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1.
J Food Sci Technol ; 56(12): 5289-5297, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31749476

RESUMO

The food product industry is increasingly looking for foods with nutritional properties that can provide health benefits. Additionally, a challenge for the food industry is the use of all raw materials. For these reasons, banana peel that is a raw material from Banana (Musa spp.) fruit emerges as potential for new food product development. Here, we developed powder blends using a lyophilization process for the preparation of flour to potential use in cookies, bread, and pasta products. Three formulations were designed; the main difference in the formulations was the use of banana peel concentration. Our results showed that blends produced with banana peel presented physical-chemical properties considered suitable for use in food industry. Moreover, the evaluated morphological parameters reveal the properties of the powders. The blends formulated with banana peel have more antioxidant properties, showing that the banana peel may be an attractive option to generate powders with high antioxidant properties.

2.
Sci Rep ; 9(1): 15741, 2019 Oct 31.
Artigo em Inglês | MEDLINE | ID: mdl-31673065

RESUMO

Reactive oxygen species (ROS) are byproducts of aerobic metabolism and may cause oxidative damage to biomolecules. Plants have a complex redox system, involving enzymatic and non-enzymatic compounds. The evolutionary origin of enzymatic antioxidant defense in plants is yet unclear. Here, we describe the redox gene network for A. thaliana and investigate the evolutionary origin of this network. We gathered from public repositories 246 A. thaliana genes directly involved with ROS metabolism and proposed an A. thaliana redox gene network. Using orthology information of 238 Eukaryotes from STRINGdb, we inferred the evolutionary root of each gene to reconstruct the evolutionary history of A. thaliana antioxidant gene network. We found two interconnected clusters: one formed by SOD-related, Thiol-redox, peroxidases, and other oxido-reductase; and the other formed entirely by class III peroxidases. Each cluster emerged in different periods of evolution: the cluster formed by SOD-related, Thiol-redox, peroxidases, and other oxido-reductase emerged before opisthokonta-plant divergence; the cluster composed by class III peroxidases emerged after opisthokonta-plant divergence and therefore contained the most recent network components. According to our results, class III peroxidases are in expansion throughout plant evolution, with new orthologs emerging in each evaluated plant clade divergence.

3.
Artigo em Inglês | MEDLINE | ID: mdl-28904552

RESUMO

In tropical America, principally in Northeastern Brazil, the leaf extract of Anacardium occidentale is traditionally used for treatment of different diseases. However, chemical and biological properties and activities of Anacardium occidentale are poorly investigated and known. Here, we evaluated the antioxidant and anti-inflammatory activities "in vitro" of leaf extract from Anacardium occidentale. Our results show that leaf extract exhibits antioxidant activity when used to treat RAW 264.7 macrophage cells. Antioxidant effects were observed by decrease in oxidative damage in macrophage cells treated with 0.5 µg/mL and 5 µg/mL of leaf extract. Moreover, leaf extract reversed oxidative damage and inflammatory parameters induced in LPS-stimulated RAW 264.7 macrophage cells. Leaf extract at 0.5 µg/mL and 5 µg/mL was able to inhibit release of TNF-α and IL-1ß in LPS-stimulated cells. Taken together, our results indicate antioxidant and anti-inflammatory effects of leaf extract from Anacardium occidentale and reveal the positive effects that intake of these products can mediate in biological system.

