Cytotoxicity Of Erythromycin On PAHs-degrading Strain And The Effects On Degradation Process

PAHs (polycyclic aromatic hydrocarbons) made serious pollution as the classicPOPs (persistent organic pollutants), and scientists discovered many kinds ofPAHs-degrading bacteria in recent years, however it is difficult to achieve the desiredgoals in the actual environmental bioremediation. Factors of environment andecological conditions are much more complex than that in the simple experimentalbacterial culture, for example，common residues in environment of antibiotics is apotential influence factor. Scholars have recognized that the abuse of antibiotics doesharm to environment just like POPs, and focus on the adsorption of antibiotics inenvironment, direct toxicity impacts on plants and animals even human. however，theeffect of antibiotics on a micro-ecological environment is less studied, andenvironment risks caused by the effects of antibiotics on pollutant degrading bacteriashould not be ignored. If PAHs biodegradation process is damaged, the consequencesare antibiotics and PAHs composite permanent pollution. The relationship betweenantibiotics and microbe is not completely opposite like “spear and shield”, and effectsof antibiotics on bacteria of environment are complex and changeable, so clarifyingthe relationship between these factors will be beneficial to make the rightenvironmental risk assessment and provide a scientific basis and reference for theeffective application of PAHs-degrading bacteria known as “environment thebeneficial bacteria”in the actual environment.This paper mainly studies the following aspects:(1) through the toxicity test oferythromycin on phenanthrene-degrading bacteria GY2B and pyrene-degradingbacteria CP13, some commonly used toxicological indexes are determined such saminimum inhibitory concentration (MIC), inhibitory curve, total superoxidedismutase (SOD), lactate dehydrogenase (LDH), in order to evaluate physiologicalconditions of the two kinds of bacteria under the influence of erythromycin;(2) thepost antibiotic effect (PAE) and the changes during it were studied to mimic theprocess containing rainwater runoff and antibiotics diluted, and the effects of strainrecovery growth ability is tested as well as the recovery mechanism in GY2B;(3) it isstudied that the effect of erythromycin on biodegradation of phenanthrene or pyrene， proliferation of bacteria in the culture medium containing erythromycin andphenanthrene or pyrene. It is also studied that the utilization of erythromycin as solecarbon source, and the effect of trace erythromycin affecting strain1months.The main results have been obtained in this paper as follows:(1) The minimal inhibitory concentration (MIC) of erythromycin on GY2B was0.25μg mL-1, the maximum tolerant concentration (99.9%mortality) of GY2B toerythromycin was25μg mL-1; the sensitivity of GY2B decrease with time；whenconcentration of erythromycin was higher than minimal inhibitory concentration(0.25μg mL-1)，it reduced significantly the total superoxide dismutase activity（SOD）of the cell, did damage to the bacteria by active oxygen and decreased the activity oflactate dehydrogenase （LDH），though the effect on the level of oxygen breathingwould be weakened gradually.(2) The minimal inhibitory concentration (MIC) of erythromycin on CP13was16μg mL-1; even the maximum drug sensitivity concentration (256μg mL-1) can onlyinhibit85.9%CP13cultured24h; CP13was resistant to erythromycin. whenconcentration of erythromycin was higher than16μg mL-1，it reduced the total SODand LDH activity of the cell, but the effect is less than that suffered by GY2B. CP13showed great surviving ability in erythromycin conditions.(3) Erythromycin had significant concentration-dependent PAE on GY2B, but itdid not change cell size; the changes of DNA content during PAE were caused bySOS repair mechanism, DNA autolysis and binary division. GY2B cells were able torecover in short exposure to erythromycin2~3h. Erythromycin had no PAE onCP13,and CP13cells can recover in short exposure to erythromycin at once.(4) Erythromycin can inhibit the proliferation of GY2B and phenanthreneutilization, and the effect was concentration-dependent. When concentration oferythromycin was25μg mL-1,48h phenanthrene-degrading rate of GY2B was lessthan10.0%. When concentration of erythromycin was256μg mL-1,3d pyrene-degrading rate of CP13was11.0%. It needed more erythromycin to inhibit CP13degrading pyrene than to inhibit GY2B degrading phenanthrene. GY2B and CP13cannot use erythromycin as the only carbon source to proliferate and PAHs content determined how long bacteria cells survived.