Zhu Yinjie, Ding Jian, Wang Xiaoxiong, Wang Xuejian, Cao Huansheng, Teng Fei, Yao Shishi, Lin Zhiru, Jiang Yuelu, Tao Yi
Guangdong Provincial Engineering Research Center for Urban Water Recycling and Environmental Safety, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen, Guangdong, 518055, China.
Key Laboratory of Microorganism Application and Risk Control (MARC) of Shenzhen, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen, Guangdong, 518055, China.
Environ Sci Ecotechnol. 2024 Jul 9;22:100455. doi: 10.1016/j.ese.2024.100455. eCollection 2024 Nov.
Harmful cyanobacterial blooms (HCBs) pose a global ecological threat. Ultraviolet C (UVC) irradiation at 254 nm is a promising method for controlling cyanobacterial proliferation, but the growth suppression is temporary. Resuscitation remains a challenge with UVC application, necessitating alternative strategies for lethal effects. Here, we show synergistic inhibition of using ultraviolet A (UVA) pre-irradiation before UVC. We find that low-dosage UVA pre-irradiation (1.5 J cm) combined with UVC (0.085 J cm) reduces 85% more cell densities compared to UVC alone (0.085 J cm) and triggers -mediated regulated cell death (RCD), which led to cell lysis, while high-dosage UVA pre-irradiations (7.5 and 14.7 J cm) increase cell densities by 75-155%. Our oxygen evolution tests and transcriptomic analysis indicate that UVA pre-irradiation damages photosystem I (PSI) and, when combined with UVC-induced PSII damage, synergistically inhibits photosynthesis. However, higher UVA dosages activate the SOS response, facilitating the repair of UVC-induced DNA damage. This study highlights the impact of UVA pre-irradiation on UVC suppression of cyanobacteria and proposes a practical strategy for improved HCBs control.
有害蓝藻水华(HCBs)构成了全球生态威胁。254纳米的紫外线C(UVC)照射是控制蓝藻增殖的一种有前景的方法,但生长抑制是暂时的。复苏仍然是UVC应用面临的一个挑战,因此需要替代策略来实现致死效果。在这里,我们展示了在UVC之前使用紫外线A(UVA)预照射的协同抑制作用。我们发现,与单独使用UVC(0.085焦耳/平方厘米)相比,低剂量UVA预照射(1.5焦耳/平方厘米)与UVC(0.085焦耳/平方厘米)联合使用可使细胞密度降低85%以上,并触发介导的程序性细胞死亡(RCD),导致细胞裂解,而高剂量UVA预照射(7.5和14.7焦耳/平方厘米)可使细胞密度增加75%-155%。我们的放氧测试和转录组分析表明,UVA预照射会损害光系统I(PSI),并且与UVC诱导的PSII损伤相结合时,会协同抑制光合作用。然而,更高的UVA剂量会激活SOS反应,促进UVC诱导的DNA损伤的修复。这项研究突出了UVA预照射对UVC抑制蓝藻的影响,并提出了一种改进有害蓝藻水华控制的实用策略。