RESUMO
The photolyase family consists of flavoproteins with enzyme activity able to repair ultraviolet light radiation damage by photoreactivation. DNA damage by the formation of a cyclobutane pyrimidine dimer (CPD) and a pyrimidine-pyrimidone (6-4) photoproduct can lead to multiple affections such as cellular apoptosis and mutagenesis that can evolve into skin cancer. The development of integrated applications to prevent the negative effects of prolonged sunlight exposure, usually during outdoor activities, is imperative. This study presents the functions, characteristics, and types of photolyases, their therapeutic and cosmetic applications, and additionally explores some photolyase-producing microorganisms and drug delivery systems.
Assuntos
Desoxirribodipirimidina Fotoliase , Reparo do DNA , Desoxirribodipirimidina Fotoliase/genética , Desoxirribodipirimidina Fotoliase/metabolismo , Flavoproteínas , Dímeros de Pirimidina , Pirimidinas , Pirimidinonas , Raios Ultravioleta/efeitos adversosRESUMO
Microalgae are complex photosynthetic organisms found in marine and freshwater environments that produce valuable metabolites. Microalgae-derived metabolites have gained remarkable attention in different industrial biotechnological processes and pharmaceutical and cosmetic industries due to their multiple properties, including antioxidant, anti-aging, anti-cancer, phycoimmunomodulatory, anti-inflammatory, and antimicrobial activities. These properties are recognized as promising components for state-of-the-art cosmetics and cosmeceutical formulations. Efforts are being made to develop natural, non-toxic, and environmentally friendly products that replace synthetic products. This review summarizes some potential cosmeceutical applications of microalgae-derived biomolecules, their mechanisms of action, and extraction methods.
Assuntos
Produtos Biológicos , Cosmecêuticos , Cosméticos , Microalgas , Anti-Inflamatórios/metabolismo , Anti-Inflamatórios/farmacologia , Antioxidantes/metabolismo , Antioxidantes/farmacologia , Produtos Biológicos/metabolismo , Produtos Biológicos/farmacologia , Biotecnologia , Cosmecêuticos/farmacologia , Cosméticos/metabolismo , Microalgas/metabolismoRESUMO
Respiratory diseases are leading causes of death and disability in developing and developed countries. The burden of acute and chronic respiratory diseases has been rising throughout the world and represents a major problem in the public health system. Acute respiratory diseases include pneumonia, influenza, SARS-CoV-2 and MERS viral infections; while chronic obstructive pulmonary disease (COPD), asthma and, occupational lung diseases (asbestosis, pneumoconiosis) and other parenchymal lung diseases namely lung cancer and tuberculosis are examples of chronic respiratory diseases. Importantly, chronic respiratory diseases are not curable and treatments for acute pathologies are particularly challenging. For that reason, the integration of nanotechnology to existing drugs or for the development of new treatments potentially benefits the therapeutic goals by making drugs more effective and exhibit fewer undesirable side effects to treat these conditions. Moreover, the integration of different nanostructures enables improvement of drug bioavailability, transport and delivery compared to stand-alone drugs in traditional respiratory therapy. Notably, there has been great progress in translating nanotechnology-based cancer therapies and diagnostics into the clinic; however, researchers in recent years have focused on the application of nanostructures in other relevant pulmonary diseases as revealed in our database search. Furthermore, polymeric nanoparticles and micelles are the most studied nanostructures in a wide range of diseases; however, liposomal nanostructures are recognized to be some of the most successful commercial drug delivery systems. In conclusion, this review presents an overview of the recent and relevant research in drug delivery systems for the treatment of different pulmonary diseases and outlines the trends, limitations, importance and application of nanomedicine technology in treatment and diagnosis and future work in this field.
RESUMO
Obesity leads to chronic oxidative stress promoting the development of cardiovascular diseases including coronary artery disease and endothelial dysfunction. Increased reactive oxygen species production associated with obesity might lead to endothelial dysfunction through cyclooxygenase (COX) pathway. We evaluated arachidonic acid (AA)-dependent coronary vascular responses and explored COX metabolism in obese C57BL/6 mice. In response to arachidonic acid (AA), isolated hearts from obese mice showed increased vasoconstriction compared with control mice. Released thromboxane (TX) A2 during AA-induced vasoconstriction phase was increased in heart perfusates from obese mice. Indomethacin and 1-benzylimidazole, both reduced vasoconstriction response in control and obese mice. Vasoconstriction response to TXA2 mimetic analog U46619 was 2.7 higher in obese mice. Obesity increased COX-2, TXS and TX receptor protein expression as well as oxidative stress evaluated by nitrotyrosine and peroxynitrite levels, compared with control mice. Obese mice treated with FeTMPyP, a peroxynitrite scavenger, reversed all these parameters to control levels. These data suggest that alterations in COX pathway may be associated with increased generation of free radicals, including peroxynitrite, that result from the oxidative stress observed in obesity.
