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This study was carried out to evaluate the occurrence of the fluoroquinolone antimicrobial agent ciprofloxacin (CIP) in the effluent of the Hospital of the Federal University of Santa Maria (HUSM). Measured environmental concentrations (MECs) of CIP in the hospital wastewater, both before (P1) and after (P2) cesspit/filter system treatment (CFTS), were determined by means of solid phase extraction and reversed-phase liquid chromatography with fluorescence detection (LC-FLD) and reversed-phase liquid chromatography with mass spectrometric detection (LC-MS/MS). The MECs (n = 7 daily composed samples) were 19 to 155 lg L -1 (average: 54 l 21 lg L -1) and 32 to 99 lg L -1 (average: 65 l 45 lg L -1 ) in P1 and P2, respectively. No relevant removal was observed from P1 to P2. In a worst case scenario, the final effluent was regarded as MECs of surface water. These MECs were generally 5 to 20,000-fold higher than what was previously known. If the present data is drawn on to form a model of the situation in developing countries, the picture provides a first rough indication that the environmental risk associated with the use and emission of pharmaceuticals into the environment in developing countries might be higher than in developed countries.

Dimercaprol is a compound used in the treatment of mercury intoxication, however with low therapeutic efficacy. It is assumed that dimercaprol acts by reactivating target sulfhydryl-containing proteins. In the present investigation we studied the inhibitory effect of mercuric chloride treatment (3 days with 2.3 or 4.6 mg/kg HgCl2, sc) in mice on cerebral, renal and hepatic delta-aminolevulinate dehydratase (ALA-D) activity, and a possible reversal of the effect of mercury by dimercaprol (0.25 mmol/kg, 24 hr after the last mercury injection). Mercuric chloride did not inhibit cerebral ALA-D at the doses injected. Dimercaprol treatment did not restore the normal enzyme activity of the liver after the 25% inhibition caused by 4.6 mg/kg HgCl2. In the kidney, dimercaprol enhanced the inhibitory effect of 4.6 mg/kg mercuric chloride (from 35% after mercury treatment alone to 65% after mercury plus dimercaprol treatment). Mercury content increased in kidney after exposure to 2.3 or 4.6 mg/kg and the levels attained were higher than in any other organ Mercury accumulated in liver only after exposure to 4.6 mg/kg HgCl2, and dimercaprol further increased mercury deposition. Dimercaprol treatment also increased the levels of mercury in brain of animals exposed to 4.6 mg/kg HgCl2 The enzymes from all sources presented similar sensitivity to the combined effect of HgCl2 and dimercaprol in vitro. In the absence of preincubation, 0-500 muM dimercaprol potentiated the inhibitory effect of HgCl2 on ALA-D activity. In the presence of preincubation, and 100 and 250 muM dimercaprol enhanced ALA-D sensitivity to mercury, whereas 500 muM dimercaprol partially protected the enzyme from mercury inhibition. Dimercaprol (500 muM) inhibited renal and hepatic ALA-D when preincubated with the enzymes. These data suggested that the dimercaprol-Hg complex may have a more toxic effect on ALA-D activity than Hg2+. Furthermore, the present data show that dimercaprol did not acts by reactivating mercury-inhibited sulfhydryl-containing ALA-D, and that indeed it may have an inhibitory effect per se depending on the tissue.

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