Preparation of selective magnetic adsorbents for dispersive micro-solid phase extraction often involves multi-step reactions which are time consuming. This study demonstrates a simplified method for the synthesis of a magnetic adsorbent, which is selective towards the adsorption of mercury(ii) ions (Hg2+). In this method, the incorporation of a metal capturing ligand (3-oxo-1,3-diphenylpropyl-2-(naphthalen-2-ylamino) ethylcarbamodithioate) and the coating of magnetic particles with silica gel was performed in a single step. This adsorbent was then used in solid-phase microextraction for the preconcentration of Hg2+ in water. In this study, a mercury analyzer was used to quantify the Hg2+. Under optimized conditions, the developed analytical method achieved a low detection limit (4.0 ng L-1), satisfactory enrichment factor (96.4) and wide linearity range (50.0-5000 ng L-1) with a good coefficient of determination (0.9985) and good repeatability (<7%). The preconcentration factor of this method was 100. This proposed method was also successfully utilized for the determination of Hg2+ in drinking water, tap water and surface water with good recovery (>91%) and high intra-day and inter-day precision.
Background: Endometrial cancer (EC) is the most common gynecologic malignancy in developed countries. Annonacin, a natural pure compound extracted from the seeds of Annona muricata, is a potential alternative therapeutic agent to treat EC.
Objective: To study the antitumor activity of annonacin and its mechanism of action in EC cells (ECCs).
Materials and Methods: Viability of ECCs treated with annonacin for 72 h was determined using methyl thiazolyl tetrazolium assay. The induction of cell cycle arrest and apoptotic cell death was evaluated using propidium iodide and annexin V-PE/7-AAD assay, respectively. DNA strand breaks were visualized using transferase dUTP nick end labeling assay, and the effects of annonacin on survival signaling were determined using western blotting.
Results: Annonacin exhibited antiproliferative effects on EC cell lines (ECC-1 and HEC-1A) and primary cells (EC6-ept and EC14-ept) with EC50values ranging from 4.62 to 4.92 μg/ml. EC cells were shown arrested at G2/M phase after treated with 4 μg/ml of annonacin for 72 h. This led to a significant increase in apoptotic cell death (65.7%) in these cells when compared to vehicle-treated cells (P < 0.005). We further showed that annonacin-mediated apoptotic cell death was associated with an increase in caspase-3 cleavage and DNA fragmentation. Cell apoptosis was accompanied with downregulation of extracellular signal-regulated kinase survival protein expression and induction of G2/M cell cycle arrest.
Conclusion: Annonacin may be a potential novel therapeutic agent for EC patients.
SUMMARY: We aimed to study the antitumor activity of annonacin and its mechanism of action in endometrial cancer cells. Annonacin exerted antiproliferation effects on both endometrial cancer cell lines and primary cells via induction of apoptosis and inhibition of extracellular signal-regulated kinase. Our data represented that annonacin could be an alternative therapeutic treatment to combat endometrial cancer. Abbreviations Used: 7-AAD: 7-Amino-Actinomycin, ATP: Adenosine diphosphate, BSA: Bovine serum albumin, DNA: Deoxyribonucleic acid, EC: Endometrial cancer, ECC-1: Endometrial cancer cell-1, EC50: Half maximal effective concentration, Ept: Epithelial, FBS: Fetal bovine serum, HEC-1A: Human endometrial carcinoma-1A, MTT: Methyl thiazolyl tetrazolium, NaCl: Sodium chloride, NADH: Nicotinamide adenine dinucleotide, RPMI 1640: Roswell Park Memorial Institute Medium, SDS: Sodium dodecyl sulfate.