Tribenuron-methyl
(TM), as one of the sulfonylurea (SU) herbicides, has been widely
and effectively applied for many kinds of plants. SUs inhibit plant
growth by restraining the biosynthetic pathway of branched-chain amino
acids (BCAAs) catalyzed by acetolactate synthase (ALS). Safeners are
agrochemicals that protect crops from herbicide injuries. To improve
the crop tolerance under TM toxicity stress, this paper evaluated
the protective effect of N-tosyloxazolidine-3-carboxamide.
It turned out that most of the tested compounds showed significant
protection against TM via enhancing the glutathione (GSH) content
and glutathione S-transferase (GST) activity. Among
all of the tested compounds, compound 16 exhibited more
excellent protection than the contrast safener R-28725 and other target
compounds. A positive correlation between the growth level, endogenous
GSH content, and GST activity was observed in this research. The GST
kinetic parameter V
max of the maize was
increased by 29.6% after treatment with compound 16,
while K
m was decreased by 51.9% compared
to the untreated control. The molecular docking model indicated that
compound 16 could compete with TM in the active site
of ALS, which could interpret the protective effects of safeners.
The present work demonstrated that N-tosyloxazolidine-3-carboxamide
derivatives could be considered as potential candidates for developing
new safeners in the future.
Herbicide safeners enhance herbicide detoxification in crops without
reducing their herbicidal efficacy against target weeds. To alleviate
maize injury caused by the sulfonylurea herbicide nicosulfuron, a
series of 1,3-disubstituted imidazolidine or hexahydropyrimidine derivatives
were rationally designed via bioisosterism and active subunit combinations.
Thirty novel compounds were synthesized using an efficient one-pot
method and low-cost raw materials and characterized by IR, 1H NMR, 13C NMR, and high-resolution mass spectrometer
(HRMS). Bioactivity and structure–activity relationship (SAR)
were evaluated for herbicide safeners tested against nicosulfuron
injury. Most of the compounds effectively protected sensitive maize
against nicosulfuron damage. The parent skeletons and substituents
of the target compounds both substantially influenced their safener
activity. Compound I-3 exhibited superior bioactivity
compared to the safener isoxadifen-ethyl. Molecular docking simulations
disclosed that compound I-3 competed with nicosulfuron
for the acetolactate synthase active site and demonstrated that this
is the protective mechanism of safeners. The target compound I-3 presented with strong herbicide safener activity in maize
and is, therefore, a potential candidate for the development of a
novel herbicide safener.
BACKGROUND: Herbicide safeners mitigate crop damage without reducing herbicide efficacy. Here, the protective effects of phenoxyacetyl oxazolidine derivatives as potential safeners were evaluated with a view toward reducing injury caused by sulfonylurea herbicide nicosulfuron to sensitive maize varieties. RESULTS: Growth indices demonstrated that the bioactivity of compound 9 (N-phenoxyacety-2-methyl-2,4-diethyl-1,3-oxazolidine) was superior to that of R-28725 and all other compounds tested. Compound 9 induced endogenous glutathione and upregulated glutathione-S-transferase (GST) in maize. Thus, it could enhance maize tolerance to nicosulfuron. Compared with the untreated water control group, the maximum reaction rate of GST was increased by 37.62%, while the maximum velocity of GST was decreased by 61.93% after treatment with compound 9. Acetolactate synthase relative activity was significantly enhanced in the case of treatment with compound 9, indicating the excellent protective effects of compound 9 against nicosulfuron in maize. CONCLUSIONS: The present work demonstrates that phenoxyacetyl oxazolidine derivatives are potentially efficacious as herbicide safeners and merit further investigation.
Doxorubicin (DOX) is an effective anticancer drug which is widely used in clinical treatment. However, the severe cardiotoxicity limits its use. Thus, it is an urgent need to attenuate the toxicity of DOX without impairing its efficacy. Many studies show that Se may protect normal tissues from damages of some anticancer drugs. Recently, Se@SiO nanocomposites emerges as better substitutes for direct element Se in treatment of cancer cells for their ideal biocompatibility. In the present article, we synthesized Se@SiO nanocomposites and confirmed their characterization according to previous studies. We accomplished a conjunctive use of Se@SiO nanocomposites with DOX then explored the toxicity and efficacy of this combination. In the in vivo experiments, the survival rate of mice with DOX treatment was significantly increased by Se@SiO. And Se@SiO has few interference to the therapeutic effect of DOX. Particularly, Se@SiO significantly attenuated DOX-induced myocardial tissue damage (serum index, apoptosis index, western-blot index) and protected mice from reduction in LVEF induced by DOX in mice model. In summary, we concluded that the protective effect of Se@SiO in DOX-induced cardiotoxicity was possibly attributable to the inhibition of ROS production, showing great potential of Se@SiO nanocomposite in the clinical use of DOX.
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