Origem do saber popular no cultivo de horto medicinal / ORIGIN OF POPULAR KNOWLEDGE ON THE CULTIVATION OF MEDICINAL GARDEN

objetivo: descrever a origem do saber popular relacionado ao cultivo de hortomedicinal em um município da região Noroeste do Rio Grande do Sul. Método: estudoexploratório, estruturado a partir de uma pesquisa qualitativa. A seleção dos participantes dapesquisa ocorreu por meio da rede de relações. A coleta dos dados aconteceu nos meses deabril e maio de 2014, contou com entrevista semiestruturada e observação participante. Naanálise dos dados, utilizou-se a proposta operativa. Resultados: a origem dos hortosmedicinais está ligada à iniciativa da Empresa de Assistência Técnica e Extensão rural e oconhecimento inerente ao cultivo é proveniente do saber popular. Considerações finais:ressalta-se a importância da inserção de profissionais da saúde nas comunidades em queatuam, considerando as dimensões dos contextos sociais que permeiam as inter-relações,planejando ações de saúde mais resolutivas.

Aim: to describe the origin of popular knowledge in medicinal gardencultivation in a municipality in the Northwestern region of Rio Grande do Sul. Method:exploratory study, structured from a qualitative research. The selection of the researchsubjects occurred through the network of relationships. Data collection took place during themonths of April and May 2014, with semi-structured interview and participant observation. Indata analysis, the operative protocol was used. Results: the origin of the medicinal plantgarden is linked to the initiative of the Technical Assistance Enterprise and Rural Extensionand the inherent knowledge to cultivation comes from popular knowledge. Finalconsiderations: the importance of the insertion of health professionals in the community inwhich they operate is important, considering the dimensions of the social contexts thatpermeate the interrelationships, planning more resolutive health actions.

Objetivo: describir el origen del conocimiento popular relacionado al cultivo dehuerto medicinal en un municipio de la región noroeste del Rio Grande do Sul. Método: estudioexploratorio, estructurado a partir de una investigación cualitativa. La selección de los sujetos dela investigación se produjo por medio de la red de relaciones. La recolección de los datos ocurrióen los meses de abril y mayo de 2014, para tanto se utilizó entrevista semiestructurada yobservación participante. En el análisis de datos se utilizó el protocolo operativo. Resultados: elorigen de los huertos medicinales está relacionado a la iniciativa de la Empresa de AsistenciaTécnica y Extensión rural y el conocimiento inherente al cultivo procede del saber popular.Consideraciones finales: se resalta la importancia de la inserción de profesionales de la salud enla comunidad donde actúan, considerando las dimensiones de los contextos sociales que permeanlas interrelaciones, planificando acciones de salud más resolutivas.

High-fat diet and hydrochlorothiazide increase oxidative stress in brain of rats.

This study evaluated the effect of possible synergic interaction between high fat diet (HF) and hydrochlorothiazide (HCTZ) on biochemical parameters of oxidative stress in brain. Rats were fed for 16 weeks with a control diet or with an HF, both supplemented with different doses of HCTZ (0.4, 1.0, and 4.0 g kg(-1) of diet). HF associated with HCTZ caused a significant increase in lipid peroxidation and blood glucose levels. In addition, HF ingestion was associated with an increase in cerebral lipid peroxidation, vitamin C and non-protein thiol groups (NPSH) levels. There was an increase in vitamin C as well as NPSH levels in HCTZ (1.0 and 4.0 g kg(-1) of diet) and HF plus HCTZ groups. Na(+)-K(+)-ATPase activity of HCTZ (4.0 g kg(-1) of diet) and HCTZ plus HF-fed animals was significantly inhibited. Our data indicate that chronic intake of a high dose of HCTZ (4 g kg(-1) of diet) or HF change biochemical indexes of oxidative stress in rat brain. Furthermore, high-fat diets consumption and HCTZ treatment have interactive effects on brain, showing that a long-term intake of high-fat diets can aggravate the toxicity of HCTZ.

Toxicological evaluation of subchronic exposure to diphenyl diselenide in rats.

The aim of this study was to investigate the effects caused by subchronic exposure to diphenyl diselenide in rats. Adult Wistar rats were exposed to diphenyl diselenide (5-300 micromol kg(-1), subcutaneously) once a day for 14 days. The subchronic administration of diphenyl diselenide at a dose of 300 micromol kg(-1) significantly increased aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in plasma. Conversely, this exposure did not alter lactate dehydrogenase (LDH) activity, urea and creatinine levels in plasma. The activity of delta-aminolevulinate dehydratase (delta-ALA-D) from liver and kidney was inhibited by high dosages of diphenyl diselenide. Diphenyl diselenide did not alter renal Na(+)/K(+)ATPase. A decline in body weight gain was associated with a decrease in food consumption in rats treated with 100 or 300 micromol kg(-1) diphenyl diselenide. At these dosages (100 and 300 micromol kg(-1)), diphenyl diselenide did not cause histological alterations in the liver of rats. Taken together, these results demonstrated that subchronic exposure to diphenyl diselenide at high doses induced minor toxicological effects.