4.
Sci Rep ; 7(1): 8795, 2017 08 18.
Artigo em Inglês | MEDLINE | ID: mdl-28821831

RESUMO

The receptor for advanced glycation endproducts (RAGE) is a pattern-recognition receptor associated with inflammation in most cell types. RAGE up-regulates the expression of proinflammatory mediators and its own expression via activation of NF-kB. Recent works have proposed a role for RAGE in Parkinson's disease (PD). In this study, we used the multimodal blocker of RAGE FPS-ZM1, which has become available recently, to selectively inhibit RAGE in the substantia nigra (SN) of rats intracranially injected with 6-hydroxydopamine (6-OHDA). FPS-ZM1 (40 µg per rat), injected concomitantly with 6-OHDA (10 µg per rat) into the SN, inhibited the increase in RAGE, activation of ERK1/2, Src and nuclear translocation of NF-kB p65 subunit in the SN. RAGE inhibition blocked glial fibrillary acidic protein and Iba-1 upregulation as well as associated astrocyte and microglia activation. Circulating cytokines in serum and CSF were also decreased by FPS-ZM1 injection. The loss of tyrosine hydroxylase and NeuN-positive neurons was significantly inhibited by RAGE blocking. Finally, FPS-ZM1 attenuated locomotory and exploratory deficits induced by 6-OHDA. Our results demonstrate that RAGE is an essential component in the neuroinflammation and dopaminergic denervation induced by 6-OHDA in the SN. Selective inhibition of RAGE may offer perspectives for therapeutic approaches.


Assuntos
Dopamina/metabolismo , Neurônios Dopaminérgicos/efeitos dos fármacos , Neurônios Dopaminérgicos/metabolismo , Oxidopamina/efeitos adversos , Receptor para Produtos Finais de Glicação Avançada/antagonistas & inibidores , Substância Negra/metabolismo , Animais , Citocinas/metabolismo , Modelos Animais de Doenças , Neurônios Dopaminérgicos/patologia , Mediadores da Inflamação/metabolismo , Masculino , NF-kappa B/metabolismo , Doença de Parkinson/etiologia , Doença de Parkinson/metabolismo , Doença de Parkinson/patologia , Ratos , Substância Negra/efeitos dos fármacos , Substância Negra/patologia , Quinases da Família src/metabolismo
5.
Intensive Care Med Exp ; 5(1): 15, 2017 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-28303482

RESUMO

BACKGROUND: Extracellular superoxide dismutase (ECSOD) protects nitric oxide (NO) bioavailability by decreasing superoxide levels and preventing peroxynitrite generation, which is important in maintaining renal blood flow and in preventing acute kidney injury. However, the profile of ECSOD expression after sepsis is not fully understood. Therefore, we intended to evaluate the content and gene expression of superoxide dismutase (SOD) isoforms in the renal artery and their relation to renal blood flow. METHODS: Sepsis was induced in Wistar rats by caecal ligation and perforation. Several times after sepsis induction, renal blood flow (12, 24 and 48 h); the renal arterial content of SOD isoforms, nitrotyrosine, endothelial and inducible nitric oxide synthase (e-NOS and i-NOS), and phosphorylated vasodilator-stimulated phosphoprotein (pVASP); and SOD activity (3, 6 and 12 h) were measured. The influence of a SOD inhibitor was also evaluated. RESULTS: An increase in ECSOD content was associated with decreased 3-nitrotyrosine levels. These events were associated with an increase in pVASP content and maintenance of renal blood flow. Moreover, previous treatment with a SOD inhibitor increased nitrotyrosine content and reduced renal blood flow. CONCLUSIONS: ECSOD appears to have a major role in decreasing peroxynitrite formation in the renal artery during the early stages of sepsis development, and its application can be important in renal blood flow control and maintenance during septic insult.

