The Role of Wastewater Treatment Plants in the Environmental Dissemination of Antibiotic Resistant Bacteria (ARB) and Resistance Genes (ARG)

This study was conducted to evaluate the influence of wastewater treatment processes on the prevalence of antibiotic resistance fecal coliform (FC) and antibiotic resistance genes (ARGs) of FC. In addition, the occurrence of antibiotic resistant bacteria (ARB) and antibiotic resistant genes (ARGs) in surface waters receiving wastewater was evaluated. Greater resistance against penicillin (P), colisitin (CT) and ampicillin (AMP) were observed for FC isolated from effluent disinfected by chlorine (71%), than that disinfected by UV (45%). The greatest resistance against six antibiotics was recorded for FC isolates from effluent disinfected by chlorine. The prevalence of tetB and blaSHV was lowest in isolates from chlorine-disinfected effluents. The occurrence of ARG blaSHV was highest in FC isolated from effluent disinfected by UV. A significant correlation was recorded between FC levels in surface waters and the level of bacterial resistance to ampicillin (P SHV in effluents and in surface waters. TetA and tetC were highly prevalent in surface water compared to tetB. The results of the study demonstrate the widespread prevalence of ARB and ARG in wastewater and receiving water bodies. The result indicates that the source of ARB and ARG in surface waters originate from wastewater. Released ARB and ARG may serve as the source of ARG to pathogenic bacteria in surface waters. Disinfection processes may influence the selection of antibiotic resistant patterns of bacteria.

Protein kinase A inhibition induces EPAC-dependent acrosomal exocytosis in human sperm

To in teract with the egg, the spermatozo on must un dergo several biochemical and motility modifications in the female reproductive tract, collectively called capacitation. Only capacitated sperm can undergo acrosomal exocytosis, near or on the egg, a process that allows the sperm to penetrate and fertilize the egg. In the present study, we investigated the invoIvement of cyclic adenosine monophosphate (cAMP)-dependent processes on acrosomal exocytosis. Inhibition of protein kinase A (PKA) at the end of capacitation induced acrosomal exocytosis. This process is cAMP-dependent;however, the addition of relatively high concentration of the membrane-permeable 8-bromo-cAMP (8Br-cAMP, 0.1 mmol l^-1) analog induced significant inhibition of the acrosomal exocytosis. The induction of acrosomal exocytosis by PKA inhibition was significantly inhibited by an exchange protein directly activated by cAMP (EPAC) ESI09 inhibitor. The EPAC selective substrate activated AE at relatively low concentrations (0.02-0.1 μmol l^1), whereas higher concerttrations (>5 pmol l^-1) were inhibitory to the AE induced by PKA inhibition. Inhibition of PKA revealed about 50% increase in intracellular cAMP levels, conditions under which EPAC can be activated to induce the AE. Induction of AE by activating the actin severing?protein, gelsolin, which causes F-actin dispersion, was inhibited by the EPAC inhibitor. The AE induced by PKA inhibition was mediated by phospholipase C activity but not by the Ca^2+-channel, CatSper. Thus, inhibition of PKA at the end of the capacitation process induced EPAC/phospholipase C-dependent acrosomal exocytosis. EPAC mediates F-actin depolymerization an d/or activation of effectors down stream to F-actin breakdown that lead to acrosomal exocytosis.