Molt-Related Sensitivity of Daphnia pulex in Toxicity Testing

1979 ◽  
Vol 36 (9) ◽  
pp. 1129-1133 ◽  
Author(s):  
David Robert Lee ◽  
Arthur L. Buikema Jr.

Continuous and short-term exposures of Daphnia pulex to 0.56 mg Cr/L showed that these animals undergo cyclic changes in susceptibility. Short-term exposure (2 h) followed by transfer to clean water for 22 h resulted in significantly higher mortality for individuals that molted during exposure. Continuous exposure to chromate resulted in significantly shorter mean survival times for animals that had molted < 4 h before being placed in chromate solution. Because laboratory cultures can be synchronized with respect to molting, the effects of cyclic sensitivity can bias bioassay results. By examining the animals at the beginning of the test, the degree of synchrony can be determined and appropriate steps taken. Key words: bioassay, Daphnia pulex, chromium toxicity, molting

1975 ◽  
Vol 5 (3) ◽  
pp. 419-423 ◽  
Author(s):  
Carey Borno ◽  
Iain E. P. Taylor

Stratified, imbibed Douglas fir (Pseudotsugamenziesii (Mirb.) Franco) seeds were exposed to 100% ethylene for times between 0 and 366 h. Germination rate and germination percentage were increased by treatments up to 48 h. The 12-h treatment gave largest stimulation; 30% enhancement of final germination percentage over control. Treatment for 96 h caused increased germination rate for the first 5 days but reduced the germination percentage. Germinants were subject to continuous exposure to atmospheres containing 0.1 – 200 000 ppm ethylene in air, but it did not stimulate growth, and the gas was inhibitory above 100 ppm. Although some effects of high concentrations of ethylene may have been due to the lowering of oxygen supplies, this alone was insufficient to account for the full inhibitory effect. The mechanism of stimulation by short-term exposure to ethylene is discussed.


2018 ◽  
Vol 204 ◽  
pp. 1-8 ◽  
Author(s):  
Zhiquan Liu ◽  
Mingqi Cai ◽  
Ping Yu ◽  
Minghai Chen ◽  
Donglei Wu ◽  
...  

Blood ◽  
1999 ◽  
Vol 94 (9) ◽  
pp. 3121-3128 ◽  
Author(s):  
Marianne G. Rots ◽  
Rob Pieters ◽  
Godefridus J. Peters ◽  
Christina H. van Zantwijk ◽  
Rob Mauritz ◽  
...  

Abstract Cellular methotrexate (MTX) resistance may cause treatment failure in childhood common/preB-acute lymphoblastic leukemia (c/preB-ALL), T-lineage ALL (T-ALL), and acute myeloid leukemia (AML). The ex vivo potency of several antifolates (MTX, trimetrexate [TMQ], GW1843U89, multitargeted antifolate [MTA], Raltitrexed, and ZD9331) was studied via in situ inhibition of thymidylate synthase (TS). After short-term exposure, relapsed c/preB-ALL (rALL, n = 21), T-ALL (n = 22), and AML (n = 22) were 3-fold, 10-fold, and 6-fold less sensitive to MTX (P ≤ .01) compared with initial c/preB-ALL (n = 43). This difference in resistance was not observed for TMQ. Also for GW1843U89 and MTA, no resistance was observed in rALL and AML compared with c/preB-ALL. T-ALL compared with c/preB-ALL tended to be less resistant to GW1843U89 (3-fold) and MTA (6-fold) than to MTX (10-fold) (P= .06). Raltitrexed was more active against c/preB-ALL compared with the other subtypes. After 21 hours continuous incubation, T-ALL and AML samples were equally sensitive as c/preB-ALL to MTX, but rALL was 3-fold resistant to MTX compared with initial c/preB-ALL (P = .003). The resistance of rALL was circumvented by TMQ (1-fold; P = .03) and GW1843U89 (1.4-fold; P= .004). Novel antifolates, except MTA, displayed a more potent TS inhibition than MTX during continuous exposure. These results suggest that MTX resistance in AML and T-ALL can be circumvented by continuous exposure, and that novel antifolates should be explored further for MTX-resistant T-ALL, rALL, and AML cells.


Blood ◽  
1999 ◽  
Vol 94 (9) ◽  
pp. 3121-3128 ◽  
Author(s):  
Marianne G. Rots ◽  
Rob Pieters ◽  
Godefridus J. Peters ◽  
Christina H. van Zantwijk ◽  
Rob Mauritz ◽  
...  

Cellular methotrexate (MTX) resistance may cause treatment failure in childhood common/preB-acute lymphoblastic leukemia (c/preB-ALL), T-lineage ALL (T-ALL), and acute myeloid leukemia (AML). The ex vivo potency of several antifolates (MTX, trimetrexate [TMQ], GW1843U89, multitargeted antifolate [MTA], Raltitrexed, and ZD9331) was studied via in situ inhibition of thymidylate synthase (TS). After short-term exposure, relapsed c/preB-ALL (rALL, n = 21), T-ALL (n = 22), and AML (n = 22) were 3-fold, 10-fold, and 6-fold less sensitive to MTX (P ≤ .01) compared with initial c/preB-ALL (n = 43). This difference in resistance was not observed for TMQ. Also for GW1843U89 and MTA, no resistance was observed in rALL and AML compared with c/preB-ALL. T-ALL compared with c/preB-ALL tended to be less resistant to GW1843U89 (3-fold) and MTA (6-fold) than to MTX (10-fold) (P= .06). Raltitrexed was more active against c/preB-ALL compared with the other subtypes. After 21 hours continuous incubation, T-ALL and AML samples were equally sensitive as c/preB-ALL to MTX, but rALL was 3-fold resistant to MTX compared with initial c/preB-ALL (P = .003). The resistance of rALL was circumvented by TMQ (1-fold; P = .03) and GW1843U89 (1.4-fold; P= .004). Novel antifolates, except MTA, displayed a more potent TS inhibition than MTX during continuous exposure. These results suggest that MTX resistance in AML and T-ALL can be circumvented by continuous exposure, and that novel antifolates should be explored further for MTX-resistant T-ALL, rALL, and AML cells.


1976 ◽  
Vol 36 (01) ◽  
pp. 221-229 ◽  
Author(s):  
Charles A. Schiffer ◽  
Caroline L. Whitaker ◽  
Morton Schmukler ◽  
Joseph Aisner ◽  
Steven L. Hilbert

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.


2016 ◽  
Vol 307 ◽  
pp. 137-144 ◽  
Author(s):  
Gaëtan Philippot ◽  
Fred Nyberg ◽  
Torsten Gordh ◽  
Anders Fredriksson ◽  
Henrik Viberg

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