6.
Intensive Care Med Exp ; 2(1): 17, 2014 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-26266917

RESUMO

BACKGROUND: The purpose of this research is to study the relationship between superoxide dismutase (SOD) and lung redox state in an animal model of sepsis. METHODS: Sepsis was induced in rats by the cecal ligation and perforation model (CLP). After 3, 6, and 12 h, CLP protein content and expression of SOD1, SOD2, and SOD3 were evaluated, and SOD activity was assessed. Oxidative damage was determined by quantifying nitrotyrosine content. Lung localization of SOD3 was performed by immunohistochemistry. The protective effect of a SOD mimetic on oxidative damage, inflammation, and lung permeability was assessed 12 and 24 h after sepsis induction. RESULTS: Lung levels of SOD1 decreased 3 and 12 h after sepsis, but SOD2 and SOD3 increased, as well as SOD activity. These alterations were not associated with changes in sod gene expression. Nitrotyrosine levels increased 3 and 12 h after sepsis. The administration of a SOD mimetic decreased nitrotyrosine and proinflammatory cytokine levels and improved lung permeability. CONCLUSIONS: SOD2 and SOD3 increased after sepsis induction, but this was insufficient to protect the lung. Treatments based on SOD mimetics could have a role in lung injury associated with sepsis.

7.
Int J Parasitol ; 43(5): 371-9, 2013 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-23369670

RESUMO

Schistosomiasis is a parasitic disease caused by trematode worms from the Schistosoma genus and is characterized by high rates of morbidity. The main organs affected in this pathology, such as liver, kidneys and spleen, are shifted to a pro-oxidant state in the course of the infection. Here, we compared oxidative stress parameters of liver, kidney and spleen with other organs affected by schistosomiasis - heart, brain cortex and lungs. The results demonstrated that mice infected with Schistosoma mansoni had altered non-enzymatic antioxidant status in lungs and brain, increased carbonyl levels in lungs, and a moderate level of oxidative stress in heart. A severe redox imbalance in liver and kidneys and decreased non-enzymatic antioxidant capacity in spleen were also observed. Superoxide dismutase and catalase activities were differently modulated in liver, kidney and heart, and we found that differences in Superoxide dismutase 2 and catalase protein content may be responsible for these differences. Lungs had decreased receptor for advanced glycation endproduct expression and the brain cortex presented altered tau expression and phosphorylation levels, suggesting important molecular changes in these tissues, as homeostasis of these proteins is widely associated with the normal function of their respective organs. We believe that these results demonstrate for the first time that changes in the redox profile and expression of tissue-specific proteins of organs such as heart, lungs and brain are observed in early stages of S. mansoni infection.


Assuntos
Estresse Oxidativo/imunologia , Receptores Imunológicos/metabolismo , Schistosoma mansoni/fisiologia , Esquistossomose mansoni/imunologia , Proteínas tau/metabolismo , Animais , Catalase/metabolismo , Córtex Cerebral/parasitologia , Córtex Cerebral/patologia , Regulação da Expressão Gênica/fisiologia , Pulmão/parasitologia , Pulmão/patologia , Camundongos , Miocárdio/patologia , Oxirredução , Receptor para Produtos Finais de Glicação Avançada , Receptores Imunológicos/genética , Esquistossomose mansoni/metabolismo , Esquistossomose mansoni/parasitologia , Superóxido Dismutase , Proteínas tau/genética
8.
Acta Pharmacol Sin ; 33(4): 558-67, 2012 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-22426700

RESUMO

AIM: Toxicity of retinol (vitamin A) has been previously associated with apoptosis and/or cell malignant transformation. Thus, we investigated the pathways involved in the induction of proliferation, deformation and proliferative focus formation by retinol in cultured Sertoli cells of rats. METHODS: Sertoli cells were isolated from immature rats and cultured. The cells were subjected to a 24-h treatment with different concentrations of retinol. Parameters of oxidative stress and cytotoxicity were analyzed. The effects of the p38 inhibitor SB203580 (10 µmol/L), the JNK inhibitor SP600125 (10 µmol/L), the Akt inhibitor LY294002 (10 µmol/L), the ERK inhibitor U0126 (10 µmol/L) the pan-PKC inhibitor Gö6983 (10 µmol/L) and the PKA inhibitor H89 (1 µmol/L) on morphological and proliferative/transformation-associated modifications were studied. RESULTS: Retinol (7 and 14 µmol/L) significantly increases the reactive species production in Sertoli cells. Inhibition of p38, JNK, ERK1/2, Akt, and PKA suppressed retinol-induced [(3)H]dT incorporation into the cells, while PKC inhibition had no effect. ERK1/2 and p38 inhibition also blocked retinol-induced proliferative focus formation in the cells, while Akt and JNK inhibition partially decreased focus formation. ERK1/2 and p38 inhibition hindered transformation-associated deformation in retinol-treated cells, while other treatments had no effect. CONCLUSION: Our results suggest that activation of multiple kinases is responsible for morphological and proliferative changes associated to malignancy development in Sertoli cells by retinol at the concentrations higher than physiological level.


