Biocompatible silver nanoparticles: An investigation into their protein binding efficacies, anti-bacterial effects and cell cytotoxicity studies.

Green synthesis of silver nanoparticles (AgNPs) has garnered tremendous interest as conventional methods include the use and production of toxic chemicals, products, by-products and reagents. In this regard, the synthesis of AgNPs using green tea (GT) extract and two of its components, (-)-epigallocatechin gallate (EGCG) and (+)-catechin (Ct) as capping/stabilizing agents, is reported. The synthesized AgNPs showed antibacterial activity against the bacterial strains Staphylococcus aureus and Escherichia coli, along with anticancer activity against HeLa cells. After administering nanoparticles to the body, they come in contact with proteins and results in the formation of a protein corona; hence we studied the interactions of these biocompatible AgNPs with hen egg white lysozyme (HEWL) as a carrier protein. Static quenching mechanism was accountable for the quenching of HEWL fluorescence by the AgNPs. The binding constant (K b) was found to be higher for EGCG-AgNPs ((2.309 ± 0.018) × 104 M-1) than for GT-AgNPs and Ct-AgNPs towards HEWL. EGCG-AgNPs increased the polarity near the binding site while Ct-AgNPs caused the opposite effect, but GT-AgNPs had no such observable effects. Circular dichroism studies indicated that the AgNPs had no such appreciable impact on the secondary structure of HEWL. The key findings of this research included the synthesis of AgNPs using GT extract and its constituent polyphenols, and showed significant antibacterial, anticancer and protein-binding properties. The -OH groups of the polyphenols drive the in situ capping/stabilization of the AgNPs during synthesis, which might offer new opportunities having implications for nanomedicine and nanodiagnostics.

Biocompatible silver nanoparticles:An investigation into their protein binding efficacies,anti-bacterial effects and cell cytotoxicity studies / 药物分析学报

Green synthesis of silver nanoparticles (AgNPs) has garnered tremendous interest as conventional methods include the use and production of toxic chemicals,products,by-products and reagents.In this regard,the synthesis of AgNPs using green tea (GT) extract and two of its components,(-)-epi-gallocatechin gallate (EGCG) and (+)-catechin (Ct) as capping/stabilizing agents,is reported.The syn-thesized AgNPs showed antibacterial activity against the bacterial strains Staphylococcus aureus and Escherichia coli,along with anticancer activity against HeLa cells.After administering nanoparticles to the body,they come in contact with proteins and results in the formation of a protein corona;hence we studied the interactions of these biocompatible AgNPs with hen egg white lysozyme (HEWL) as a carrier protein.Static quenching mechanism was accountable for the quenching of HEWL fluorescence by the AgNPs.The binding constant (Kb) was found to be higher for EGCG-AgNPs ((2.309 ± 0.018) × 104 M-1)than for GT-AgNPs and Ct-AgNPs towards HEWL.EGCG-AgNPs increased the polarity near the binding site while Ct-AgNPs caused the opposite effect,but GT-AgNPs had no such observable effects.Circular dichroism studies indicated that the AgNPs had no such appreciable impact on the secondary structure of HEWL.The key findings of this research included the synthesis of AgNPs using GT extract and its con-stituent polyphenols,and showed significant antibacterial,anticancer and protein-binding properties.The-OH groups of the polyphenols drive the in situ capping/stabilization of the AgNPs during synthesis,which might offer new opportunities having implications for nanomedicine and nanodiagnostics.

EFHC1 mutation in Indian juvenile myoclonic epilepsy patient.

OBJECTIVE: Juvenile myoclonic epilepsy (JME) is the most common form of idiopathic generalized epilepsies (IGEs) and is genetically heterogeneous. Mutations in EFHC1 cause JME. Because about 2 million people in India are affected by JME alone, we investigated the prevalence of mutations in the EFHC1 gene in the Indian population with JME. We studied 63 patients with JME and 80 healthy controls. METHODS: Clinical identification of JME was evaluated using established criteria. Following clinical evaluation of the patients and confirming presence of JME, blood samples were collected from each patient and healthy individual. Subsequently, genomic DNA was extracted from the blood samples. Eleven exons of the EFHC1 gene were individually amplified by polymerase chain reaction (PCR) for each DNA sample. The PCR products were then purified and sequenced commercially. The identified DNA variants were sequenced at least twice in both the forward and reverse directions and compared with the Exome Aggregation Consortium (ExAC) database. RESULTS: We found five heterozygous and one homozygous variant. We found three novel coding variants 661C→T, 779 G →A, and 730 C→T, which lead to R221C, R260Q, and R244STOP amino acid substitutions, respectively. The coding variant 475 C→T, resulting in the amino acid substitution R159W, reported earlier as polymorphism, was also identified in both patient and control populations. SIGNIFICANCE: Detection of these three novel variants, excluding R159W, which is considered polymorphism, expands the range of possible mutations in the EFHC1 gene. The novel variants that we are reporting herein have not been mentioned before as occurring in JME patients of other ethnic population. Therefore, these novel coding variants may be confined to the Indian JME population. Further studies on the mutational spectrum of EFHC1 in a larger number of Indian JME patients concurrent with their mode of inheritance and underlying functional assays should establish whether EFHC1 could be a panethnic gene for JME.