One-time ozone treatment improves the postharvest quality and antioxidant activity of Actinidia arguta fruit.

The major aim of this study was to check the effect of one-time ozonation on selected quality parameters and antioxidant status of Actinidia arguta fruit. For this purpose, A. arguta fruit was ozonated with gas at a concentration of 10 and 100 ppm, which was carried out successively for 5, 15 and 30 min. Next, the selected quality attributes, antioxidants level as well as NADPH and mitochondrial energy metabolism in mini-kiwi fruit after ozonation were analysed. Our research has shown that ozonation reduced the level of yeast and mould without affecting the content of soluble solids or acidity. In turn, ozonation clearly influenced the antioxidant activity and the redox status of the fruit. The ozonated fruit was characterised by a lower level of ROS due to the higher level of low molecular weight antioxidants, as well as the higher activity of superoxide dismutase and catalase. In addition, improved quality and antioxidant activity of the fruit were indirectly due to improved energy metabolism and NADPH level. The ozonated fruit showed a higher level of ATP, due to both higher activity of succinate dehydrogenase and higher availability of NADH. Moreover, the increased level of NAD+ and the activity of NAD+ kinase and glucose-6-phosphate dehydrogenase contributed to higher levels of NADPH in the fruit.

Antioxidant Action of an Aqueous Extract of Royal Sun Medicinal Mushroom, Agaricus brasiliensis (Agaricomycetes), in Rats with Adjuvant-Induced Arthritis.

The purpose of this study was to evaluate possible effects of the administration of an aqueous Agaricus brasiliensis extract on the oxidative state of the liver, brain, and plasma in adjuvant-induced arthritic rats, a model for human rheumatoid arthritis. Daily doses of 400 mg · kg-1 were administered by gavage for 23 days. This treatment produced significant diminutions in protein carbonylation and lipid damage in the liver, brain, and plasma. It also diminished the tissue reactive oxygen species and increased the antioxidant capacity of the plasma. Antioxidant defenses, which are diminished by arthritis, were improved by treatment with the A. brasiliensis extract, as revealed by preservation of the reduced glutathione and protein thiol levels and by the tendency of the activities of some antioxidant enzymes to normalize. The increased glucose-6-phosphate dehydrogenase activity was also almost normalized by the treatment. In addition, there were indications that A. brasiliensis can inhibit the initiation of structural events that can lead to hepatocyte necrosis. In conclusion, A. brasiliensis aqueous preparations can, in principle, be visualized as potential auxiliaries in the treatment of patients with rheumatoid arthritis as a result of their capacity to reduce oxidative stress. This effect was exerted in multiple organs, as can be judged from the results obtained in the liver, brain, and plasma. The continuous ingestion of A. brasiliensis as specific preparations or as a food supplement can possibly help to attenuate the systemic effects of rheumatoid arthritis and improve the quality of life of patients affected by this disease.

Triagem neonatal para deficiência de enzima desidrogenase de glicose hepática (glicose-6- fosfato desidrogenase, G-6-PD) / Neonatal screening for enzyme deficiency hepatic glucose dehydrogenase (glucose-6- phosphate dehydrogenase, G-6-PD)