Assuntos
Proliferação de Células/efeitos dos fármacos , Radicais Livres/metabolismo , Células de Sertoli/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Vitamina A/farmacologia , Vitaminas/farmacologia , Animais , Apoptose/efeitos dos fármacos , Células Cultivadas , Ativação Enzimática/efeitos dos fármacos , Masculino , Proteínas Quinases/metabolismo , Ratos , Células de Sertoli/citologia , Células de Sertoli/metabolismo , Células de Sertoli/patologia
9.
Brain Res Bull ; 87(4-5): 432-44, 2012 Mar 10.
Artigo em Inglês | MEDLINE | ID: mdl-22274401

RESUMO

Even though vitamin A has been viewed as an antioxidant molecule, recent findings demonstrate that such vitamin elicits pro-oxidant effects in vivo. Moreover, vitamin A supplements utilization may increase mortality rates among healthy subjects. However, the mechanism by which vitamin A elicits such effects remains to be better analyzed. In this regard, we investigated here the consequences of vitamin A supplementation at 500, 1000, or 2500 IU/kg day(-1) for 3 months on adult rat substantia nigra and striatum total and mitochondrial redox state (both oxidative and nitrosative stress markers), electron transfer chain activity, monoamine oxidase (MAO) enzyme activity, endoplasmic reticulum stress marker (BiP), α- and ß-synucleins, ß-amyloid peptide (1-40), dopamine D2 receptor (D2R), receptor for advanced glycation end products (RAGE), caspase-3 and caspase-8 enzyme activity and tumor necrosis factor-α (TNF-α) levels. Also, nigrostriatal mitochondria were isolated and challenged with 50 µM H2O2 in vitro after vitamin A supplementation and complexes I-III, II-III, and IV enzyme activity was recorded. We observed both total and mitochondrial oxidative and nitrosative stress, increased MAO enzyme activity, and increased levels of α-synuclein, ß-amyloid peptide, RAGE, and TNF-α, but decreased D2R in both rat brain areas. Furthermore, vitamin A supplementation induced a decrease in nigral, but not striatal, ß-synuclein levels in this work. Moreover, mitochondria isolated from both substantia nigra and striatum of vitamin A-treated rats were more sensitive to H2O2 than control mitochondria as assessed through the in vitro assay. Overall, these data may be useful to explain how vitamin A elicits neurotoxic effects chronically.


Assuntos
Corpo Estriado/efeitos dos fármacos , Suplementos Nutricionais/toxicidade , Espécies Reativas de Oxigênio/toxicidade , Substância Negra/efeitos dos fármacos , Vitamina A/toxicidade , Peptídeos beta-Amiloides/metabolismo , Animais , Corpo Estriado/metabolismo , Transporte de Elétrons/efeitos dos fármacos , Peróxido de Hidrogênio/toxicidade , Masculino , Mitocôndrias/efeitos dos fármacos , Monoaminoxidase/metabolismo , Oxidantes/toxicidade , Oxirredução/efeitos dos fármacos , Ratos , Ratos Wistar , Substância Negra/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
10.
Toxicol In Vitro ; 26(2): 304-14, 2012 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-22186154

