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New insight into the residual inactivation of Microcystis aeruginosa by dielectric barrier discharge.

Li L, Zhang H, Huang Q - Sci Rep (2015)

Bottom Line: Our results showed that the numbers of both dead and apoptotic cells increased with DBD treatment delay time, and hydrogen peroxide produced by DBD was the main reason for the time-delayed inactivation effect.However, apart from the influence of hydrogen peroxide, the DBD-induced initial injures on the algal cells during the discharge period also played a considerable role in the inactivation of the DBD treated cells, as indicated by the measurement of intracellular reactive oxygen species (ROS) inside the algal cells.We therefore propose an effective approach to utilization of non-thermal plasma technique that makes good use of the residual inactivation effect to optimize the experimental conditions in terms of discharge time and delay time, so that more efficient treatment of cyanobacterial blooms can be achieved.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Ion Beam Bio-engineering, Institute of Biotechnology and Agriculture Engineering, Hefei Institutes of Physical Science, Chinese Academy of Sciences, 230031.

ABSTRACT
We report the new insight into the dielectric barrier discharge (DBD) induced inactivation of Microcystis aeruginosa, the dominant algae which caused harmful cyanobacterial blooms in many developing countries. In contrast with the previous work, we employed flow cytometry to examine the algal cells, so that we could assess the dead and living cells with more accuracy, and distinguish an intermediate state of algal cells which were verified as apoptotic. Our results showed that the numbers of both dead and apoptotic cells increased with DBD treatment delay time, and hydrogen peroxide produced by DBD was the main reason for the time-delayed inactivation effect. However, apart from the influence of hydrogen peroxide, the DBD-induced initial injures on the algal cells during the discharge period also played a considerable role in the inactivation of the DBD treated cells, as indicated by the measurement of intracellular reactive oxygen species (ROS) inside the algal cells. We therefore propose an effective approach to utilization of non-thermal plasma technique that makes good use of the residual inactivation effect to optimize the experimental conditions in terms of discharge time and delay time, so that more efficient treatment of cyanobacterial blooms can be achieved.

No MeSH data available.


H2O2 concentration after DBD treatment for different discharge times.The measurements were repeated for three times.
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f4: H2O2 concentration after DBD treatment for different discharge times.The measurements were repeated for three times.

Mentions: This delayed inactivation is also called residual inactivation effect, which is ascribed to hydrogen peroxide generated from the DBD treatment. To verify this, we measured the change of hydrogen peroxide vs. discharge time, as shown in Fig. 4. It shows that H2O2 concentration can be raised up to 8 mM in the DBD treated sample’s supernatant solution for discharge time at 8 min. With H2O2 produced in solution, the living cells can be continuously inactivated. Figure 5 shows the quantitative analysis of residual inactivation based on the flow cytometry assessment method (Supplementary Fig. S5 and Fig. S6). Figure 5(A) shows that the inactivation rate increases with the prolongation of delay time, where the samples were harvested with different DBD treatment time and delay time. Besides, it shows that when discharge time is less than 2 min, the residual inactivation effect is not pronounced. In addition, we also took the DBD treated algal cells out of the DBD-treated solution, re-suspended them in pure water, and then measured the residual inactivation rate, with the result presented in Fig. 5(B). It shows no significant change of inactivation rate with delay time, further confirming that H2O2 plays the role in the residual inactivation effect.


New insight into the residual inactivation of Microcystis aeruginosa by dielectric barrier discharge.

Li L, Zhang H, Huang Q - Sci Rep (2015)

H2O2 concentration after DBD treatment for different discharge times.The measurements were repeated for three times.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4561898&req=5

f4: H2O2 concentration after DBD treatment for different discharge times.The measurements were repeated for three times.
Mentions: This delayed inactivation is also called residual inactivation effect, which is ascribed to hydrogen peroxide generated from the DBD treatment. To verify this, we measured the change of hydrogen peroxide vs. discharge time, as shown in Fig. 4. It shows that H2O2 concentration can be raised up to 8 mM in the DBD treated sample’s supernatant solution for discharge time at 8 min. With H2O2 produced in solution, the living cells can be continuously inactivated. Figure 5 shows the quantitative analysis of residual inactivation based on the flow cytometry assessment method (Supplementary Fig. S5 and Fig. S6). Figure 5(A) shows that the inactivation rate increases with the prolongation of delay time, where the samples were harvested with different DBD treatment time and delay time. Besides, it shows that when discharge time is less than 2 min, the residual inactivation effect is not pronounced. In addition, we also took the DBD treated algal cells out of the DBD-treated solution, re-suspended them in pure water, and then measured the residual inactivation rate, with the result presented in Fig. 5(B). It shows no significant change of inactivation rate with delay time, further confirming that H2O2 plays the role in the residual inactivation effect.

Bottom Line: Our results showed that the numbers of both dead and apoptotic cells increased with DBD treatment delay time, and hydrogen peroxide produced by DBD was the main reason for the time-delayed inactivation effect.However, apart from the influence of hydrogen peroxide, the DBD-induced initial injures on the algal cells during the discharge period also played a considerable role in the inactivation of the DBD treated cells, as indicated by the measurement of intracellular reactive oxygen species (ROS) inside the algal cells.We therefore propose an effective approach to utilization of non-thermal plasma technique that makes good use of the residual inactivation effect to optimize the experimental conditions in terms of discharge time and delay time, so that more efficient treatment of cyanobacterial blooms can be achieved.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Ion Beam Bio-engineering, Institute of Biotechnology and Agriculture Engineering, Hefei Institutes of Physical Science, Chinese Academy of Sciences, 230031.

ABSTRACT
We report the new insight into the dielectric barrier discharge (DBD) induced inactivation of Microcystis aeruginosa, the dominant algae which caused harmful cyanobacterial blooms in many developing countries. In contrast with the previous work, we employed flow cytometry to examine the algal cells, so that we could assess the dead and living cells with more accuracy, and distinguish an intermediate state of algal cells which were verified as apoptotic. Our results showed that the numbers of both dead and apoptotic cells increased with DBD treatment delay time, and hydrogen peroxide produced by DBD was the main reason for the time-delayed inactivation effect. However, apart from the influence of hydrogen peroxide, the DBD-induced initial injures on the algal cells during the discharge period also played a considerable role in the inactivation of the DBD treated cells, as indicated by the measurement of intracellular reactive oxygen species (ROS) inside the algal cells. We therefore propose an effective approach to utilization of non-thermal plasma technique that makes good use of the residual inactivation effect to optimize the experimental conditions in terms of discharge time and delay time, so that more efficient treatment of cyanobacterial blooms can be achieved.

No MeSH data available.