CONTEXTO: Proposta de incorporação do teste de G-6-PD no material colhido para o teste do pezinho do Programa Nacional de Triagem Neonatal (PNTN). Entretanto, atualmente, não há um consenso universal sobre o rastreamento neonatal de G-6-PD, fundamentalmente por causa das incertezas sobre a razão entre seus riscos e benefícios. TECNOLOGIA: Rastreamento diagnóstico de glicose-6-fosfato desidrogenase (G-6-PD) em recém-nascidos, no Programa Nacional de Triagem Neonatal (PNTN). PERGUNTAS: Qual é a história natural, características clínicas, incidência, morbimortalidade, qualidade de vida e tratamento disponível para a deficiência de G-6-PD? O teste de rastreamento é seguro, efetivo e eficiente o suficiente para modificar as condutas e os desfechos imediatos e em longo prazo nos pacientes diagnosticados? Caso afirmativo, a que custo para o Sistema Único de Saúde do Brasil? MÉTODOS: Realizaram-se duas buscas sistemáticas nas principais bases de dados eletrônicas (PubMed, Embase, Cochrane, etc.) para recuperar informações relevantes sobre a doença e testes de triagem para apoiar a tomada de decisões no Brasil. EVIDÊNCIAS CIENTÍFICAS: Foram identificados 63 estudos originais: 26 abrangendo aspectos da doença e 37 sobre triagem. Todos os estudos foram de coortes retro- ou prospectivas nos quais se relatam taxas de detecção da deficiência de G-6-PD com testes diversos sem relato das condutas subsequentes ou das consequências para a saúde da população. Houve 12 estudos realizados com recém-nascidos no Brasil demonstrando uma prevalência que variou nas regiões, desde 1% no Sul até 9% na Amazônia, com diversos tipos de coleta e testes, taxas variadas de falsos positivos e sem acompanhamento dos pacientes ou relatos de desfechos. Nos estudos internacionais também não se relatou acompanhamento dos pacientes ou relatos de desfechos. Não há estudos de qualidade de vida dos pacientes. Não existem estudos comparativos adequados que permitam determinar a acurácia do teste para a deficiência de G-6-PD no PNTN, em comparação a não triagem ou a outras medidas de prevenção para mortalidade precoce (protocolos de alerta, programa de educação e triagem oportunista). AVALIAÇÃO ECONÔMICA: A avaliação econômica não foi realizada. {A inclusão de exames no programa de triagem de recém-nascidos masculinos no Líbano (com 1% de prevalência) foi considerada eficiente. DISCUSSÃO: A efetividade clínica comparativa em relação a não rastrear ou à implementação de outros programas é desconhecida. Em resumo, a evidência existente continua a ser insuficiente para estabelecer a adequação do rastreamento de recém-nascidos para a deficiência de G-6-PD, embora benefícios para a saúde possam ser esperados se o diagnóstico e o tratamento precoce da hiperbilirrubinemia (< 3 dias entre 1 a 7dias) forem alcançados. Para que o rastreamento neonatal seja implementado no Brasil, seria importante que um programa piloto fosse implementado a priori para avaliar a taxa de falsos positivos de maneira representativa, adequar a linha de cuidados e garantir que o diagnóstico precoce não seja retardado. A OMS considera importante a colaboração no campo dos programas para TN, de modo a unificar critérios, recomendações e avaliações de desempenho dos testes e dos processos assistenciais correlatos. RECOMENDAÇÃO INICIAL DA CONITEC: Os membros da CONITEC presentes no plenário em sua 66ª reunião ordinária no dia 10 de maio de 2018 emitiram recomendação inicial desfavorável à incorporação do teste de detecção da enzima G-6-PD para identificação de deficiência dessa enzima em neonatos no Programa Nacional de Triagem Neonatal do SUS ("teste do pezinho"). Essa matéria será enviada para consulta pública com recomendação inicial de não incorporação desse teste ao SUS. CONSULTA PÚBLICA: A consulta pública n° 30/2018 foi realizada entre os dias 25/05/2018 e 13/06/2018. Foram recebidas ao total 14 contribuições. Dentre as contribuições enviadas, 61% (n= 17) se referiram a contribuições de profissionais de saúde, 21% (n= 6) representações de pacientes (paciente, familiar, amigo ou cuidador de paciente) e 18% (n= 5) de outros interessados no tema. Entre as 05 contribuições (18%) com concordância total foi citado que: (i) apesar de considerar urgente a ampliação da triagem neonatal, há outras doenças que são mais indicadas antes da deficiência de G6PD como as aminoacidopatias e os defeitos de beta-oxidação; (ii) depoimento do programa de 6 anos de triagem neonatal expandido com G6PD por força de Lei, no Distrito Federal, que apesar das melhorias, usa muitos recursos e não faz diferença na clínica. Dentre as 18 contribuições (64%) que discordaram totalmente da recomendação preliminar da CONITEC, houve 5 (18%) que não apresentaram sugestões adicionais, 4 (14%) que apresentaram comentários referente a outras tecnologias diversas e outras 9 (32%) apresentaram comentários substantivos, 2 inclusive com sugestões adicionais. Nas 2 destas que contribuíram com 2 publicações anexadas, analisou-se que já haviam sido consideradas no texto desse Relatório Técnico. RECOMENDAÇÃO FINAL DA CONITEC: No dia 02 de agosto de 2018 durante a 69ª reunião ordinária da Comissão, após realizada a avaliação das sugestões, os membros do Plenário da CONITEC presentes deliberaram por unanimidade recomendar a não incorporação da detecção da deficiência de glicose-6-fostato desidrogenase em papel-filtro no teste do pezinho para deficiência de glicose-6-fosfato desidrogenase. Foi assinado o registro de deliberação nº 362/2018. DECISÃO: Não incorporar o procedimento de detecção da deficiência de glicose-6-fosfato desidrogenase em papel-filtro no teste do pezinho para deficiência de glicose-6-fosfato desidrogenase, no âmbito do Sistema Único de Saúde ­ SUS. Dada pela Portaria nº 44 de 31 de outubro de 2018, publicada no Diário Oficial da União nº 210, de 31 de outubro de 2018, seção 1, página 40.