RESUMO

Usnic acid (UA) is the most common and abundant lichenic secondary metabolite with potential therapeutic application. Anti-inflammatory and antitumour properties have already been reported and UA-enriched extracts are widely used to treat several diseases in the folk medicine. First, we performed in silico evaluation of UA interactions with genes/proteins and important compounds for cellular redox balance and NO pathway. Then, we assessed UA redox properties against different reactive species (RS) generated in vitro, and evaluated its action on SH-SY5Y neuronal like cells upon hydrogen peroxide (H(2)O(2)), since no in vitro neurotoxicological data has been reported so far. Total reactive antioxidant potential index (TRAP) showed a significant antioxidant capacity of UA at the highest tested concentration; UA was also effective against hydroxyl radicals and reduced the formation of nitric oxide. In vitro, lipoperoxidation was enhanced by UA and changed the cellular viability at highest concentration of 20µg/mL for 1 and 4h, as well as 2 and 20µg/mL for 24h of treatment, according to MTT reduction assay. Moreover, UA did not display protective effects against H(2)O(2)-induced cell death in any case. Evaluation of intracellular RS production by the DCFH-based assay indicated that UA was able to induce changes in basal RS production at concentration of 20µg/mL for 1h and from 2ng/mL to 20µg/mL for 4 and 24h. In conclusion, UA could display variable redox-active properties, according to different system conditions and/or cellular environment. Moreover, our results suggest that potential neurotoxicological effects of UA should be further studied by additional approaches; for instance, in vivo and clinical studies.


Assuntos
Benzofuranos/toxicidade , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Humanos , Peróxido de Hidrogênio/metabolismo , Radical Hidroxila/metabolismo , Óxido Nítrico/metabolismo , Oxirredução , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
11.
Toxicol In Vitro ; 25(2): 462-8, 2011 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-21111802

RESUMO

Atranorin (ATR) is a lichenic secondary metabolite with potential uses in pharmacology. Antinociceptive and antiinflammatory actions have been reported, and the use of atranorin-enriched lichen extracts in folk medicine is widespread. Nonetheless, very few data on ATR biological actions are available. Here, we evaluated free radical scavenging activities and antioxidant potential of ATR using various in vitro assays for scavenging activity against hydroxyl radicals, hydrogen peroxide, superoxide radicals, and nitric oxide. The total reactive antioxidant potential (TRAP) and total antioxidant reactivity (TAR) indexes and in vitro lipoperoxidation were also evaluated. Besides, we determined the cytoprotective effect of ATR on H(2)O(2)-challenged SH-SY5Y cells by the MTT assay. ATR exerts differential effects towards reactive species production, enhancing hydrogen peroxide and nitric oxide production and acting as a superoxide scavenger; no activity toward hydroxyl radical production/scavenging was observed. Besides, TRAP/TAR analysis indicated that atranorin acts as a general antioxidant, although it demonstrated to enhance peroxyl radical-induced lipoperoxidation in vitro. ATR was not cytotoxic, and also protected SH-SY5Y cells against H(2)O(2)-induced cell viability impairment. Our results suggest that ATR has a relevant redox-active action, acting as a pro-oxidant or antioxidant agent depending on the radical. Also, it will exert cytoprotective effects on cells under oxidative stress induced by H(2)O(2).


Assuntos
Antioxidantes/farmacologia , Citoproteção , Hidroxibenzoatos/farmacologia , Células Cultivadas , Humanos , Peróxido de Hidrogênio/metabolismo , Oxirredução
12.
Reprod Toxicol ; 30(3): 452-6, 2010 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-20679000

RESUMO

Vitamin A is an essential micronutrient that regulates many biological processes through modulation of retinoic acid receptor-responsive genes. Vitamin A acts as a systemic antioxidant, participating in the modulation of diverse redox mechanisms involved in physiological and pathological processes. Different studies, however, observed that vitamin A and other retinoids may induce pro-oxidant/deleterious actions under certain conditions, leading to impairment of brain and lung function. Here, we studied the effect of vitamin A treatment at oral doses of 100 IU/kg, 200 IU/kg, and 300 IU/kg to female rats (Rattus norvegicus) during pregnancy and lactation on oxidative parameters of lungs from the offspring vitamin A supplementation induced increases in lipoperoxidation, protein carbonyl, activities of the antioxidant enzymes superoxide dismutase and catalase (200 IU/kg, and 300 IU/kg), and decreased sulphydryl protein (500 IU/kg) content in the neonatal lung.


