Natural bee-honey based biostimulants confer salt tolerance in onion via modulation of the antioxidant defence system

2019 ◽  
Vol 94 (5) ◽  
pp. 632-642 ◽  
Author(s):  
Wael Morad Semida ◽  
Taia Ali Abd El-Mageed ◽  
Khaulood Hemida ◽  
Mostafa Mohamed Rady
2016 ◽  
Vol 10 (07) ◽  
pp. 1030-1039 ◽  
Author(s):  
Wael M. Semida ◽  
◽  
Taia A. Abd El-Mageed ◽  
Saad M. Howladar ◽  
Mostafa M. Rady ◽  
...  

2000 ◽  
Vol 27 (3) ◽  
pp. 273 ◽  
Author(s):  
María P. Benavídes ◽  
Patricia L. Marconi ◽  
Susana M. Gallego ◽  
María E. Comba ◽  
María L. Tomaro

A relationship between the antioxidant defence system and salt tolerance in two clones of potato (Solanum tuberosum L.) differing in salt sensitivity was studied. The antioxidant defence system of the sensitive clone responded differently to 100 and 150 mM NaCl. At 100 mM NaCl, growth, dehydroascorbate reductase and catalase activities remained unaltered, but chlorophyll and reduced glutathione content decreased (23% and 35%, respectively), while ascorbate content and superoxide dismutase activity were increased 34% and 63%, with respect to the control (0 mM NaCl). The superoxide dismutase increment was higher under 150 mM NaCl treatment, while a general decrease (except for dehydroascorbate reductase and catalase activities) in all the antioxidant parameters studied was observed in the sensitive clone. Reduced glutathione and ascorbate, the main antioxidant soluble defences, and all antioxidant enzymes (except catalase) were significantly elevated in the tolerant clone compared to the sensitive one when both were grown in the absence of NaCl. Under 100 and 150 mM NaCl treatments, no changes in the antioxidant stress parameters were detected in the tolerant clone. These results suggest a relationship between salt tolerance and the antioxidant defence system in the two clones.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Ana Maria Murta Santi ◽  
Paula Alves Silva ◽  
Isabella Fernandes Martins Santos ◽  
Silvane Maria Fonseca Murta

Abstract Background Superoxide dismutase (SOD), a central component of the antioxidant defence system of most organisms, removes excess superoxide anions by converting them to oxygen and hydrogen peroxide. As iron (Fe) SOD is absent in the human host, this enzyme is a promising molecular target for drug development against trypanosomatids. Results We obtained Leishmania infantum mutant clones with lower FeSOD-A expression and investigated their phenotypes. Our attempts to delete this enzyme-coding gene using three different methodologies (conventional allelic replacement or two different CRISPR/methods) failed, as FeSOD-A gene copies were probably retained by aneuploidy or gene amplification. Promastigote forms of WT and mutant parasites were used in quantitative reverse-transcription polymerase chain reaction (RT-qPCR) and western blot analyses, and these parasite forms were also used to assess drug susceptibility. RT-qPCR and western blot analyses revealed that FeSOD-A transcript and protein levels were lower in FeSOD-A−/−/+L. infantum mutant clones than in the wild-type (WT) parasite. The decrease in FeSOD-A expression in L. infantum did not interfere with the parasite growth or susceptibility to amphotericin B. Surprisingly, FeSOD-A−/−/+L. infantum mutant clones were 1.5- to 2.0-fold more resistant to trivalent antimony and 2.4- to 2.7-fold more resistant to miltefosine. To investigate whether the decrease in FeSOD-A expression was compensated by other enzymes, the transcript levels of five FeSODs and six enzymes from the antioxidant defence system were assessed by RT-qPCR. The transcript level of the enzyme ascorbate peroxidase increased in both the FeSOD-A−/−/+ mutants tested. The FeSOD-A−/−/+ mutant parasites were 1.4- to 1.75-fold less tolerant to oxidative stress generated by menadione. Infection analysis using THP-1 macrophages showed that 72 h post-infection, the number of infected macrophages and their intracellular multiplication rate were lower in the FeSOD-A−/−/+ mutant clones than in the WT parasite. Conclusions The unsuccessful attempts to delete FeSOD-A suggest that this gene is essential in L. infantum. This enzyme plays an important role in the defence against oxidative stress and infectivity in THP-1 macrophages. FeSOD-A-deficient L. infantum parasites deregulate their metabolic pathways related to antimony and miltefosine resistance. Graphic Abstract


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