Biomonitoring of selenoprotein P in human serum by fast affinity chromatography coupled to ICP-MS

Most of the Se in human serum is bound to selenoprotein P (SEPP1) in which Se is present in form of selenocysteine. The SEPP1 is a new possible biomarker for the Se status and for this reason we developed a fast, simple and reliable method for the quantitative determination of SEPP1 in serum by affinity chromatography coupled to ICP-MS. It is possible to separate SEPP1 from other selenoproteins in serum in only 5?min, which allows high sample throughput in clinical laboratories. Measured and certified concentrations of total Se and Se(SEPP1) are in good agreement for the reference material SRM 1950. The SEPP1 concentration was stable in serum samples of 3 persons for a minimum of 2 weeks. Further results of method validation were described including internal and external quality assurance.The analytical method was applied for a biomonitoring study of the SEPP1 and total Se concentration in human serum of 50 occupationally non-exposed persons living in northern Germany. Concentration ranges and mean concentrations for Se(SEPP1) are 31.1–59.7 and 46.2?μg/L, respectively. The corresponding values for total Se are 62–120 and 83.5?μg/L. The mean percentage of total Se in serum present as SEPP1 is 58%.     

Deficits in trace fear conditioning in a rat model of fetal alcohol exposure: dose–response and timing effects

In humans, prenatal alcohol exposure can result in significant impairments in several types of learning and memory, including declarative and spatial memory. Animal models have been useful for confirming that many of the observed effects are the result of alcohol exposure, and not secondary to poor maternal nutrition or adverse home environments. Wagner and Hunt (2006) reported that rats exposed to ethanol during the neonatal period (postnatal days [PDs] 4–9) exhibited impaired trace fear conditioning when trained as adolescents, but were unaffected in delay fear conditioning. The present series of three experiments represent a more detailed analysis of ethanol-induced deficits in trace conditioning. In Experiment 1, the dose of ethanol given to neonates was varied (3.0, 4.0, or 5.0 g/kg/day). There was a dose-dependent reduction in trace conditioning, with the poorest performance observed in animals treated with the highest dose. In Experiment 2, it was found that the impairment in trace conditioning resulting from neonatal ethanol exposure was dependent on the duration of the trace interval used for training; less learning was evident in ethanol-exposed animals trained with longer trace interval durations. These results confirm other reports of delay-dependent memory deficits. Finally, Experiment 3 determined that ethanol exposure limited to the first half of the neonatal period (PDs 4–6) was more detrimental to later trace conditioning than exposure during the second half (PDs 7–9). These results support the hypothesis that trace-conditioning impairments resulting from early ethanol exposure are due to the drug's teratogenic effects on the developing hippocampus, as the findings parallel those observed in animals with discrete hippocampal lesions. Comparisons between delay and trace fear-conditioning performance in animals exposed to ethanol during the brain growth spurt provide a model system to study both selective learning impairments and possible treatment approaches for humans with fetal alcohol spectrum disorders.     

Induction and localization of hepatic CYP4501A in flounder and rainbow trout exposed to benzo[a]pyrene

The hepatic detoxification system in Baltic flounder and rainbow trout was characterized under experimental conditions. Fish were exposed to benzo[a]pyrene (BaP, 10 and 50mg/kg, ip) or vehicle for 2, 5, and 10 days (in rainbow trout also for 20 days) and then sacrificed. Control fish were sampled at days 0 and 10 (flounder) or day 20 (rainbow trout). The hepatic distribution of CYP1A was analyzed immunohistochemically and microsomal ethoxyresorufin O-deethylase activity was determined spectrophotometrically. The kinetics of the CYP1A responses (EROD) was similar in both species, while a species-specific difference in the magnitude of the response was observed. CYP1A was demonstrated in the hepatocytes in both fish species 2 days after BaP administration and throughout the experiment. In rainbow trout a CYP1A response in the vascular endothelium of liver parenchyma was detected 2 days postadministration, while the corresponding reaction in flounder was seen 5 days postadministration. Thus, our results confirm previous reports that the CYP1A response is species specific. Furthermore, the induction of hepatic CYP1A in Baltic flounder reflects pathophysiological effects induced by polycyclic aromatic hydrocarbon compounds and, consequently, is a parameter useful when monitoring the anthropogenic effects on the Baltic Sea environment.