TY - JOUR
T1 - Combined impact of silver nanoparticles and chlorine on the cell integrity and toxin release of Microcystis aeruginosa
AU - Singh, Abhishek
AU - Hou, Wen Che
AU - Lin, Tsair Fuh
N1 - Funding Information:
A.S. gratefully acknowledges the financial support from National Cheng Kung University. This work was supported by the Taiwan Ministry of Science and Technology ( MOST 107-2221-E-006-195-MY3).
Funding Information:
TEM images of 0.6 mg/L AgNPs after 20 min of exposure to NaOCl (0.2–0.6 mg/L) with and without M. aeruginosa are shown in Fig. 3. At low NaOCl level (0.2 mg/L, Fig. 3a and (d)) the shape of AgNP appears to be irregular. In comparison, the AgNP looks fragmented and smaller in size (Fig. 3b and (e)), and it further fragments into smaller pieces as seen in Fig. 3c and (f). On the contrary, there was no change in the morphology of AgNPs in the NR water only (Fig. S6). A previous study looking into the reactions of AgNPs with NaOCl, hydrogen peroxide, and potassium permanganate have found changes in the morphology of AgNPs (Qin et al., 2018). However, the previous study did not mention any fragmentation of AgNPs, possibly due to different experimental conditions from the present study. The TEM images (Fig. 3) reveal changes in the morphology of the AgNPs after reacting with the NaOCl, thus supporting that the dissolution of AgNPs occurs in the presence of NaOCl.The release and degradation of MCs were measured for all samples at 20 min to see whether the presence of AgNPs could change MCs levels in the present study. AgNPs may cause potential biases in ELISA methods (Petersen et al., 2020), but in the current study interferences from AgNPs (Fig. S8) was minimal. Fig. 5 shows the release and oxidation of MCs under individual and combined levels (0.2–0.4 mg/L) of AgNPs and NaOCl. The level of intracellular (IC) MCs in NR water prior to any exposure (i.e. control) was 4.8 μg/L. In comparison, the extracellular (EC) MCs (the difference between total and intracellular MCs) was 0.28 μg/L (5.1 μg/L total MCs). For NaOCl only samples, the IC MCs were reduced by around 48% (0.2 mg/L) and 95% (0.4–0.6 mg/L). In comparison the EC MCs increased to 2.8, 1.9 and 0.4 μg/L for 0.2, 0.4, and 0.6 mg/L NaOCl, respectively. The AgNPs (0.2–0.6 mg/L) only M. aeruginosa samples saw negligible changes in MCs (IC = 4.5–4.8 μg/L, and EC = 0.25–0.30 μg/L) levels compared to the control sample. The MCs level for AgNP + 0.2 mg/L NaOCl decreased by 47%, 60%, and 81% for IC MCs with increasing AgNPs from 0.2 to 0.6 mg/L, while the EC MCs increased to 2.7, 3.0, and 3.6 μg/L for 0.2, 0.4 and 0.6 mg/L AgNP, respectively. In case for 0.2–0.6 mg/L AgNP + 0.4 mg/L NaOCl samples, the IC MCs were reduced to ≤ 0.16 μg/L, while the EC toxin level was between 1.9 and 2.15 μg/L. Finally for 0.2–0.6 mg/L AgNP + 0.6 mg/L NaOCl samples, the IC MCs were reduced to ≤ 0.15 μg/L (ND at 0.6 mg/L AgNP and NaOCl) while the EC toxin level was between 0.38 and 0.52 μg/L. The observed toxin (IC and EC) released here also supports the percentage of cell lysis seen (Fig. 1) at various NaOCl levels. The lowest NaOCl (0.2 mg/L) dosage with AgNPs caused a significant release of IC MCs but not able to oxidize it, thus resulting in increased detection of EC MCs. The reason behind this seems to be the complete consumption of free chlorine (Fig. S5), as the free chlorine is responsible for the oxidation of MCs (Fan et al., 2016; Lin et al., 2009). At 0.4 mg/L NaOCl, almost all the IC MCs were released (total MCs = 2.0–2.4 μg/L) as it was evident that nearly all total MCs were measured as EC. Hence, at 0.4 mg/L NaOCl, the MCs were rapidly degraded but not completely removed (<1 μg/L). This aspect might be due to chlorine residual (Fig. S5) being insufficient to rapidly remove the dissolved toxin within 20 min (Lin et al., 2009). In contrast, complete toxin release and its degradation (total MCs = 0.57–0.52 μg/L) below the WHO threshold value (1 μg/L MC for drinking water) can be seen at the highest 0.6 mg/L NaOCl for all the samples. It is clear from Fig. S5 that enough residual free chlorine was available (0.6 mg/L NaOCl) after rapidly oxidizing cells, AgNPs, and MCs. Moreover, it was observed earlier that released Ag+ also helped in cell lysis, so this might leave more available NaOCl to react with the MCs. Previous studies have also shown complete removal of MCs at higher free available chlorine dosages (Fan et al., 2016; Zamyadi et al., 2013). Hence, it is clear the AgNP/Ag+ have a role in the release of MCs by helping NaOCl in faster cell lysis, but NaOCl was also responsible for reducing the MCs in the AgNP + NaOCl systems.A.S. gratefully acknowledges the financial support from National Cheng Kung University. This work was supported by the Taiwan Ministry of Science and Technology (MOST 107-2221-E-006-195-MY3).
