Lipid regulators are among the most prescribed human pharmaceuticals worldwide. Gemfibrozil, which belongs to this class of pharmaceuticals, is one of the most frequently encountered in the aquatic environment. However, there is limited information concerning the mechanisms involved in gemfibrozil effects to aquatic organisms, particularly to marine organisms. Based on this knowledge gap, the current study aimed to assess biochemical and behavioral effects following a sublethal exposure to gemfibrozil (1.5, 15, 150, 1500 and 15,000 μg L-1) in the estuarine/marine fish Sparus aurata. After the exposure to 1.5 μg L-1 of gemfibrozil, fish had reduced ability to swim against a water flow and increased lipid peroxidation in the liver. At concentrations between 15-15,000 μg L-1, the activities of some enzymes involved in antioxidant defense were induced, appearing to be sufficient to prevent oxidative damage. Depending on the organ, different responses to gemfibrozil were displayed, with enzymes like catalase being more stimulated in gills, whereas glutathione peroxidase was more activated in liver. Although there were no obvious concentration-response relationships, the integrated biomarker response version 2 (IBRv2) analysis revealed that the highest concentrations of gemfibrozil (between 150-15,000 μg L-1) caused more alterations. All the tested concentrations of gemfibrozil induced effects in S. aurata, in terms of behavior and/or oxidative stress responses. Oxidative damage was found at a concentration that is considered environmentally relevant, suggesting a potential of this pharmaceutical to impact fish populations.

One hundred twelve fecal samples of healthy children were recovered in Portugal during October 2007 and February 2008 and were tested for extended-spectrum β-lactamases (ESBLs) containing Escherichia coli isolates and vancomycin-resistant enterococci (VRE). Three of the 112 fecal samples (2.7%) harbored ESBL-positive E. coli isolates and the bla _CTX-M-1 , bla _TEM-52 , and bla _SHV-12 genes were identified in these isolates. The bla _TEM-52 -containing isolate showed a phenotype of multiresistance that included fluoroquinolones, tetracycline, trimethoprim–sulfamethoxazole, and chloramphenicol; sul 1, sul 3, and cml A genes were detected in this isolate, in addition to two amino acid changes in GyrA (Ser83Leu + Asp87Asn) and one in ParC protein (Ser80Ile). The ESBL isolates corresponded to phylogroup A (one isolate), B1 (one isolate), and D (one isolate). van A-containing Escherichia faecium isolates were detected in 13 of the 112 fecal samples (11.6%), and van C-1 isolates were found in 2 samples. A diversity of resistance genes [( tet (M), tet (L), erm (B), aph (3′)-IIIa, ant (6)-Ia, cat A, and vat (E)] were found in VRE isolates. These results show that the intestinal tract of healthy children constitutes a reservoir of ESBL-containing E. coli and VRE isolates.