Low toxicity of diphenyl diselenide in rabbits: a long-term study.

Selenium compounds, like diphenyl diselenide (Ph(2)Se(2)), possess glutathione peroxidase (GSHPx)-like activities and other antioxidant properties. The aim of this study was to evaluate the effects of a long-term oral supplementation with Ph(2)Se(2) on various toxicological parameters in rabbits. Adult New Zealand male rabbits were divided into four groups: Group I served as control; Groups II, III and IV received 0.3, 3.0 and 30 p.p.m. of Ph(2)Se(2) pulverized in the chow for 8 months. A number of toxicological parameters were examined in liver, kidney, cerebral cortex and hippocampus, such as delta-aminolaevulinic acid dehydratase (delta-ALA-D), catalase (CAT), GSHPx activities, non-protein thiol (-SH), lipid peroxidation and ascorbic acid levels. The results indicated that supplementation 30 p.p.m. Ph(2)Se(2 )significantly increased delta-ALA-D activity in liver and in cerebral cortex. Non-protein -SH levels were significantly increased in liver but not in kidney, cerebral cortex and hippocampus of rabbits. Ascorbic acid content was significantly lower in the liver and cerebral cortex after supplementation with 30 p.p.m. Ph(2)Se(2). Conversely, no alterations in GSHPx and CAT activities, nor in thiobarbituric acid reactive substances levels were observed in rabbit tissues. These results indicate that oral supplementation with Ph(2)Se(2) is relatively secure in rabbits after 8 months of exposure. The findings encourage further experiments on the potential therapeutic effects of such compound.

Effects of diphenyl-diselenide on orofacial dyskinesia model in rats.

Recently, we have described the beneficial effects of Diphenyl diselenide, an organochalcogen with glutathione peroxidase-like activity, on reserpine-induced orofacial dyskinesia in old rats. In this study, our aim was to examine the effects of diselenide on haloperidol-induced orofacial dyskinesia in rats. Male wistar rats received one single dose of Haloperidol decanoate (57 mg/kg/im) or control. After this dose, the animals received daily administration of diphenyl diselenide (1, 5 or 10 mg/kg/sc) or control, during 28 days. Twenty-four hours after the last diselenide or control solution injection, all the rats were observed for quantification of oral dyskinesia through the frequency of vacuous chewing movements (VCM) and tongue protrusion (TP) and the duration of facial twitching (FT). Haloperidol caused a significant increase in VCM, TP and FT observed in the 4 weekly evaluations (p<0.05). The co-administration of diselenide (5 mg/kg) reversed this effect for all the parameters in four behavioral sessions. The results of the present study demonstrate the possible protective activity of diphenyl diselenide on haloperidol-induced orofacial diskinesia. This effect is in accordance to the involvement of neurotoxicity in orofacial dyskinesia and suggest that studies be continued with new antioxidant compounds.

Changes in biochemical parameters in rabbits blood after oral exposure to diphenyl diselenide for long periods.

The concept that selenium-containing molecules may be better antioxidants than classical antioxidants, has led to the design of synthetic organoselenium compounds. The present study was conducted to evaluate the potential toxicity of long time oral exposure to diphenyl diselenide (PhSe)2 in rabbits. Male adult New Zealand rabbits were divided into four groups, group I served as control; groups II, III and IV received 0.3, 3.0 and 30 ppm of (PhSe)2 pulverized in the chow for 8 months. A number of parameters were examined in blood as indicators of toxicity, including delta-aminolevulinate dehydratase (delta-ALA-D), catalase, glutathione peroxidase (GPx), alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, creatinine, TBARS, non-protein-SH, ascorbic acid and selenium. The results demonstrated that 6 and 8 months of 30 ppm (PhSe)2 intake caused a significant increase in blood delta-ALA-D activity. Erythrocyte non-protein thiol levels were significantly increased after 2 months of 30 ppm (PhSe)2 intake and then return to control levels after prolonged periods of intake. Ingestion of 3.0 ppm of (PhSe)2 for 8 months significantly increased catalase activity in erythrocytes. Conversely, no alterations in GPx, ALT, AST, TBARS and selenium levels were observed in rabbit serum, conversely, selenium levels in peri-renal adipose tissue were significantly increased after 8 months of 30 ppm (PhSe)2 intake, indicating its great lipophylicity. The present results suggest that diphenyl diselenide was not hepato- or renotoxic for rabbits, but caused some biochemical alterations that can be related to some pro-oxidant activity of the compound (particularly the reduction in Vitamin C).