Assuntos
Tromboxanos , Vasoconstrição , Animais , Ácido Araquidônico/metabolismo , Ciclo-Oxigenase 2 , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Obesos , Obesidade/metabolismo , Ácido Peroxinitroso/farmacologia , Tromboxano A2RESUMO
BACKGROUND: Obesity is a serious health problem associated with the pathogenesis of various metabolic diseases. Nitric Oxide (NO) plays an important role in kidney function and altered NO levels have been associated with the pathogenesis of obesity. Therefore, we aimed to study whether an early stage of obesity contributes with progression of renal failure through further NO impairment. METHODS: Male C57BL/6 mice were fed with a high-fat diet (HFD) or a normal diet (ND) during 2 weeks. All mice underwent either sham surgery (sham) or 5/6 nephrectomy (Np). One group of HFD Np mice was treated with antioxidants plus L-arginine. Kidney damage parameters were assessed and eNOS metabolism was evaluated. RESULTS: Mice on a HFD increased body weight, eNOS protein and mRNA expression, and radical oxygen species (ROS). Urine nitrites excretion, urine volume, and plasma BH4 were decreased. In HFD mice, 5/6 Np further increased BH2 and urine protein concentration, ROS levels, and eNOS mRNA expression. The decrease in BH4 plasma levels and urine nitrites excretion was accentuated. NO synthesis stimulation with the antioxidants + L-arginine treatment prevented all these changes. CONCLUSIONS: The early changes in NO metabolism are associated with an early stage of obesity. This effect on NO potentiates kidney damage development.
Assuntos
Rim/metabolismo , Óxido Nítrico/metabolismo , Obesidade/metabolismo , Insuficiência Renal/metabolismo , Animais , Antioxidantes/farmacologia , Biomarcadores/sangue , Biomarcadores/urina , Biopterinas/análogos & derivados , Biopterinas/sangue , Dieta Hiperlipídica , Modelos Animais de Doenças , Progressão da Doença , Regulação para Baixo , Rim/cirurgia , Masculino , Camundongos Endogâmicos C57BL , Nefrectomia , Óxido Nítrico/urina , Óxido Nítrico Sintase Tipo III/genética , Óxido Nítrico Sintase Tipo III/metabolismo , Obesidade/etiologia , Obesidade/genética , Estresse Oxidativo , Proteinúria/etiologia , Proteinúria/metabolismo , RNA Mensageiro/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Insuficiência Renal/etiologia , Insuficiência Renal/genética , Insuficiência Renal/prevenção & controle , Fatores de Risco , Aumento de PesoRESUMO
Cyclooxygenase (COX)-dependent prostaglandins are necessary for normal kidney function. These prostaglandins are associated with inflammation, maintenance of sodium and water homeostasis, control of renin release, renal vasodilation, vasoconstriction attenuation, and prenatal renal development. COX-2 expression is regulated by the renin-angiotensin system, glucocorticoids or mineralcorticoids, and aldosterone, supporting a role for COX-2 in kidney function. Indeed, COX-2 mRNA and protein levels as well as enzyme activity are increased, along with PGE2, during kidney failure. In addition, changes in COX-2 expression are associated with increased blood pressure, urinary volume, sodium and protein and decreased urinary osmolarity. Intrarenal mechanisms such as angiotensin II (Ang II) production, increased sodium delivery, glomerular hypertension, and renal tubular inflammation have been suggested to be responsible for the increase in COX-2 expression. Although, specific COX-2 pharmacological inhibition has been related to the prevention of kidney damage, clinical studies have reported that COX-2 inhibition may cause side effects such as edema or a modest elevation in blood pressure and could possibly interfere with antihypertensive drugs and increase the risk of cardiovascular complications. Thus, administration of COX-2 inhibitors requires caution, especially in the presence of underlying cardiovascular disease.