End Of Uptake Period Research Articles

Accumulation, depuration and risk assessment of cadmium (Cd) and lead (Pb) in clam Corbicula fluminea (O. F. Müller, 1774) under laboratory conditions

The present study investigated the accumulation and depuration of two heavy metals Cd and Pb in the freshwater clam Corbicula fluminea under laboratory conditions. Treated clam was exposed to single and combined treatments of Cd and Pb at the concentration of 5 mg/L and 10.5 mg/L for 10 days, respectively. The animal was then placed in metal free water in the following 5 days for depuration experiment. Heavy metal concentrations were determined by an inductively coupled plasma optical emission spectrometer (ICP OES). The limit of detection (LOD) and recovery for Cd and Pb were 0.01, 0.06 µg/g WW, and 80, 83% respectively. Results showed that the clam was able to accumulate Cd and Pb at the maximum rate of 0.26 and 0.37 (µg/g/day), respectively; and depurates at the rate of 0.32 and 0.08 (µg/g/day), respectively. At the end of uptake period, the concentrations of Cd and Pb in the soft tissues of single and combined exposures were 1.8 and 1.1 µg/g wet weight (WW) and 1.2 and 0.8 µg/g WW, respectively. The clam also showed rapid depuration of Cd and Pb. At the end of depuration, the concentrations of Cd and Pb in the soft tissues were only 0.2 and 0.8 µg/g WW in single and 0.17 and 0.4 µg/g WW in combined exposure, respectively. The results of the present study also shown that there was a competition between Cd and Pb in the tissues of the clam. The total target hazard quotients and the hazard index indicated that people might experience adverse health effects through consuming contaminated C. fluminea.

Dietary exposure of American kestrels (Falco sparverius) to decabromodiphenyl ether (BDE-209) flame retardant: Uptake, distribution, debromination and cytochrome P450 enzyme induction

Accumulation and evidence of debromination of the flame retardant 2,2′,3,3′,4,4′,5,5′,6,6′-decabromodiphenyl ether (BDE-209) have been reported for biota, including raptorial birds, based on PBDE congener residues in tissues and eggs. However, in vivo studies with BDE-209-exposed birds are rare and unknown for a raptorial species. In the present study, males (n=22) of raptorial American kestrels (Falco sparverius) were exposed to 116,000ng of BDE-209 (high purity, >98%; in safflower oil) per day for 21days (~2,436,000ng total BDE-209 exposure over this uptake period), followed by a 25-day depuration period. Control males (n=11) received the safflower vehicle only. In the exposed birds, BDE-209 was quantifiable in all plasma (end of uptake and depuration period) as well as liver and fat (end of depuration only) samples. The mean (±SE) BDE-209 level in plasma was 1474±1145ng/g wet weight (ww) at the end of the uptake period, and was significantly (p<0.001) lower (88%) at 174±148ng/g ww after the 25day depuration period. This equates to a mean reduction rate of 52ng/g ww per day and a rough estimation of the BDE-209 half-life in plasma of approximately 14days. The mean (±SE) BDE-209 levels were 4668±6192ng/g ww in the fat, and 338±311ng/g ww in the liver, of exposed individuals, which were significantly (p≤0.001) greater than mean concentrations (25±20 in fat and 2.6±0.9ng/g ww in liver) in the control birds. In addition to BDE-209, lower brominated PBDE congeners, and mainly meta- and para-debromination products of BDE-209 were also quantified in plasma, liver and/or fat. We estimated based on the dose that at least 80% of the non-BDE-209 concentration in the kestrel tissues and plasma must be derived from BDE-209 debromination by the kestrels. Where quantifiable, lower brominated PBDE concentrations were significantly (0.023>p>0.001) higher in the exposed relative to the control bird samples (except for BDE-154 and -153 in fat). Additional PBDE congeners found in plasma included nona-BDEs (208, 207 and 206), followed by octa-BDEs (197, 196, 201 and 203), and in liver and/or fat, the hepta-BDEs 180 and 183 and BDE-153. Higher hepatic EROD activity (cytochrome P450 1A1 monooxygenase-mediation) in the exposed birds compared to control birds was strongly suggested to be PBDE-induced, and was consistent with BDE-209 and congener metabolism in the exposed kestrels. The mean EROD activity rate was 36.1pmol/min/mg protein relative to the (n=4) control birds whose activity was just above the detection limit (10.3pmol/min/mg protein). Overall, the results demonstrated that following diet exposure of kestrels to high purity BDE-209, uptake occurred as well as BDE-209 degradation via debromination to lower brominated PBDE congeners.

Nitrate Accumulation, Assimilation, and Transport by Decapitated Corn Roots

The effects of accumulated [(14)N]nitrate and its utilization in decapitated, 5-day-old dark-grown corn roots on influx, accumulation, xylem deposition, and reduction of concurrently absorbed nitrate during an 18-hour exposure to 0.5 millimolar K(15)NO(3) nutrient solution were examined. A 20-hour pretreatment in 15.0 millimolar K(14)NO(3) high nitrate (HN) resulted in a 2-fold greater tissue nitrate level than pretreatment in 0.5 millimolar K(14)NO(3) low nitrate (LN). Upon transfer to the 0.5 millimolar K(15)NO(3) solution, the net nitrate uptake rate in HN roots after 2 hours was 52% of the LN rate, but increased to 93% at the end of the uptake period. Despite an enhanced [(14)N]nitrate efflux from HN roots to the uptake solution, the efflux differences between the two pretreatments did not compensate for the decrease in net nitrate uptake. The [(15)N]nitrate influx rate was initially restricted by 33% in the HN roots compared to LN roots, but it had decreased to 7% by the end of the 18-hour uptake period. At this time, the total tissue nitrate levels were similar for both pretreatments. The rate of accumulation of [(15)N]nitrate in the tissue was relatively constant for both pretreatments, but was 25% less in HN roots. Of the previously accumulated [(14)N]nitrate, 52 and 46% remained after 18 hours in the LN and HN roots, respectively. The [(14)N]nitrate decline for HN roots was initially more rapid than in the LN roots which was linear over time. Xylem transport and efflux more than accounted for the decline in [(14)N]nitrate of LN roots and all but 4% in the HN roots which was attributed to reduction. Compartmentation of the previously accumulated nitrate was evident from the higher atom per cent (15)N of xylem nitrate compared to that of the tissue nitrate of both LN and HN roots. During the first 2 hours, xylem transport of [(14)N]nitrate by the HN roots was 49% greater than for LN roots, while [(15)N]nitrate transport was 9% less in HN roots compared to LN roots. Even though the reduction of [(15)N]nitrate in HN roots was 31% less than LN roots during the first 2 hours, [(15)N]nitrate was reduced more rapidly than the previously accumulated [(14)N]nitrate. After the first 4 hours, the relative partitioning of absorbed [(15)N]nitrate between accumulation, reduction, and translocation was similar regardless of pretreatment.