Toxic concentrations of metronidazole to Microcystis protocystis.

Antimicrobials are among the most commonly used drugs and have become a class of contaminants with great environmental importance. Metronidazole is an antimicrobial used for the therapeutic management of several human diseases. The toxicity of antimicrobials on aquatic species may affect sensitive microorganisms and reduce metabolic processes. Cyanobacteria is a group of organisms that are of great ecological importance in aquatic environments. Studies indicate that cyanobacteria are very sensitive to some antimicrobials. Therefore, it is necessary to evaluate the effects of metronidazole contamination on phytoplankton. The aim of this study was to investigate the effects of metronidazole on the growth of the cyanobacterium Microcystis protocystis and to evaluate the stability of this antimicrobial agent in the culture medium over a period of 96 hours. M. protocystis was resistant to growth inhibition by metronidazole. The EC50 of this antimicrobial for M. protocystis was 117.3 mg L(-1). Under the growth inhibition test conditions, neither a significant change in the MNZ concentration nor the presence of drug metabolites or degradation products was observed. These results indicate low cellular uptake of the antimicrobial agent and its persistence in the culture medium.

Involvement of membrane galactose in the in vivo and in vitro sequestration of desialylated erythrocytes.

The influence of terminal beta-galactose residues for the in vitro and in vivo sequestration of sialidase-treated erythrocytes by macrophages was investigated. Preincubation of rat peritoneal macrophages with galactose, oligosaccharides, glycoproteins and glycolipids with terminal beta-galactose residues inhibits both binding and phagocytosis of sialidase-treated erythrocytes by masking a beta-galactose-specific lectin on the macrophage cell membrane. These inhibition studies show that binding via demasked erythrocyte surface beta-galactosyl residues to this lectin is necessary for the subsequent phagocytosis step. According to these observations, repeated injections of lactose (30mM serum concentration) and asialo-fetuin (10-30 microM serum concentration) into the blood stream of rabbits led to a reduction of the rapid sequestration rate of sialidase-treated erythrocytes. Asialo-fetuin proved to be a much more potent inhibitor than lactose, in accordance with the in vitro experiments. This inhibition is reversible, as after the disappearance of the inhibitory effect, the sialidase-treated erythrocytes were again rapidly removed from the circulation to an extent similar to that of the experiments without inhibitors. No significant influence on binding and phagocytosis was measured in the presence of sialyllactose and native fetuin in vitro, or of native fetuin on sequestration in vivo. The experiments with rabbits show that a beta-galactosyl-specific lectin seems to be involved in the mechanism of sequestration of desialylated erythrocytes in vivo, as has been observed in vitro with rat peritoneal macrophages.