Antidiabetic activity of alcoholic stem extract of Gymnema montanum in streptozotocin-induced diabetic rats.

In the present study, the effect of alcoholic stem extract of Gymnema montanum (GMSt) on blood glucose, plasma insulin, and carbohydrate metabolic enzymes were studied in experimental diabetes. Diabetes mellitus was induced by a single intraperitoneal injection of STZ (60 mg/kg bw). Five days after STZ induction, diabetic rats received GMSt orally at the doses of 25, 50, 100 and 200mg/kg daily for 3 weeks. Graded doses of stem extract showed a significant reduction in blood glucose levels and improvement in plasma insulin levels. The effect was more pronounced in 100 and 200mg/kg than 50mg/kg. GMSt showed significant increase in hexokinase, Glucose-6-phosphate dehydrogenase and glycogen content in liver of diabetic rats while there was significant reduction in the levels of glucose-6-phosphatase and fructose-1,6-bisphosphatase. The present study clearly indicated significant antidiabetic effect with the stem extract of G. montanum and lends support for its traditional usage.

The efficiacy of bismuth subnitrate against genotoxicity and oxidative stress induced by aluminum sulphate.

Aluminum (Al) is commonly used in industrial processes and drugs and is thought to induce erythrocytes damage via activation of oxidative stress. Recently, bismuth (Bi)-containing drugs are used in the treatment of various diseases. However, uncertain effects of Bi in blood tissue may participate in the therapeutic efficacy of Bi compounds as related to metals. Hence, this study aimed to determine the roles on human blood cells of the various concentrations of aluminum sulphate (Al(2)(SO(4))(3)) and bismuth subnitrate (BSN), separate and together. With this aim, oxidative status was assessed on erythrocytes by measuring following oxidative stress markers: reduced glutathione (GSH), superoxide dismutase (SOD), glucose-6-phosphate dehydrogenase (G-6-PDH) and catalase (CAT). Two chemicals were tested for their ability to induce cytogenetic change in human lymphocytes using assays for chromosome aberrations (CAs) and sister chromatid exchanges (SCEs). Our results showed that high dose of Al(2)(SO(4))(3) (20 µg/mL) caused oxidative stress and increased CA and SCE frequencies. Whereas, BSN doses did not change CA and SCE rates. Moreover, it led to changes of antioxidant capacity at different concentrations. After concomitant treatment with Al(2)(SO(4))(3) and BSN, the effects of BSN doses were different on enzyme activities and decreased the genotoxic damage. However, the high dose of BSN and Al(2)(SO(4))(3) was shown to enhance the frequencies of CAs and SCEs in a synergistic manner. In conclusion, BSN could be effective in the protection against the blood toxicity of Al(2)(SO(4))(3).

Effect of dietary ascorbate on lipogenesis and lipolysis activities in black sea bream, Acanthopagrus schlegelii.

To assess the effect of dietary ascorbate on lipid metabolism, 1-year black sea bream (Acanthopagrus schlegelii) were reared on a casein-based purified diet and an ascorbate fortified diet (1,100 mg of L: -ascorbyl-2- monophosphate-Mg/kg diet). The fortified ascorbate was effectively incorporated into the fish body and elevated muscle carnitine content. Fortifications of dietary ascorbate depressed activities of glucose-6-phosphate dehydrogenase and NADP-isocitrate dehydrogenase as lipogenic enzymes in the hepatopancreas and intraperitoneal fat body. Starvation after feeding experiment activated carnitine palmitoyltransferase as a lipolysis enzyme in the hepatopancreas in both control and vitamin C(VC) groups, while the lipolysis activity was significantly higher in VC group. These results confirmed that dietary ascorbate depressed lipogenesis and activated lipolysis, i.e., influenced the lipid metabolism of black sea bream.