Ethanol inhibits δ-aminolevulinate dehydratase and glutathione peroxidase activities in mice liver: Protective effects of ebselen and N-acetylcysteine.

Changes in sulfhydryl status have been shown to be involved with the ethanol-induced hepatotoxicity. In addition, evidence shows the importance of replenishing thiols in patients with alcoholic liver disease. This study was undertaken to examine the possible beneficial effects of the individual and simultaneous treatments with two antioxidant drugs (N-acetylcysteine and ebselen) against ethanol-induced changes in thiol status, as well as on the activities of δ-aminolevulinate dehydratase (δ-ALA-D) and glutathione peroxidase (GPx) in mice liver. Daily ethanol administrations (3g ethanol/kg, by gavage) decreased liver nonprotein thiols (NPSH) concentration after 30 days of treatment and N-acetylcysteine (300mg/kg once a day, i.p.) or ebselen (5mg/kg once a day, subcutaneously) treatment restored this variable to control levels. However, additive beneficial effects concerning NPSH levels were not observed after the simultaneous administration with both drugs. While liver GPx and δ-ALA-D activities were inhibited by ethanol exposure and these inhibitions were significantly blunted by N-acetylcysteine or ebselen treatment, the simultaneous administration with both drugs did not show additive beneficial effects in relation to the enzymes' activities. NPSH levels were positively correlated with GPx and δ-ALA-D activities. The results presented herein show that ebselen and N-acetylcysteine alone are able to restore ethanol-induced thiols as well as the inhibition of hepatic enzymes whose catalytic functions depend on their thiol (δ-ALA-D) and selenol (GPx) groups.

Ebselen and diphenyl diselenide do not change the inhibitory effect of lead acetate on delta-aminolevulinate dehidratase.

It is known that lead is toxic to several species of animals, and growing data support the participation of oxidative in lead toxicity. Selenium compounds, like diphenyl diselenide and Ebselen have a thiol-peroxidase like and other antioxidant properties. In this work, we determine whether these non-thiol-containing compounds with antioxidant properties could reverse the toxicity produced by Pb(2+). Lead acetate injection followed by injection with Ebselen or diphenyl diselenide did not change the levels of non-protein thiol groups (NPSH), whereas simultaneous treatment with lead plus Ebselen reduced NPSH levels in liver. Lead and Ebselen caused a marked reduction in TBARS level in kidney, whereas lead or selenium compounds did not change TBARS levels in brain or liver. Lead acetate inhibited, δ-aminolevulinate dehydratase (ALA-D) activity in blood, liver, kidney and brain. Selenium compounds did not change enzyme activity nor the inhibitory effect of lead acetate in kidney and liver. Ebselen reversed brain ALA-D inhibition caused by Pb(2+). Reactivation index for ALA-D by DTT was higher in lead-treated groups than control groups in all tissues. Lead acetate or selenium compounds did not demonstrate alteration on [(3)H]-glutamate uptake by synaptosomes, whereas lead acetate plus Ebselen showed an increase on [(3)H]-glutamate uptake. The results of the present study indicate that ALA-D inhibition antecedes the overproduction of reactive oxygen species, which is becoming well documented in the literature.

Effects of mercury and selenite on delta-aminolevulinate dehydratase activity and on selected oxidative stress parameters in rats.

The present study evaluates the effects of Na(2)SeO(3) and HgCl(2) on kidney and liver of adult rats. In vivo, HgCl(2) (17 micromol/kg, sc) reduced ascorbic acid levels in liver ( approximately 15%), whereas in kidney it reduced ALA-D activity ( approximately 60%) and ascorbic acid levels ( approximately 35%) and increased TBARS content ( approximately 50%). Na(2)SeO(3) (17 micromol/kg, sc) exposure increased the content of nonprotein thiol groups in liver (35-60%) and kidney ( approximately 50-160%), partially prevented mercury-induced ALA-D inhibition in kidney, and completely prevented a mercury-induced increase of TBARS content and decrease of ascorbic acid levels in kidney. In vitro, HgCl(2) and Na(2)SeO(3) inhibited renal and hepatic ALA-D, while HgCl(2) increased TBARS in renal and hepatic tissue preparations. Na(2)SeO(3) increased the rate of glutathione oxidation in vitro. Results indicated that Na(2)SeO(3) protected against HgCl(2) effects in vivo (prevention of mercury interaction with thiol groups and of mercury-induced oxidative damage). In vitro, Na(2)SeO(3) did not prevent mercury effects, but potentiated ALA-D inhibition by mercury, probably due to its ability to oxidize thiol groups.