Phenol and nitrogenous heterocyclic compounds (NHCs) are typical organic pollutants in coal gasification wastewater which are difficult to deal with. Unlike phenol, the stable molecular structure of NHCs make them nearly impossible to degrade under aerobic or anaerobic condition. In this paper, biodegradation of phenol and NHCs as carbon sources for denitrification was studied in a laboratory-scale anoxic reactor. Denitrifiers could degrade 490 mg/L phenol and 321.5 mg/L NO3(-)-N within 12 hours with removal efficiencies of 99.8% and 99.6%, respectively. The inhibition of pyridine on the microbes could be reduced by adding phenol into influent and the experimental results showed that pyridine could be degraded as the sole carbon source with the maximum organic loading rate of 4.38 mg/(g MLSS·h) (MLSS: mixed liquor suspended solids). When phenol was included as a growth substrate, the degradation performance of quinoline and pyrrole was improved due to co-degradation, and removal rate of NHCs increased according with increment of phenol in influent.

The aim of this study was to develop physiologically based pharmacokinetic (PBPK) models capable of simulating cefadroxil concentrations in plasma and tissues in mouse, rat, and human. PBPK models in this study consisted of 14 tissues and 2 blood compartments. They were established using measured tissue to plasma partition coefficient (Kp) in mouse and rat, absolute expression levels of hPEPT1 along the entire length of the human intestine, and the transporter kinetic parameters. The PBPK models also assumed that all the tissues were well-stirred compartments with perfusion rate limitations, and the ratio of the concentration in tissue to the unbound concentration in plasma is identical across species. These PBPK models were validated strictly by a series of observed plasma concentration–time profile data. The average fold error (AFE) and absolute average fold error (AAFE) values were all less than 2. The models’ rationality and accuracy were further demonstrated by the almost consistent Vss calculated by the PBPK model and noncompartmental method, as well as the good allometric scaling relationship of Vss and CL. The model suggests that hPEPT1 is the major transporter responsible for the oral absorption of cefadroxil in human, and the plasma concentration–time profiles of cefadroxil were not sensitive to dissolution rate faster than T85% = 2 h. The cefadroxil PBPK model in human is reliable and can be used to predict concentration–time profile at infected tissue. It may be useful for dose selection and informative decision-making during clinical trials and dosage form design of cefadroxil and provide a reference for the PBPK model establishment of hPEPT1 substrate.