Beneficiary effect of Tinospora cordifolia against high-fructose diet induced abnormalities in carbohydrate and lipid metabolism in Wistar rats.

High intake of dietary fructose has been shown to exert a number of adverse metabolic eff ects in humans and experimental animals. The present study was designed to investigate the eff ect of the aqueous extract of Tinospora cordifolia stem (TCAE) on the adverse eff ects of fructose loading toward carbohydrate and lipid metabolism in rats. Adult male Wistar rats of body weight around 200 g were divided into four groups, two of which were fed with starch diet and the other two with high fructose (66 %) diet. Plant extract of TC (400 mg/kg/day) was administered orally to each group of the starch fed rats and the highfructose fed rats. At the end of 60 days of experimental period, biochemical parameters related to carbohydrate and lipid metabolism were assayed. Hyperglycemia, hyperinsulinemia, hypertriglyceridemia, insulin resistance, and elevated levels of hepatic total lipids, cholesterol, triglycerides, and free fatty acids (p < 0.05) observed in fructose-fed rats were completely prevented with TCAE treatment. Alterations in the activities of enzymes of glucose metabolism (hexokinase, phosphofructokinase, pyruvate kinase, glucose-6-phosphatase, fructose-1,6-bisphosphatase, and glucose-6-phosphate dehydrogenase) and lipid metabolism (fatty acid synthetase, lipoprotein lipase, and malic enzyme) as observed in the high fructose-fed rats were prevented with TCAE administration. In conclusion, our fi ndings indicate improvement of glucose and lipid metabolism in high-fructose fed rats by treatment with Tinospora cordifolia, and suggest that the plant can be used as an adjuvant for the prevention and/or management of insulin resistance and disorders related to it.

Massive acute haemolysis and severe neonatal hyperbilirubinemia in glucose-6-phosphate dehydrogenase-deficient preterm triplets.

Premature triplets (2 boys and 1 girl) were delivered at 34 weeks, with both boys identified as Glucose-6-phosphate dehydrogenase (G6PD) deficient. Despite having similar quantitative levels of G6PD in their cord blood, only one boy had severe hyperbilirubinemia and anaemia caused by acute haemolysis requiring exchange transfusion. G6PD-deficient infants with the similar genetic, demographic, maternal, clinical factors and G6PD quantification levels can have different severity of presentation of neonatal jaundice in similar environmental set up. This supports the massive acute haemolysis can occur in infant with G6PD deficiency in the absence of any obvious blood group incompatibilities, infection, or ingestion of oxidising agents known to trigger haemolysis.

Effect of Semecarpus anacardium Linn. nut milk extract on glutathione and its associated enzymes in experimentally induced mammary carcinoma.

Reduced glutathione (GSH) is a ubiquitous thiol-containing tripeptide that plays a key role in the etiology of many diseases and, in particular, cancer. GSH, the foremost internal protective system, participates directly in the destruction of free radical compounds and detoxification of carcinogens. The effect of Semecarpus anacardium nut milk extract was studied for gaining insight into the disease relationship to GSH and its metabolizing enzymes. Mammary carcinoma was induced by giving 7,12-dimethylbenz[a]anthracene (DMBA) (25 mg/mL of olive oil) perorally by gastric intubation, and nut milk extract of S. anacardium was administered orally (200 mg/kg of body weight/day) for 14 days to mammary carcinoma-bearing rats. The levels of GSH and its metabolizing enzyme activities were determined in liver and kidney homogenates. Significant decreases in GSH, glutathione peroxidase, glutathione S-transferase, glutathione reductase, and gamma-glutamylcysteine synthetase and a concomitant increase in oxidized glutathione, gamma-glutamyl transpeptidase, and glucose 6-phosphate dehydrogenase were observed in DMBA-induced mammary carcinoma in rats, while drug treatment reversed the conditions to near normal levels. There was a marked increase in GSH level and gamma-glutamylcysteine synthetase activity in drug control rats. These findings suggest that S. anacardium can exert its protective effect in maintaining the glutathione redox status by restoring the associated enzymes against oxidative stress in experimental mammary carcinoma.

