Enhanced suppression effects on Microcystis aeruginosa by combining hydrogen peroxide and intermittent UVC irradiation: the importance of triggering advanced oxidation process within cells

• Published in: Journal of hazardous materials 2024-02, Vol.463, p.132826, Article 132826
• Main Authors: Zheng, Jie, Teng, Fei, Zhou, Tingru, Cao, Huansheng, Wang, Xuejian, Zhu, Yinjie, Tao, Yi
• Format: Article
• Language: English
• Subjects: Apoptosis-like cell death; Hydrogen peroxide; Microcystis aeruginosa; Reactive oxygen species; Ultraviolet-C irradiation
• ISSN: 0304-3894; 1873-3336; 1873-3336
• DOI: 10.1016/j.jhazmat.2023.132826

In order to strengthen the inhibitory effect of UVC/H2O2 on Microcystis aeruginosa growth, this study designed a novel strategy for inducing an advanced oxidation process in algal cells by splitting UVC irradiation into two rounds. The first irradiation of UVC upon adding H2O2 facilitated the delivery of H2O2 into the cell cytoplasm, which induced an intracellular advanced oxidation process after the second irradiation of UVC. The intermittent treatment of UVC/H2O2 could further attack the Ca-Mn and Fe-S clusters in the photosynthetic electron transport chain. In contrast, conventional simultaneous treatment of UVC/H2O2 only attacked the interaction subunits between PSII cores and the phycobilisome. The block of the photosynthetic electron transport chain, shedding of the Ca-Mn cluster, and damage of the Fe-S cluster gave rise to massive intracellular H2O2, O2•−, and HO•. Consequently, ROS acted as a mediator and led to caspase-3(-like) activation and the subsequent initiation of apoptosis-like cell death. The remarkable functional mechanisms make the intermittent treatment of UVC/H2O2 an ideal method for the practical application of suppressing HABs (target-selective, long-lasting, cost-minimized, and eco-friendly). Microcystis aeruginosa blooms frequently occur worldwide and cause severe damage. Most reported algicides are known to cause growth inhibition and cell death by generating oxidative radicals in water as massive extracellular oxidative stress. In the present study, an intermittent treatment of UVC/H2O2 was introduced to enhance the intracellular oxidative stress in Microcystis cells significantly. UV light and hydrogen peroxide can cross the cell membrane and produce radicals inside the cells. The strain from UV, hydrogen peroxide, and radicals attack the Ca-Mn cluster and Fe-S cluster in the photosynthetic electron transport chain and causes damage to the interaction subunits between PSII and phycobilisome. Due to the complete disruption of the photosynthetic system, ROS were unavoidably produced when the absorption of light energy by the phycobilisome exceeds the capacity for photochemical transformation. Therefore, the photodamage of both PSII and PSI can cause long-lasting cell inactivation by intracellular advanced oxidation processes while avoiding adverse effects on non-target species in the ecosystem. In addition, such an approach to induce intracellular oxidative stress can be transplanted into disinfection processes for water and wast