RESUMO
The mercuric ion (Hg2+) is a hazardous pollutant that is widely distributed in living organisms, foods, and environments with highly toxic and bio-accumulative properties. In the present study, a fluorescent probe based on aptamer gold nanoclusters (apt-AuNCs) was prepared for the ultrasensitive detection of Hg2+ in food. The principle underlying the prepared probe was the quenching of the fluorescence of apt-AuNCs in the presence of Hg2+ due to the strong metallophilic interactions between the 5d10 centers of Hg2+ and Au+. Under optimal conditions, the proposed fluorescent probe exhibited a linear relationship with Hg2+ concentration within the range of 2-200 nM (R2 = 0.9960). In addition, the limit of detection (LOD) was 0.0158 nM, which is below the Chinese standard value of 25 nM for Hg2+ in food. Furthermore, the apt-AuNCs were applied to detect Hg2+ in spinach and crawfish samples, with recovery percentages of 91.99%â¼108.06%, meaning that apt-AuNCs could be used as a promising probe to detect Hg2+ in complex food samples.
Assuntos
Mercúrio , Nanopartículas Metálicas , Corantes Fluorescentes , Ouro , Espectrometria de FluorescênciaRESUMO
Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease which represents a wide spectrum of hepatic damage. Several studies have reported that NAFLD is a strong independent risk factor for coronary artery disease (CAD). And patients with NAFLD are at higher risk and suggested undergoperiodic cardiovascular risk assessment. Cardiovascular disease (CVD) is responsible for the main cause of death in patients with NAFLD, and is mostly influenced by genetic factors. Both NAFLD and CAD are heterogeneous disease. Common pathways involved in the pathogenesis of NAFLD and CAD includes insulin resistance (IR), atherogenic dyslipidemia, subclinical inflammation, oxidative stress, etc. Genomic characteristics of these two diseases have been widely studied, further research about the association of these two diseases draws attention. The gene polymorphisms of adiponectin-encoding gene (ADIPOQ), leptin receptor (LEPR), apolipoprotein C3 (APOC3), peroxisome proliferator-activated receptors (PPAR), sterol regulatory elementbinding proteins (SREBP), transmembrane 6 superfamily member 2 (TM6SF2), microsomal triglyceride transfer protein (MTTP), tumor necrosis factors-alpha (TNF-α) and manganese superoxide dismutase (MnSOD) have been reported to be related to NAFLD and CAD. In this review, we aimed to provide an overview of recent insights into the genetic basis of NAFLD and CAD.
Assuntos
Doença da Artéria Coronariana/genética , Hepatopatia Gordurosa não Alcoólica/genética , Polimorfismo Genético , Adiponectina/genética , Apolipoproteína C-III/genética , Proteínas de Transporte/genética , Humanos , Proteínas de Membrana/genética , Receptores Ativados por Proliferador de Peroxissomo/genética , Receptores para Leptina/genética , Proteínas de Ligação a Elemento Regulador de Esterol/genética , Superóxido Dismutase/genética , Fator de Necrose Tumoral alfa/genéticaRESUMO
Nonalcoholic fatty liver disease (NAFLD) is a metabolic stress-induced liver disease that is closely related not only to genetic susceptibility but also to insulin resistance and highly linked with metabolic syndrome. In recent years, the prevalence of NAFLD has increased rapidly, paralleling the epidemic of type 2 diabetes mellitus and obesity leading to cardiovascular disease. It has been demonstrated that NAFLD is highly associated with atherosclerosis. With recently gained knowledge, it appears that NAFLD may induce insulin resistance, dyslipidemia, oxidative stress, inflammation, and fluctuation of adipokines associated with atherosclerosis. In this review, we aimed to summarize recent discoveries related to both NAFLD and atherosclerosis, and to identify possible mechanisms linking them.
