Journal of hazardous materials · 2025
Signal molecule nitric oxide exerts stronger regulation on the cell death of oxidative stress-sensitive harmful algae species under allelochemical exposure.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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He Yan, Zhou Zijian, Ding Yuan, Liu Yan, Yang Zhanbiao, Luo Ling, Chen Zhilin, He Jinsong
Аннотация
The relationship between the regulatory effect of nitric oxide (NO) and oxidative stress tolerance in controlling HABs under allelopathic effect remains unclear. In this study, the impact of NO on four species of algae blooms was examined under allelochemical N-phenyl-1-naphthylamine (P1NA) exposure. Results revealed that the regulatory effect of NO was constrained by the sensitivity of algae to oxidative stress. The addition of the NO scavenger L-NAME alleviated allelopathic stress of P1NA with the increase of OD680 value and esterase activity of two algae (Microcystis aeruginosa and Chlorella vulgaris), accompanied by a significant decrease of antioxidant enzyme activity (SOD and CAT), respectively. In contrast, the obvious decline of NO level did not result in significant alterations in the antioxidant indices of the other two species (Anabaena flosaguas and Scenedesmus quadricauda). The principal component analysis (PCA) further displayed a strong correlation between antioxidant parameters and NO regulation, with the first two PCs explaining 67.5 % of the overall variance. Transcriptomic data revealed the impact of NO on redox balance differed with two algae, M. aeruginosa and S. quadricauda. L-NAME significantly reduced transcript levels of signal transduction and homeostasis-related genes (ntrC and AHP1) in oxidative stress-sensitive M. aeruginosa. However, in oxidative stress-insensitive S. quadricauda, only the expression of genes (fadE and pal) associated with irreversible proteolysis was detected. It is firstly proposed that the sensitivity to oxidative stress plays a pivotal role in determining the regulatory effect of NO for accelerating the algae cell death for controlling HABs.