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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.


The variation of inactivation rate (A) and apoptotic cells (B) after DBD treated 3 minutes and delayed for different hours (a) the samples containing H2O2, (b) the samples discarding H2O2 and re-suspended in pure water.
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f7: The variation of inactivation rate (A) and apoptotic cells (B) after DBD treated 3 minutes and delayed for different hours (a) the samples containing H2O2, (b) the samples discarding H2O2 and re-suspended in pure water.

Mentions: Furthermore, we are also interested in the investigation of apoptosis of algal cell as observed with flow cytometry and confirmed by the apoptosis assays but essentially ignored in previous studies. The foregoing experiments prove that the H2O2 can cause the residual effect on M. aeruginosa, which includes both the direct inactivated dead cells and apoptotic cells. This result is consistent with the report by Ding30 that H2O2 can induce cell death and apoptosis. We also observed that the number of apoptotic cells also increased with delay time (Supplementary Fig. S7). This indicates that H2O2 plays a role in the apoptosis of M. aeruginosa. But it arouses the question whether all the apoptotic cells stem from extracellular H2O2 effect? To answer this question, we then carried out the following research, with the result as shown in Fig. 7. In the experiment, to exclude the H2O2 effect, we compared three kinds of samples: (a) the samples containing both algal cells and the DBD treated solution with the DBD produced H2O2; (b) the sample discarding the supernatant containing H2O2 and then re-suspended the algal cells with same volume pure water; and (c) the samples containing the untreated normal algal cells but suspended in the DBD treated sample’s supernatant. A schematic diagram for illustrating the preparation of these three kinds of samples is shown in Supplementary Figure S8. Then the three types of samples were examined for the residual inactivation effect, respectively. From the analysis of the samples (a, b and c), we can conclude that not only H2O2 contributes to the residual effect, but also the initial direct damage induced by DBD on the cells plays a considerable role. In the data analysis, the effect by sole H2O2 can be estimated by subtracting the inactivation efficiency of sample (b) from that of sample (a). Figure 7(A,B) illustrate the efficiencies of the direct inactivation and delayed inactivation vs. delay time, respectively. The insets in both Fig. 7(A,B) unambiguously demonstrate that more cells become dead and apoptotic without the presence of H2O2. This thus suggests that the initial even mild damage on the cells can also play an important role in the residual inactivation effect. Moreover, the comparison between the sample (a) and (c) reveals that the DBD treated sample is indeed more sensitive to H2O2 (Supplementary Fig. S9), which also verifies that the DBD-induced initial damage on the cells is partly responsible for the residual interaction effect.


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

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

The variation of inactivation rate (A) and apoptotic cells (B) after DBD treated 3 minutes and delayed for different hours (a) the samples containing H2O2, (b) the samples discarding H2O2 and re-suspended in pure water.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f7: The variation of inactivation rate (A) and apoptotic cells (B) after DBD treated 3 minutes and delayed for different hours (a) the samples containing H2O2, (b) the samples discarding H2O2 and re-suspended in pure water.
Mentions: Furthermore, we are also interested in the investigation of apoptosis of algal cell as observed with flow cytometry and confirmed by the apoptosis assays but essentially ignored in previous studies. The foregoing experiments prove that the H2O2 can cause the residual effect on M. aeruginosa, which includes both the direct inactivated dead cells and apoptotic cells. This result is consistent with the report by Ding30 that H2O2 can induce cell death and apoptosis. We also observed that the number of apoptotic cells also increased with delay time (Supplementary Fig. S7). This indicates that H2O2 plays a role in the apoptosis of M. aeruginosa. But it arouses the question whether all the apoptotic cells stem from extracellular H2O2 effect? To answer this question, we then carried out the following research, with the result as shown in Fig. 7. In the experiment, to exclude the H2O2 effect, we compared three kinds of samples: (a) the samples containing both algal cells and the DBD treated solution with the DBD produced H2O2; (b) the sample discarding the supernatant containing H2O2 and then re-suspended the algal cells with same volume pure water; and (c) the samples containing the untreated normal algal cells but suspended in the DBD treated sample’s supernatant. A schematic diagram for illustrating the preparation of these three kinds of samples is shown in Supplementary Figure S8. Then the three types of samples were examined for the residual inactivation effect, respectively. From the analysis of the samples (a, b and c), we can conclude that not only H2O2 contributes to the residual effect, but also the initial direct damage induced by DBD on the cells plays a considerable role. In the data analysis, the effect by sole H2O2 can be estimated by subtracting the inactivation efficiency of sample (b) from that of sample (a). Figure 7(A,B) illustrate the efficiencies of the direct inactivation and delayed inactivation vs. delay time, respectively. The insets in both Fig. 7(A,B) unambiguously demonstrate that more cells become dead and apoptotic without the presence of H2O2. This thus suggests that the initial even mild damage on the cells can also play an important role in the residual inactivation effect. Moreover, the comparison between the sample (a) and (c) reveals that the DBD treated sample is indeed more sensitive to H2O2 (Supplementary Fig. S9), which also verifies that the DBD-induced initial damage on the cells is partly responsible for the residual interaction 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.