Quinolones are broad-spectrum synthetic antibacterial drugs first obtained during the synthesis of chloroquine. Nalidixic acid, the prototype of quinolones, first became available for clinical consumption in 1962 and was used mainly for urinary tract infections caused by Escherichia coli and other pathogenic Gram-negative bacteria. Recently, significant work has been carried out to synthesize novel quinolone analogues with enhanced activity and potential usage for the treatment of different bacterial diseases. These novel analogues are made by substitution at different sites—the variation at the C-6 and C-8 positions gives more effective drugs. Substitution of a fluorine atom at the C-6 position produces fluroquinolones, which account for a large proportion of the quinolones in clinical use. Among others, substitution of piperazine or methylpiperazine, pyrrolidinyl and piperidinyl rings also yields effective analogues. A total of twenty six analogues are reported in this review. The targets of quinolones are two bacterial enzymes of the class II topoisomerase family, namely gyrase and topoisomerase IV. Quinolones increase the concentration of drug-enzyme-DNA cleavage complexes and convert them into cellular toxins; as a result they are bactericidal. High bioavailability, relative low toxicity and favorable pharmacokinetics have resulted in the clinical success of fluoroquinolones and quinolones. Due to these superior properties, quinolones have been extensively utilized and this increased usage has resulted in some quinolone-resistant bacterial strains. Bacteria become resistant to quinolones by three mechanisms: (1) mutation in the target site (gyrase and/or topoisomerase IV) of quinolones; (2) plasmid-mediated resistance; and (3) chromosome-mediated quinolone resistance. In plasmid-mediated resistance, the efflux of quinolones is increased along with a decrease in the interaction of the drug with gyrase (topoisomerase IV). In the case of chromosome-mediated quinolone resistance, there is a decrease in the influx of the drug into the cell.

In this study, the sorption behavior of Pleurotus ostreatus toward Ni(II) is examined with respect to pH, temperature, contact time, and concentration. The good correlation coefficient and close agreement between experimental and theoretical values of biosorption capacity confirm that the pseudo-second-order kinetic model is best applicable to the kinetics data. The sorption of Ni(II) is found to be dependent upon the pH and temperature of the solution. The adsorption of Ni(II) onto P. ostreatus is maximum at higher pH values and decreases with an increase in temperature in the range of 298–318 K. Both X_m and K_b values decrease with increase in temperature, indicating the exothermic nature of the process. Different thermodynamic parameters were calculated for adsorption of Ni(II) onto P. ostreatus. The negative value of ΔS indicates a decrease in randomness at the solid/liquid interface. The values of isosteric heat of adsorption are decreasing with increases in surface coverage, which reveal the heterogeneous nature of the solid surface. The FTIR spectra show that the carbonyl groups of P. ostreatus are responsible for adsorption of Ni(II) onto P. ostreatus.