The Toxicity And Inhibition On Bio-enzyme Activity Of Polycyclic Aromatic Hydrocarbons And Organophosphate Esters

The development of science and technology not only provides technical support for industrial boom,but also brings potential environmental risks to the society.Polycyclic aromatic hydrocarbons(PAHs)and Organophosphate esters(OPEs)are two representative pollutants.Industrial activities cause large amounts of pollutants to enter in the environment and biological body.Pollutants into the biological body,will cause a variety of hazards including immunotoxicity,reproductive toxicity and carcinogenic toxicity.Therefore,the control and treatment of PAHs and OPEs have also attracted the attention of the environmental research community.However,the pollutants with different structures are not clearly stipulated in the total amount control of pollutant,and environmental standards,and toxicological studies are necessary for the ecological and health risk assessment of environmental pollutants.Because pollutants interfere with the human system,they must first directly interact with biological macromolecules in metabolic reactions,the research at the molecular level on the toxic effects of pollutants and biological macromolecules helps to further reveal the toxicity mechanism of pollutants.This will provide an important basis for the ecological and health risk assessment of environmental pollutants and provide theoretical support for the determination of concentration standards for pollution control and treatment.In this paper,7 PAHs and 12 OPEs were used as research objects to determine the acute toxic effect of the contaminant on the growth of E.coli.The toxicity intensity of PAHs increases with the increase of the number of benzene rings.For PAHs with the same number of benzene rings,PAHs with"canyon"distortion has a stronger inhibitory effect than linear PAHs.LogK_ow,benzene ring number and local structure are important properties affecting acute toxicity.For12 OPEs,aryl phosphate esters have the most toxic inhibitory effect on E.coli,followed by chlorinated phosphate esters and finally alkyl phosphate esters.Acute toxicity was enhanced with the addition of alkyl chains and chlorine atoms(except for Tris(2-butoxyethyl phosphate,TBEP)).As for the toxic effect of OPEs on PC12 cells,the number of chlorine atoms and the space volume of substituents in OPEs are important factors affecting the proliferation of PC12 cells.In the paper,the HPLC with pre-column benzoyl chloride derivation was used to determine the inhibitory effect of PAHs on the activity of diamine oxidase(DAO),and the 50%inhibition concentration(IC₅₀)of PAHs on the inhibition of DAO activity was determined at the optimized DAO/humide concentration.The benzene ring number,LogK_ow and"canyon"distortion structure of PAHs are important factors to determine the inhibition effect.Molecular docking analysis shows that the binding energies of 7 PAHs and DAO are-5.62?-9.97 Kcal/M,and the physical properties(benzene ring number and LogK_ow)and local structure of PAHs determine the combination mode of PAHs and DAO,and then determine the inhibitory effect of PAHs on DAO.The effect of OPEs on the activity of Fatty acid amide hydrolase(FAAH)was determined by fluorescent assay using arachidonyl 7-amino,4-methyl coumarin amide(AAMCA)as substrate.The IC₅₀ value of OPEs against the inhibition of FAAH activity was tested under optimized FAAH/AAMCA conditions.Compared with alkyl phosphate esters,chlorinated phosphate esters and show more obvious inhibitory effect on FAAH.The inhibitory effect of OPEs on FAAH activity was enhanced with the increase of alkyl chain and chlorine atoms,except for TBEP.Molecular docking analysis showed that the binding energies of 12 OPEs and FAAH ranged from-9.90 to-3.15 Kcal/M.Toxicity of OPEs molecules to FAAH is determined by the binding pattern,which is mainly affected by the size of the space and the type of substituents.