Assuntos
Lactação/metabolismo , Pulmão/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Vitamina A/análogos & derivados , Vitaminas/efeitos adversos , Animais , Animais Recém-Nascidos , Antioxidantes/metabolismo , Catalase/metabolismo , Diterpenos , Relação Dose-Resposta a Droga , Feminino , Peroxidação de Lipídeos/efeitos dos fármacos , Pulmão/enzimologia , Pulmão/crescimento & desenvolvimento , Pulmão/metabolismo , Troca Materno-Fetal , Gravidez , Carbonilação Proteica/efeitos dos fármacos , Ratos , Compostos de Sulfidrila/metabolismo , Superóxido Dismutase/metabolismo , Vitamina A/administração & dosagem , Vitamina A/efeitos adversos , Vitamina A/farmacocinética , Vitaminas/administração & dosagem , Vitaminas/farmacocinética
13.
Cell Biochem Funct ; 28(3): 190-6, 2010 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-20232491

RESUMO

Exercise training has been used for treatment/prevention of many cardiovascular diseases, but the mechanisms need to be clarified. Thus, our aim was to compare oxidative stress parameters between rats submitted to a swimming training and sedentary rats (control). Twelve male rats were divided into two groups: control and exercise training. The exercise training had daily 1 h swimming sessions for 8 weeks and a load (5% of its body mass) was placed in rat's tail. Thereafter the animals were killed, aorta and heart were surgically removed and blood was collected. Body mass gain, thiobarbituric acid reactive species (TBARS), carbonyl content, total reactive antioxidant potential (TRAP), total antioxidant reactivity (TAR), superoxide dismutase (SOD) activity and catalase (CAT) activity were evaluated. The trained rats showed a lower body mass gain and no modifications on heart. An increased SOD activity was observed on aorta after the training, but no changes were seen for CAT activity, which led to an increased SOD/CAT ratio. The arterial TBARS was also increased for trained rats. The decrease in TRAP in exercise training was the single modification on plasma. Our findings suggest that the increased SOD activity could play a role in vascular adaptations to exercise training.


Assuntos
Aorta/metabolismo , Miocárdio/metabolismo , Oxirredução , Estresse Oxidativo , Condicionamento Físico Animal/fisiologia , Adolescente , Adulto , Animais , Antioxidantes/metabolismo , Catalase/metabolismo , Criança , Feminino , Humanos , Masculino , Carbonilação Proteica , Ratos , Superóxido Dismutase/metabolismo , Tiobarbitúricos/metabolismo
14.
J Med Food ; 12(6): 1375-80, 2009 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-20041796

RESUMO

Lungs require an adequate supply of vitamin A (retinol) for normal embryonic development, postnatal maturation, and maintenance and repair during adult life. However, recent intervention studies revealed that supplementation with retinoids resulted in higher incidence of lung cancer, although the mechanisms underlying this effect are still unknown. Here, we studied the effect of vitamin A supplementation on oxidative stress parameters in lungs of Wistar rats. Vitamin A supplementation at either therapeutic (1,000 and 2,500 IU/kg) or excessive (4,500 and 9,000 IU/kg) doses for 3, 7, or 28 days induced lipid peroxidation, protein carbonylation, and oxidation of protein thiol groups, as well as change in catalase and superoxide dismutase activity. Together, these results suggest that vitamin A supplementation causes significant changes in redox balance, which are frequently associated with severe lung dysfunction.