Attenuation of cerebral oxygen toxicity by sound conditioning.

HYPOTHESIS: Sound conditioning might reduce cerebral oxygen toxicity. BACKGROUND: Cerebral oxygen toxicity is related to high levels of reactive oxygen species. Noise-induced hearing loss has been shown to result from ischemia-reperfusion, in which reactive oxygen species play a major role. Repeated exposure to loud noise at levels below that which produces permanent threshold shift prevented noise-induced hearing loss and was associated with significant elevation of the antioxidant enzymes measured in the inner ear. We tested the hypothesis that sound conditioning might reduce cerebral oxygen toxicity. METHODS: Forty-five guinea pigs were prepared for electroencephalography and auditory brainstem recording. The auditory brainstem recording detection threshold was determined to confirm baseline normal hearing. The animals were divided into three equal groups and subjected to the following procedures: Group 1, electroencephalography electrode implantation and auditory brainstem recording only; Group 2, exposure to oxygen at 608 kPa (the latency to the first electrical discharge in the electroencephalogram preceding the appearance of seizures was measured); and Group 3, sound conditioning followed by oxygen exposure. The animals were killed, and the brains were excised and homogenized. Brain levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase, glutathione reductase, glucose-6-phosphate dehydrogenase, and thiobarbituric acid reactive substances were compared among the groups. RESULTS: Latency to the first electrical discharge was compared between Groups 2 and 3, and was found to be significantly longer in Group 3 (27.9 +/- 11 versus 20.4 +/- 7.6 min, p < 0.03). No significant changes were found in brain levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase, glutathione reductase, glucose-6-phosphate dehydrogenase, or thiobarbituric acid reactive substances. CONCLUSION: Our data show that sound conditioning prolongs the latency to oxygen-induced convulsions. This effect was not accompanied by significant changes in whole-brain antioxidant enzyme activity or the magnitude of lipid peroxidation.

Oral Candida albicans and Candida dubliniensis differentiation by multilocus enzyme electrophoresis and sodium dodecylsulphate-polyacrylamide gel electrophoresis.

Five oral strains of Candida albicans and five C. dubliniensis, as well as their respective type-strains, were analyzed by multilocus enzyme electrophoresis (MLEE) and sodium dodecyl-sulfate polyacrylamide gel electrophoresis (SDS-PAGE). After electrophoreses and numerical analyses, we obtained two distinct species-specific taxa, which may justify the use of MLEE and SDS-PAGE as reliable methods for differentiation and complementary identification of C. dubliniensis.

Protective effects of Panax ginseng on muscle injury and inflammation after eccentric exercise.

Eccentric muscle contraction causes fibre injury associated with disruption of the myofibrillar cytoskeleton. The medicinal plant Panax ginseng C.A. Meyer, known for its therapeutic properties, was studied to explore its protective effects after eccentric contraction. A crude extract and a standardised extract (G115) of different saponin compositions were tested as to their efficacy in reducing lipid peroxidation, inflammation and release of myocellular proteins after the realisation of an eccentric contraction protocol on a rat treadmill. Plasma creatine kinase (CK) levels were significantly reduced by approximately 25% after ingestion of both extracts of ginseng. Both extracts reduced lipid peroxidation by approximately 15% as measured by malondialdehyde levels. beta-Glucuronidase concentrations and glucose-6-phosphate dehydrogenase (G6PDH) levels, which can be considered markers of inflammation, were also significantly reduced. The values of beta-glucuronidase were increased from 35.9+/-1.5 to 128.4+/-8.1 in vastus and to 131.1+/-12.1 U x g(-1) in rectus, the protection due to ginseng administration being approximately 40% in both muscles. Both extracts appeared to be equally effective in reducing injuries and inflammation caused by eccentric muscle contractions.

Neonatal jaundice in very low birth weight babies.

