes no município de Uruguaiana (RS), Brasil. A coleta de dados foi realizada a partir de um questionário sobre comportamento de risco e estilo de vida, composto de 13 questões com variáveis demográficas, socioeconômicas e comportamentais. Os comportamentos de risco prevalentes foram nunca/raramente uso de preservativos nas relações sexuais, o consumo de bebidas alcoólicas e o envolvimento em brigas. Cerca de 30% dos adolescentes apresentaram pelo menos um comportamento de risco, e 20% apresentaram dois ou mais desses. Dada a frequência de exposição, torna-se necessário a implementação de medidas de saúde no contexto escolar visando a diminuição da exposição a esses fatores de risco, promovendo a saúde desses adolescentes.

The aim of this study was to examine the prevalence of health risk behaviors such as inactivity, poor nutrition, alcoholism, drug addition, involvement in physical fights and the lack of use of condoms during sex, in adolescents of Uruguaiana (RS), Brazil. The data were collected using a questionnaire on risk behavior and lifestyle, consisting of 13 questions with demographic, socioeconomic, and behavioral variables. We have founded that the risk behaviors more prevalent were never/ rarely use of condoms during sexual intercourse, consumption of alcohol and engaging in fights. About 30% of adolescents presented, at least, one risk behavior and 20% presented two or more risk behaviors. Given this frequency of exposure to its risks, it is necessary to implement health measures in the school context, aimed to reduce exposure to these risk factors, promoting the health of adolescents.

The antioxidant properties of different phthalocyanines.

Oxidative stress is involved in the etiology of several chronic diseases, including cardiovascular disease, diabetes, cancer, and neurodegenerative disorders. From this perspective, we have evaluated the possible antioxidant capacities of five different phthalocyanines (PCs), consisting of four metallophthalocyanines (MPCs) and one simple phthalocyanine (PC) in order to explore, for the first time, the potential antioxidant activities of these compounds. Our results show that all PCs tested in this study have significant antioxidant activity in lipid peroxidation assay, providing protection from sodium nitroprusside -induced oxidative damage to supernatant from the homogenized liver, brain, e rim of mice. Compared to the non-induced control, the PCs were generally more efficient in reducing malondialdehyde levels in all assays on lipid peroxidation induced by sodium nitroprusside; the order of approximate decrease in efficiency was as follows: manganese-PC (better efficiency)>copper-PC>iron-PC>zinc-PC>PC (worst efficiency). Furthermore, the copper-PC and manganese-PC compounds exerted a significant protective effect in deoxyribose degradation assays, when employing Fe(2+), Fe(2+)+H(2)O(2), and H(2)O(2) solutions. In conclusion, all PCs tested here were shown to be promising compounds for future in vivo investigations, because of their potential antioxidant activities in vitro.