ABSTRACT
Meat products are a staple of many diets around the world, but they have been subject to criticism due to their potential negative impact on human health. In recent years, there has been a growing interest in developing novel approaches to improve the healthy characteristics of meat products, with a particular focus on reducing the levels of harmful salts, lipids, and nitrites. This review aims to provide an overview of the latest research on the various methods being developed to address these issues, including the use of alternative salts, lipid-reducing techniques, and natural nitrite alternatives. By exploring these innovative approaches, we can gain a better understanding of the potential for improving the nutritional value of meat products, while also meeting the demands of consumers who are increasingly concerned about their health and well-being.
ABSTRACT
The complex fac-[Mo(CO)(3)(histidinate)]Na has been reported to be an effective CO-Releasing Molecule in vivo, eliciting therapeutic effects in several animal models of disease. The CO releasing profile of this complex in different settings both in vitro and in vivo reveals that the compound can readily liberate all of its three CO equivalents under biological conditions. The compound has low toxicity and cytotoxicity and is not hemolytic. CO release is accompanied by a decrease in arterial blood pressure following administration in vivo. We studied its behavior in solution and upon the interaction with proteins. Reactive oxygen species (ROS) generation upon exposure to air and polyoxomolybdate formation in soaks with lysozyme crystals were observed as processes ensuing from the decomposition of the complex and the release of CO.
Subject(s)
Carbon Monoxide/metabolism , Coordination Complexes/chemistry , Organometallic Compounds/chemistry , Prodrugs/chemistry , Animals , Binding Sites , Cell Line , Cell Survival/drug effects , Coordination Complexes/chemical synthesis , Coordination Complexes/toxicity , Crystallography, X-Ray , Hemodynamics , Hemoglobins/chemistry , Hemoglobins/metabolism , Hemolysis , Hep G2 Cells , Humans , Mice , Muramidase/chemistry , Muramidase/metabolism , Organometallic Compounds/chemical synthesis , Organometallic Compounds/toxicity , Prodrugs/chemical synthesis , Prodrugs/toxicity , Protein Structure, Tertiary , Serum Albumin/chemistry , Serum Albumin/metabolismABSTRACT
BACKGROUND AND AIMS: Iron deposits in the liver and abnormalities in serum iron biochemistry are frequently observed in patients with chronic liver diseases, but data for patients with hepatitis B virus (HBV) infection are scarce. Moreover, the role of HFE mutations in iron deposits in this condition remains unknown. The aim of the present study was to determine the prevalence of serum iron biochemical abnormalities and iron deposits in the liver of chronic HBV patients, and to evaluate the consequences for the activity and severity of liver disease. Additionally, we studied the role of HFE gene mutations in iron deposits. METHODS: Eighty-one male non-cirrhotic HBV patients were studied. Serum iron biochemistry, liver enzymes and C282Y/H63D mutations were investigated. Liver biopsies were scored for necroinflammatory activity (histological activity index [HAI]), fibrosis and iron deposits. RESULTS: Elevated transferrin saturation (TS) was found in 27.1% of patients and liver iron deposits in 48.7%; these deposits were mild in 68.4% and moderate in 31.6%. Patients with liver iron deposits exhibited significantly higher scores for HAI and fibrosis than those without iron deposits. HFE mutations were identified in 23.4% of patients (14 H63D heterozygotes, four H63D homozygotes, one compound mutation). No difference in the prevalence of C282Y and H63D mutations was observed between HBV patients (1.2% and 23.4%, respectively) and the general population (4.1% and 27.8%, respectively). No association was detected between HFE mutations and elevated TS or liver iron deposits. CONCLUSIONS: Elevated TS and liver iron deposits were frequent in non-cirrhotic HBV patients. Iron deposits were mainly mild and associated with higher activity and severity of liver disease, but not with HFE mutations.
Subject(s)
Hepatitis B, Chronic/genetics , Hepatitis B, Chronic/pathology , Iron/analysis , Liver/chemistry , Adolescent , Adult , Humans , Liver/enzymology , Liver Function Tests , Male , Middle Aged , Mutation , Polymerase Chain Reaction , Prospective Studies , Severity of Illness Index , Statistics, NonparametricABSTRACT
A Doença de Graves (DG) é a causa mais freqüente de hipertireoidismo. Sua origem é multifatorial, complexa, na qual a susceptibilidade genética interage com o meio ambiente e fatores endógenos para causar a doença. Os alelos do Complexo Principal de Histocompatibilidade (CPH) de classe II têm sido associados com a DG, em populações de diferentes etnias e muitas evidências apontam para a associaçäo do antígeno HLA-DR3 em caucasianos. O envolvimento dos alelos do CPH na nossa populaçäo, altamente miscigenada, foi estudado em pacientes com a DG e em indivíduos-controle da mesma área geográfica, utilizando-se DNA genômico amplificado e hibridado com iniciadores de sequência específica (SSP). O alelo HLA-DRB1*0301 esteve presente com maior freqüência (44,7 por cento) em pacientes com DG, relativamente à populaçäo-controle (22,3 por cento, pc=0,0068), conferindo Risco Relativo (RR) de 2,8 e uma Fraçäo Etiológica de 28,7, enquanto o alelo HLA-DQB1*0602 esteve, significativamente, diminuído nesses pacientes (8 por cento) em relaçäo aos pacientes-controle (31,9 por cento, pc=0,00062), conferindo RR de 1,8 e uma Fraçäo Preventiva de 26,7. Apesar de a populaçäo brasileira ser altamente miscigenada, a confirmaçäo do alelo HLA-DRB1*0301, conferindo susceptibilidade à doença, aponta esse alelo com um marcador importante na predisposiçäo à doença. Em contraste, a proteçäo conferida pelo alelo HLA-DQB1*0602 parece ser peculiar aos pacientes brasileiros
Subject(s)
Humans , Animals , Male , Female , Adult , Disease Susceptibility , Graves Disease/genetics , Major Histocompatibility Complex , Alleles , Brazil , Graves Disease/immunologyABSTRACT
Os antígenos de histocompatibilidade HLA-B8 e -DR3 säo os mais comumente associados à doença de Graves em várias populaçöes caucasianas estudadas. Näo existem publicaçoes completas sobre a tipagem de antígenos ou alelos HLA na populaçao brasileira com doença de Graves. Neste estudo, avaliamos a freqüência dos antígenos HLA de classe II em pacientes com doença de Graves com ou sem oftalmopatia procedentes do Hospital das Clínicas da FMRP-USP. Foram estudados também 191 controles procedentes da mesma área geográfica. Os antígenos foram tipados utilizando a técnica de microlinfocitotoxicidade dependente de complemento. A análise estatística foi realizada usando o teste exato de Fisher bicaudal. Os resultados mostraram que a especificidade HLA-DR3 estava significativamente aumentada em nossos pacientes, conferindo um risco relativo de 4,17 e uma fraçäo etiológica de 0,42. Por outro lado, observamos também diminuiçäo significante das freqüências das especificidades HLA-DR53 e -DQ3, conferindo risco relativo de 0,24 e 0,12, e fraçäo preventiva de 0,98 e 0,99, respectivamente. Embora a populaçäo brasileira seja bastante miscigenada, este estudo mostra que a especificidade HLA-DR3 também confere suscetibilidade à doença em nossa populaçäo. Além disso, acrescenta que as especificidades HLA-DR53 e -DQ3 podem atuar como fatores de proteçäo ao desenvolvimento da doença. Na presença ou na ausência de oftalmopatia a freqüência dos antígenos de histocompatibilidade estudados foi semelhante.