Very low birth weight (VLBW) neonates born between January 1995 to December 1998, who survived for > 2 days, were studied for the incidence, causes and interventions required for neonatal jaundice. Significant neonatal jaundice was defined as the total serum bilirubin (TSB) level beyond which baby required intervention (phototherapy and/or exchange transfusion) for neonatal jaundice. The incidence of significant neonatal jaundice (NNJ) was 76.6% and 37.3% required exchange transfusion. It was 82.9% at gestational age < or = 28 weeks reduced whereas to 56.9% at gestational age of 35-36 weeks. The incidence was 75.3%, 78.5% and 76.7% in the birth weight group of 750-799 grams, 1000-1249 grams and 1250-1499 grams respectively. Glucose 6 phosphatase dehydrogenase (G-6-PD) deficiency (12.1%) was the commonest cause of jaundice. There is a need for evaluation of prophylactic therapies that enhances liver function or decreases production of bilirubin, which would prevent the rise of TSB to dangerous levels and thus would decrease the need for exchange transfusions.

Effect of dietary chitosans with different viscosity on plasma lipids and lipid peroxidation in rats fed on a diet enriched with cholesterol.

To investigate the effect of dietary chitosan on lipid metabolism, male SD (Sprague-Dawley) rats were fed a cholesterol-enriched diet containing 5% cellulose (CE), 5% chitosan (CCS; high viscosity), or 5% chitosan (FCS; low viscosity) for 4 weeks. The two types of chitosan with a comparable degree of deacetylation had a different molecular weight and intrinsic viscosity. Significantly (p < 0.05) lower plasma total cholesterol, LDL-cholesterol and VLDL-cholesterol concentrations were observed in the rats fed on the chitosan diets. In addition, chitosan significantly increased the fecal cholesterol and triglyceride contents. Although no significant difference in body weight was found among the dietary groups, the rats fed on the chitosan diets had lower relative liver weight when compared with those fed on the cellulose diet. Both of the chitosan groups had significantly lower liver total lipid and total cholesterol contents compared to the cellulose group, although the FCS group was less effective. The plasma and liver thiobarbituric acid reactive substances (TBAR) values were similar in the CE and FCS groups, while the CCS group had increased liver TBAR values. Although a significant increase in liver glucose-6-phosphate dehydrogenase activity was observed in the CCS group, no significant change was found in the FCS group. The observed influence of chitosans with different viscosity on the plasma lipid level, liver lipids and lipid peroxidation suggests that, while the hypocholesterolemic action of chitosans with different viscosity was similar, changes in the liver lipids and liver peroxidation status depended on their molecular weight when the deacetylation degree was comparable.

Oxidative stress and antioxidant status in mouse liver: effects of dietary lipid, vitamin E and iron.

The purpose of this study was to determine the effects of dietary fat, vitamin E and iron on oxidative damage and antioxidant status. Male Swiss-Webster mice (1 mo old) were fed a basal vitamin E-deficient diet that contained either 8% fish oil + 2% corn oil or 10% lard with or without 1 g dl-alpha-tocopheryl acetate. The diets without vitamin E contained either 0.21 or 0.95 g ferric citrate/kg. Diets were fed for 4 wk/kg diet. Compared with the vitamin E-supplemented groups, mice fed diets without vitamin E (with or without supplemental iron) had significantly (P < 0.05) higher hepatic levels of thiobarbituric acid-reactive substances (TBARS), conjugated dienes and protein carbonyls when they were fed fish oil, but not lard. The levels of TBARS were further increased by iron supplementation in the mice fed fish oil. Significantly lower concentrations of alpha-tocopherol and higher glutathione (GSH) were found in the liver of mice fed fish oil and vitamin E than in those fed lard and vitamin E (P < 0.05). The activities of superoxide dismutase and glucose-6-phosphate dehydrogenase were lower in the fish oil-fed mice than in those fed lard (P < 0.05). The activities of Se-GSH peroxidase, non-Se-GSH peroxidase, catalase, and glutathione reductase were not altered by dietary fat or vitamin E/iron. The results obtained provide experimental evidence of the prooxidative effects of high dietary fish oil and iron, and suggest that vitamin E protects not only lipid-soluble compounds, but also water-soluble constituents, against oxidative damage. Further, dietary lipid plays a key role in determining cellular susceptibility to oxidative stress.

