RESUMO
Cystinuria, is an autosomal recessive genetic disorder involving increasingly high levels of poorly soluble cysteine in urine leading to formation of stones. Developing a facile, low-cost, point-of-care and selective sensor for diagnosis of cysteine is imperative. Accordingly, for the detection of cysteine, the present study demonstrates an inexpensive colorimetric, paper-based vertical flow plasmonic micro-well device with a two-minute turn-around time. The method encompasses the use of microbially-synthesized silver nanoparticles (AgNPs) that change from light brown / yellow to dark brown upon binding with Sulphur present in cysteine. This technique allows for visual detection up to 1 × 10-5 mM cysteine and can be easily offered as a rapid diagnostic test even at setups with minimal resources.
Assuntos
Colorimetria/instrumentação , Cisteína/análise , Papel , Colorimetria/economia , Custos e Análise de Custo , Limite de Detecção , Nanopartículas Metálicas/química , Prata/química , SoftwareRESUMO
Gold nanoparticles have been investigated extensively for their molecular mechanisms of action and anticancer potential. We report a novel, tubulin-targeted antiproliferative mechanism of action of tryptone-stabilized gold nanoparticles (TsAuNPs). TsAuNPs, synthesized using HAuCl4·3H2O and tryptone and characterized by a variety of spectroscopic methods and transmission electron microscopy, were found to be inhibitory to viability of human pancreatic (PANC-1), cervical (HeLa), and breast (MDA-MB-231) cancer cell lines in a concentration-dependent manner, with highest efficacy against PANC-1 cells. The particles strongly inhibited the clonogenic propagation of PANC-1 cells. TsAuNPs-mediated inhibition of cell viability involved an unusual mode of cell cycle arrest (arrest at both G0/G1 phase and S-phase) followed by apoptosis. In vitro, TsAuNPs bound purified tubulin, competitively inhibited anilinonaphthalene sulfonate binding to tubulin, and suppressed tubulin assembly. In cells, tubulin-TsAuNPs interactions were manifested as a disrupted microtubule network, defective reassembly of cold-disassembled microtubules, and induction of tubulin acetylation. Our data indicate that TsAuNPs inhibit cell viability by inducing differential cell cycle arrest possibly through disrupted dynamicity of cellular microtubules.