ArticleApplied microbiology and biotechnology2022
Oxidative stress of Microcystis aeruginosa induced by algicidal bacterium Stenotrophomonas sp. KT48.
Article in Applied microbiology and biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Response of particle-attached and free-living bacterial communities to Microcystis blooms.Applied microbiology and biotechnology · 2024Article
- Biotechnological approaches for suppressing Microcystis blooms: insights and challenges.Applied microbiology and biotechnology · 2024Review
- Pilot-Scale Fermentation ofBiology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Cyanobacterial harmful algal blooms are a worldwide problem with substantial adverse effects on the aquatic environment as well as human health. Among the multiple physicochemical and biotic approaches, algicidal bacterium is one of the most promising and eco-friendly ways to control bloom expansion. In this study, Stenotrophomonas sp. KT48 isolated from the pond where cyanobacterial blooms occurred exhibited a strong inhibitory effect on Microcystis aeruginosa. However, the algicidal performance and mechanisms of Stenotrophomonas sp. remain under-documented. To explore the algicidal performance and physiological response againt M. aeruginosa, further works were implemented here. Our results indicated that the algicidal rate of strain KT48 cultured in 1/8 LB medium supplemented with 0.3% starch or glucose was about 30% higher than that in 1/8 LB medium. Strain KT48 culture, cell-free filtrate, and cells re-suspended were inoculated into the M. aeruginosa culture, and the Chl-a content was determined. Those results indicated that the algicidal activity of cells re-suspended was far higher than that of cell-free filtrate and culture. Thus, strain KT48 exhibited algicidal activity mainly through direct attacking M. aeruginosa rather than excretion of algicides. Furthermore, strain KT48 led to an increase in cellular reactive oxygen species (ROS) and caused lipid peroxidation as supported by the increase in malondialdehyde (MDA) levels. The ROS and MDA levels in algal cells treated with strain KT48 cells re-suspended were about 3.23-fold and 2.80-fold higher than those of untreated algal cells on day 11. And a further inhibition to the antioxidant system is suggested by a sharp decrease in the superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD) activities. In addition, we also observed that the morphology of most algal cells changed from integrity to break. This study not only indicated strain KT48 with strong algicidal activity, but also explored the underlying algicidal mechanisms to provide a source of bacterial agent for the biocontrol of cyanobacterial blooms. KEY POINTS: • Strain KT48 exhibited strong algicidal activity mainly through direct attacking M. aeruginosa. • The addition of glucose could enhance the algicidal rate of strain KT48 by about 30%. • Strain KT48 led to an increase in cellular reactive oxygen species (ROS) level that causes membrane damage as supported by the increase in malondialdehyde (MDA) levels.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.