Role of iron and iron chelation therapy in oxygen free radical mediated tissue injury in an ascending mouse model of chronic pyelonephritis.

The contribution of iron towards the free radical generation leading to renal tissue damage was assessed using a non-obstructive ascending mouse model for chronic pyelonephritis. The parameters studied include luminol dependent chemiluminescence (LDCL), histopathology and some biochemical investigations. We found that iron enhanced the renal tissue damage and led to renal scarring, and end point in chronic renal inflammation, irrespective of the bacterial strain studied. In addition a role of iron chelation therapy as a treatment for chronic renal inflammation is also suggested.

Nickel deficiency alters liver lipid metabolism in rats.

The present investigation was designed to examine the effect of nickel deficiency on lipid metabolism in liver and serum lipoproteins of rats. Therefore, a study over two generations was conducted feeding a nickel-deficient diet containing 13 microg/kg nickel or a nickel-adequate diet supplemented with 1 mg/kg nickel. Male 7-wk-old pups from the second offspring were studied. Pups fed a diet poor in nickel tended to have lower weight gains (P < 0.15), nickel concentrations in liver (P < or = 0.1) and iron levels in serum (P < 0.1) than nickel-adequate rats. They were classified as nickel-deficient on the basis of significantly lower erythrocyte counts, hemoglobin concentrations, hematocrits and nickel concentrations in kidney compared with nickel-adequate rats. Nickel deficiency caused a significant triacylglycerol accumulation in liver, with greater concentrations of saturated fatty acids, monounsaturated fatty acids, and polyunsaturated fatty acids than nickel-adequate rats. Nickel deficiency had slight but significant effects on the fatty acid composition of liver total lipids and phosphatidylcholine and phosphatidylethanolamine. Moreover, nickel-deficient rats had significantly lower activities of the lipogenic enzymes glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malic enzyme and fatty acid synthase than nickel-adequate rats. Nickel-depleted pups had significantly higher concentrations of triacylglycerols and phospholipids in serum VLDL, and cholesterol in serum LDL than nickel-adequate pups. Most of these alterations in lipid metabolism are similar to those obtained in several iron-deficiency studies. Because nickel deficiency also slightly compromised iron status, it is possible that at least some of the observed alterations are due to the moderate iron deficiency.

Effect of moderate levels of dietary fish oil on insulin secretion and sensitivity, and pancreas insulin content in normal rats.

The effect of omega-3 fatty acids derived from fish and marine mammals on subjects with normal glucose tolerance is still unclear. The aim of the present study was to test whether the hypolipidemia that follows the chronic administration of cod liver oil, rich in polyunsaturated fatty acids (omega-3), to normal rats is accompanied by changes in glucose metabolism, insulin secretion and sensitivity, and pancreatic insulin content. To achieve this goal, male Wistar rats were fed with a semisynthetic diet (w/w): 62.5% cornstarch, 7% cod liver oil plus 1% corn oil, and 17% protein (CD + CLO). Control rats were fed with the same semisynthetic diet with the only exception that the source of fat was 8% (w/w) corn oil (CD). Both diets were administered ad libitum for 1 month. At the end of the experimental period, the results obtained were as follows (mean +/- SEM): serum triacylglycerol (mM): CD + CLO 0.21 +/- 0.04 vs. CD 0.58 +/- 0.05 (p < 0.05); free fatty acids (microM): CD + CLO 257 +/- 20 vs. CD 288 +/- 22 (p = NS); total cholesterol (mM): CD + CLO 1.13 +/- 0.09 vs. CD 1.82 +/- 0.06 (p < 0.05); high-density lipoprotein cholesterol (mM): CD + CLO 0.58 +/- 0.08 vs. CD 1.07 +/- 0.04 (p < 0.05); plasma glucose (mM): CD + CLO 6.30 +/- 0.29 vs. CD 6.28 +/- 0.10 (p = NS); liver triacylglycerol (mumol/liver): CD + CLO 104.1 +/- 11.4 vs. CD 136.8 +/- 4.3 (p < 0.05); glycogen (mumol/g wet weight): CD + CLO 298.3 +/- 21.0 vs. CD 297.0 +/- 19.0 (p = NS); glucose-6-phosphate dehydrogenase (U/liver): CD + CLO 37.9 +/- 2.2 vs. CD 58.8 +/- 5.0 (p < 0.05); triacylglycerol secretion (nmol/min/100 g body weight): CD + CLO 101.0 +/- 2.0 vs. CD 166.0 +/- 9.7 (p < 0.01); removal of fat emulsion (K2% min-1): CD + CLO 15.0 x 10(-2) +/- 0.8 x 10(-2) vs. CD 8.2 x 10(-2) +/- 0.2 x 10(-2) (p < 0.01); intravenous glucose tolerance (kg 10(-2): CD + CLO 2.68 +/- 0.37 vs. CD 2.70 +/- 0.14 (p = NS); immunoreactive insulin (microU/ml/ min): with the area under the curve between 0 and 30 min CD + CLO 544 +/- 60 vs. CD 1,050 +/- 38 (p < 0.05), with the area under the curve between 0 and 60 min CD + CLO 1,188 +/- 150 vs. CD 2,160 +/- 137 (p < 0.05), and pancreas insulin content (microU/mg pancreas): CD + CLO 1.85 +/- 0.29 vs. CD 2.04 +/- 0.12 (p = NS). In conclusion, the present study shows that the strong hypolipidemic effect produced by the administration of low doses of fish oil to normal rats is accompanied by a significant reduction of plasma insulin levels without changes in glucose tolerance. Since no changes in pancreatic insulin content were observed, lower plasma insulin levels, both basal and after an intravenous glucose challenge, may be the result of an increased peripheral insulin sensitivity in normoglycemic animals.

