This research provides valuable insights into the application of ZnO nanoparticles in photocatalytic wastewater treatment. Process optimization was carried out by determining the ratio of the surface area to the energy band gap (S/E) in the photocatalysis rate under different sources of light (UV light, visible light, sunlight). The nanoparticles were synthesized using the precipitation technique, and the calcination process was carried out within a temperature range of 400 to 700 °C. The structural, morphological, and optical properties of materials were investigated using X-ray powder diffraction (XRD), scanning electron microscopy (SEM), UV-Vis diffuse reflectance (UV-Vis DRS), Raman spectroscopies, and Fourier transform infrared (FTIR) spectroscopies. The study demonstrates that calcination temperature significantly influences the photocatalytic activity of ZnO nanoparticles by altering their size, surface properties, shape, and optical behavior. Optimal decomposition efficiencies of Rhodamine B were achieved at 400 °C, with yields of 24%, 92%, and 91% under visible, UV, and sunlight irradiation, respectively. Additionally, the surface area decreased from 12.556 to 8.445 m²/g, the band gap narrowed slightly from 3.153 to 3.125 eV, and crystal growth increased from 0.223 to 0.506 µm as the calcination temperature rose. The photocatalytic properties of ZnO nanoparticles were assessed to determine their efficiency in decomposing Rhodamine B dye under operational parameters, including pollutant concentration (C0), sample amount, pH level, and reaction time. The sample exhibited the best breakdown rates with C0 = 5 mg/L, solid-to-liquid ratio (S/L) = 50 mg/L, pH = 7, and reaction time = 1 h. Additionally, we combined two oxidation processes, namely H₂O₂ and photocatalytic oxidation processes, which significantly improved the Rhodamine B removal efficiency, where 100% of RhB was degraded after 60 min and 100 µL of H₂O₂.

The search for effective anti-cancer therapies has led to the exploration of dual inhibition strategies targeting multiple key molecular pathways. In this study, we aimed to design a novel candidate capable of dual inhibition targeting both EGFR (Epidermal Growth Factor Receptor) and PARP-1 (poly(ADP-ribose)polymerase-1), two crucial proteins implicated in cancer progression and resistance mechanisms. Through molecular hybridization and structure-based drug design approaches, we synthesized a series of compounds based on spirooxindole with triazole scaffolds with the potential for dual EGFR and PARP-1 inhibition. Interestingly, compounds 4a, 4b and 4f showed potent cytotoxicity against HepG2 cells with IC₅₀ values of 3.6, 4.6, and 1.9 μM compared to doxorubicin (IC₅₀ = 2.78 μM), with poor cytotoxicity against THLE2 cells with IC₅₀ values higher than 40 μM in a selective way. They exhibited potent EGFR and PARP-1 inhibition with IC₅₀ values of 74.6, 85.3, and 116.1 nM compared to Erlotinib (IC₅₀ = 80 nM, 94.7%). Additionally, they exhibited potent PARP-1 inhibition, with IC₅₀ values of 2.01, 3.6, and 18.4 nM compared to Olaparib (IC₅₀ = 1.49 nM, 94.5%). Furthermore, compound 4a-treatment induced increased apoptosis by 6.6-fold, as the effective cell death mechanism. Overall, our study underscores the importance of multi-targeted approaches in developing effective anti-cancer agents.

The unique structure of spirooxindoles and their ability to feature various pharmacophoric motifs render them privileged scaffolds for tailoring new multitarget anticancer agents. Herein, a stereoselective multicomponent reaction was utilized to generate a small combinatorial library of pyrazole-tethered spirooxindoles targeting DNA and CDK2 with free radical scavenging potential as an extra bonus. The designed spirooxindoles were directed to combat NSCLC via inducing apoptosis and alleviating oxidative stress. The series' absolute configuration was assigned by X-ray diffraction analysis. Cytotoxicity screening of the developed spirooxindoles against NSCLC A549 and H460 cells compared to normal lung fibroblasts Wi-38 revealed the sensitivity of A549 cells to the compounds and raised 6e and 6h as the study hits (IC₅₀ ∼ 0.09 μM and SI > 3). They damaged DNA at 24.6 and 35.3 nM, and surpassed roscovitine as CDK2 inhibitors (IC₅₀ = 75.6 and 80.2 nM). Docking and MDs simulations postulated their receptors binding modes. The most potent derivative, 6e, induced A549 apoptosis by 40.85% arresting cell cycle at G2/M phase, and exhibited antioxidant activity in a dose-dependent manner compared to Trolox as indicated by DPPH scavenging assay. Finally, in silico ADMET analysis predicted the drug-likeness properties of 6e.

The synthesis and X-ray structure analysis of the new [PdLCl₂]*0.5 CH₂Cl₂ complex where L is hydrazono-s-triazine di-morpholine derivative, were presented. In the neutral inner sphere of this complex, the organic ligand L is acting as a NN-bidentate chelate via the pyridine and hydrazone N-atoms. The coordination configuration of the Pd(II) is completed by two chloride ions at cis-positions. The tetra-coordinated Pd(II) showed a distorted square planar geometry. The outer sphere comprised half methylene chloride molecule per [PdLCl₂] as crystal solvent. The crystal stability is dominated by a number of weak C-H…N, C-H…Cl, and C-H…O non-covalent interactions. Based on Hirshfeld analysis, the H…H, N…H, H…Cl, O…H, Pd…C, and Cl…C intermolecular interactions contributed by 45.2, 9.3, 21.5, 5.8, 2.3, and 3.4%, respectively. DFT studies revealed closed shell characters for the Pd-N and Pd-Cl coordinate bonds. The net charge of Pd is also predicted to be 0.311 e and the amount of electron density transferred from the ligand groups is 1.689 e. The Pd(II) complex exhibited potent cytotoxic activity against MCF-7, HepG2, and A549 cells with IC₅₀ values of 1.18, 4.74, and 5.22 μg/mL, compared to cisplatin with IC₅₀ values of 4.1, 9.7, and 12.3 μg/mL, respectively. Additionally, it exhibited poor cytotoxicity against WISH cells with much higher IC₅₀ values (IC₅₀ = 37.2 μg/mL). Investigating apoptosis-induction, the Pd(II) complex induced apoptotic cell death by an 11-fold change in MCF-7 cells arresting the cell phase at the G0–G1 phase. Accordingly, Pd(II) complex can be developed as a promising anti-breast cancer agent.