Assuntos
Suplementos Nutricionais/efeitos adversos , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Vitamina A/efeitos adversos , Animais , Masculino , Distribuição Aleatória , Ratos , Ratos Wistar , Vitamina A/administração & dosagem
15.
Biol Pharm Bull ; 30(8): 1488-96, 2007 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-17666809

RESUMO

Aqueous and hydro-ethanolic extracts of Bauhinia microstachya leaves (AEBM and HEBM) were investigated for their phenolic content and phytochemical profile (by spectrophotometry and HPLC), and for their antioxidant activities and free radical scavenging potential in different in vitro systems (TRAP, TEAC, TBARS, nitric oxide, superoxide and hydroxyl radical). HEBM presented a 27.4% higher content of phenolics when compared to AEBM and a distinct phytochemical profile was observed. Our work suggests that both extracts have potent antioxidant activities and that their antioxidant capacity and efficiency vary according to the radical-generating system. In general, HEBM was more effective than AEBM in avoiding ROS-generating damage and in scavenging the various radicals formed. Nevertheless, when results were normalized to total phenolic content, a different profile of antioxidant activities and free radical scavenging potential was observed, particularly against oxidative lipid damage and superoxide radical. B. microstachya extracts may be considered an interesting source of natural antioxidants as well as other phenolic-rich plants.


Assuntos
Antioxidantes/metabolismo , Bauhinia/química , Flavonoides/farmacologia , Depuradores de Radicais Livres/farmacologia , Fenóis/farmacologia , Cromanos/farmacologia , Cromatografia Líquida de Alta Pressão , Etanol , Flavonoides/química , Radical Hidroxila/metabolismo , Luminescência , Óxido Nítrico/metabolismo , Fenóis/química , Extratos Vegetais/química , Extratos Vegetais/farmacologia , Folhas de Planta/química , Polifenóis , Solventes , Espectrofotometria Ultravioleta , Superóxidos/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Água , Xantina Oxidase/metabolismo
16.
Life Sci ; 80(1): 43-50, 2006 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-16978664

RESUMO

Mobile telephones and their base stations are an important ultra high frequency-electromagnetic field (UHF-EMF) source and their utilization is increasing all over the world. Epidemiological studies suggested that low energy UHF-EMF emitted from a cellular telephone may cause biological effects, such as DNA damage and changes on oxidative metabolism. An in vivo mammalian cytogenetic test, the micronucleus (MN) assay, was used to investigate the occurrence of chromosomal damage in erythrocytes from rat offspring exposed to a non-thermal UHF-EMF from a cellular phone during their embryogenesis; the irradiated group showed a significant increase in MN occurrence. In order to investigate if UHF-EMF could also alter oxidative parameters in the peripheral blood and in the liver - an important hematopoietic tissue in rat embryos and newborns - we also measured the activity of antioxidant enzymes, quantified total sulfhydryl content, protein carbonyl groups, thiobarbituric acid-reactive species and total non-enzymatic antioxidant defense. No significant differences were found in any oxidative parameter of offspring blood and liver. The average number of pups in each litter has also not been significantly altered. Our results suggest that, under our experimental conditions, UHF-EMF is able to induce a genotoxic response in hematopoietic tissue during the embryogenesis through an unknown mechanism.


Assuntos
Campos Eletromagnéticos , Eritrócitos/efeitos da radiação , Feto/efeitos dos fármacos , Micronúcleos com Defeito Cromossômico/efeitos da radiação , Fosfatase Ácida/análise , Animais , Eritrócitos/metabolismo , Eritrócitos/ultraestrutura , Feminino , Glutationa Peroxidase/metabolismo , Isoenzimas/análise , Tamanho da Ninhada de Vivíparos , Oxirredução , Gravidez , Ratos , Ratos Wistar , Compostos de Sulfidrila/análise , Fosfatase Ácida Resistente a Tartarato
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