In this study, climate change and human impacts on water quality in five major urban areas of Pakistan, including Karachi, Lahore, Peshawar, Abbottabad, and Gilgit, were determined. Secondary data on various physical, chemical, and bacteriological water quality parameters were taken from published papers, reports, and theses. Surface and groundwater were the major sources of drinking water in these cities. The physicochemical parameters were total turbidity, pH, dissolved solids (TDS), sulphates, chlorides, calcium, sodium, HCO₃, potassium, magnesium, nitrates, fluorides, arsenic, and hardness. The bacteriological parameters were total coliform, total faecal coliform, and total plate counts. The data revealed that pH, TDS, fluoride, chloride, HCO₃, sodium, and hardness were above the limits in Karachi. MCB Market, Goth Ibrahim, and Malir Town were the main contaminated areas in Karachi. In Lahore, arsenic was found above the limits in all sampling locations. Turbidity, pH, HCO₃, calcium, magnesium, and hardness were found above the limits in Peshawar. In Gilgit city, all physicochemical parameters were found within the limits except turbidity, which was 10 NTU in Nomal valley. Nitrates were higher in the water sources in Abbottabad. Bacterial contamination was found in the water of all five cities. Most of the studies revealed that this contamination could be human-induced. The improper disposal of solid waste, sewage, and animal waste and the excessive use of fertilisers deteriorate the quality of the water. Precipitation, a rise in temperature, and seasonal variation are climate variables that affect water quality and are responsible for major outbreaks of waterborne diseases. There is an urgent need for regular analysis, proper management, and proper treatment of drinking water before it is supplied to the local community in these cities.

The effectiveness of all antibiotics in the β-lactam group to cure bacterial infections has been impaired by the introduction of the New Delhi Metallo-β-lactamase (NDM-1) enzyme. Attempts have been made to discover a potent chemical as an inhibitor to this enzyme in order to restore the efficacy of antibiotics. However, it has been a challenging task to develop broad-spectrum inhibitors of metallo-β-lactamases. Lack of sequence homology across metallo-β-lactamases (MBLs), the rapidly evolving active site of the enzyme, and structural similarities between human enzymes and metallo-β-lactamases, are the primary causes for the difficulty in the development of these inhibitors. Therefore, it is imperative to concentrate on the discovery of an effective NDM-1 inhibitor. This study used various in silico approaches, including molecular docking and molecular dynamics simulations, to investigate the potential of phytochemicals to inhibit the NDM-1 enzyme. For this purpose, a library of about 59,000 phytochemicals was created from the literature and other databases, including FoodB, IMPPAT, and Phenol-Explorer. A physiochemical and pharmacokinetics analysis was performed to determine possible toxicity and mutagenicity of the ligands. Following the virtual screening, phytochemicals were assessed for their binding with NDM-1using docking scores, RMSD values, and other critical parameters. The docking score was determined by selecting the best conformation of the protein–ligand complex. Three phytochemicals, i.e., butein (polyphenol), monodemethylcurcumin (polyphenol), and rosmarinic acid (polyphenol) were identified as result of pharmacokinetics and molecular docking studies. Furthermore, molecular dynamics simulations were performed to determine structural stabilities of the protein–ligand complexes. Monodemethylcurcumin, butein, and rosmarinic acid were identified as potential inhibitors of NDM-1 based on their low RMSD, RMSF, hydrogen bond count, average Coulomb–Schrödinger interaction energy, and Lennard–Jones–Schrödinger interaction energy. The present investigation suggested that these phytochemicals might be promising candidates for future NDM-1 medication development to respond to antibiotic resistance.