Dietary polyunsaturated fatty acids and aging modulate glutathione-related antioxidants in rat liver.

The effects of dietary polyunsaturated fatty acids (PUFA) on the age-dependent changes in liver glutathione antioxidant system were investigated in male Wistar rats fed diets supplying either balanced amounts of linoleic acid and alpha-linolenic acids (control) or deficient in alpha-linolenic acid [n-3) deficient]. The animals were studied at the age of 6 or 24 mo. Glutathione antioxidative metabolism was markedly affected by aging. Cytosolic concentration of reduced glutathione (GSH) was lower (P < 0.01), whereas that of oxidized glutathione (GSSG) as well as the GSSG:GSH ratio were greater (P<0.001) in the 24-mo-old as compared with the 6-mo-old rats, regardless of the diet. Glutathione peroxidase activities were lower (P < 0.001) in 24-mo-old rats, though more markedly in those fed the control diet. The lipid composition of rat liver microsomal membranes was strongly modified by both diet and aging. The age-related changes mainly involved the polyunsaturated fatty acids. These results suggest that the nature of dietary PUFA and not only their degree of unsaturation affects the cellular glutathione-dependent antioxidant system and thus may modify the age-related changes in metabolic reactions.

Effects of n-3 and n-6 polyunsaturated fatty acid-enriched diets on lipid metabolism in periportal and pericentral compartments of female rat liver lobules and the consequences for cell proliferation after partial hepatectomy.

The effects of a low fat diet or diets enriched with either n-6 or n-3 polyunsaturated fatty acids (safflower or fish oil, respectively) on lipid metabolism in periportal and pericentral zones of female rat liver lobules were investigated in relation with cell proliferation after partial hepatectomy. It was found that cell proliferation was localized almost exclusively in periportal and midzonal areas and was significantly reduced by 60% after a fish oil diet only. The fish oil diet caused a strongly increased beta-oxidation capacity in peroxisomes and a moderately increased catalase activity. Catalase activity was mainly localized pericentrally, particularly after partial hepatectomy, whereas the capacity of lipid peroxidation product formation was doubled only in periportal zones in rats on a fish oil diet. The capacity of glucose-6-phosphate dehydrogenase activity to produce NADPH was distinctly lower in both zones of liver lobules as a result of the fish oil diet. Localization patterns and activity in liver lobules of NADPH-cytochrome c (P450) reductase were not significantly affected by fish oil diet. Therefore, it is concluded that elevated peroxisomal beta-oxidation and increased lipid peroxidation capacity in periportal zones of liver lobules coincide with reduced cell proliferation in hepatectomized rats on fish oil diet. These findings support the hypothesis that lipid peroxidation products are involved in the regulation of cell proliferation.