Publisher Copyright:
© 2021 Elsevier Ltd
PY - 2021/6
Y1 - 2021/6
N2 - Silver nanoparticles (AgNPs) have shown to be toxic to freshwater cyanobacterial species, and sodium hypochlorite (NaOCl) is a common oxidant for the treatment of cyanobacterial cells. AgNPs have a high possibility of co-existing with the cyanobacterial cells in the aqueous environments leading to its exposure to NaOCl during water treatment; however, their combined effects on the cyanobacterial cells are largely undocumented. This work compares the individual and combined effect of AgNP and NaOCl on the integrity and toxin (microcystins) release of Microcystis aeruginosa at varying levels. The results show that the AgNP (0.2–0.6 mg/L) alone has negligible effects on the cell lysis, while NaOCl alone shows concentration-dependent (0.2 < 0.4 < 0.6 mg/L) rupturing of cells. In contrast, the AgNP + NaOCl (0.2–0.6 mg/L) samples show increasing loss in cell integrity at higher AgNP (0.4 and 0.6 mg/L) levels than the NaOCl only samples. NaOCl exposure results in increasing dissolution of AgNPs with time, releasing silver ions (Ag+), affecting its size and morphology. The cell-associated total Ag declines over time with an increase in NaOCl levels, maybe due to increasing cell-lysis or NaOCl induced oxidative dissolution of AgNPs. The cell-associated total Ag and released Ag+ possibly weaken the cellular membrane, thus assisting NaOCl in faster cell-lysis. The combined exposure of AgNP and NaOCl also results in a higher release of toxin from the cells. This work collectively reveals that the AgNPs combined with NaOCl can enhance the cell lysis and release of toxins.
AB - Silver nanoparticles (AgNPs) have shown to be toxic to freshwater cyanobacterial species, and sodium hypochlorite (NaOCl) is a common oxidant for the treatment of cyanobacterial cells. AgNPs have a high possibility of co-existing with the cyanobacterial cells in the aqueous environments leading to its exposure to NaOCl during water treatment; however, their combined effects on the cyanobacterial cells are largely undocumented. This work compares the individual and combined effect of AgNP and NaOCl on the integrity and toxin (microcystins) release of Microcystis aeruginosa at varying levels. The results show that the AgNP (0.2–0.6 mg/L) alone has negligible effects on the cell lysis, while NaOCl alone shows concentration-dependent (0.2 < 0.4 < 0.6 mg/L) rupturing of cells. In contrast, the AgNP + NaOCl (0.2–0.6 mg/L) samples show increasing loss in cell integrity at higher AgNP (0.4 and 0.6 mg/L) levels than the NaOCl only samples. NaOCl exposure results in increasing dissolution of AgNPs with time, releasing silver ions (Ag+), affecting its size and morphology. The cell-associated total Ag declines over time with an increase in NaOCl levels, maybe due to increasing cell-lysis or NaOCl induced oxidative dissolution of AgNPs. The cell-associated total Ag and released Ag+ possibly weaken the cellular membrane, thus assisting NaOCl in faster cell-lysis. The combined exposure of AgNP and NaOCl also results in a higher release of toxin from the cells. This work collectively reveals that the AgNPs combined with NaOCl can enhance the cell lysis and release of toxins.
UR - http://www.scopus.com/inward/record.url?scp=85103104759&partnerID=8YFLogxK
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U2 - 10.1016/j.chemosphere.2021.129825
DO - 10.1016/j.chemosphere.2021.129825
M3 - Article
C2 - 35534960
AN - SCOPUS:85103104759
SN - 0045-6535
VL - 272
JO - Chemosphere
JF - Chemosphere
M1 - 129825
ER -