Salinity induced changes in cell membrane stability, protein and RNA contents

2012 ◽  
Vol 11 (24) ◽  
Author(s):  
Muhammad Jamil
2015 ◽  
Vol 38 (1) ◽  
pp. 63-69 ◽  
Author(s):  
Sepideh Sadat Jamali ◽  
Azam Borzouei ◽  
Mustafa Aghamirzaei ◽  
Hamid Reza Khosronejad ◽  
Milad Fathi

2002 ◽  
Vol 32 (8) ◽  
pp. 1351-1359 ◽  
Author(s):  
Paul G Schaberg ◽  
Donald H DeHayes ◽  
Gary J Hawley ◽  
Paula F Murakami ◽  
G Richard Strimbeck ◽  
...  

We evaluated the influence of protracted low-level nitrogen (N) fertilization on foliar membrane-associated calcium (mCa), sugar and starch concentrations, membrane stability, winter cold tolerance, and freezing injury of red spruce (Picea rubens Sarg.) trees growing in six experimental plots on Mount Ascutney, Vermont. For 12 consecutive years before this evaluation, each plot received one of three treatments: 0, 15.7, or 31.4 kg N·ha–1·year–1 supplied as NH4Cl. In comparison with trees from control plots, the current-year foliage of trees from N-addition plots had lower mCa concentrations, higher levels of electrolyte leakage, reduced cold tolerance, and greater freezing injury. Levels of mCa, membrane stability, and cold tolerance did not differ between N treatments, but trees in high-N treated plots experienced greater freezing injury. Although no differences in carbohydrate nutrition were detected in September, foliar sugar and starch concentrations from trees in N-treated plots were higher than control plot trees in January. We propose that foliar mCa deficiencies reduced cell membrane stability, decreased cold tolerance, and increased freezing injury for trees in N addition plots relative to controls. Declines in mCa may also help account for increases in respiration previously measured. Because soil, root, and mycorryhizal conditions were not evaluated, it is unknown how treatment-induced changes in these compartments may have influenced the alterations in foliar mCa and physiological parameters measured in this study.


1991 ◽  
Vol 42 (2) ◽  
pp. 167-171 ◽  
Author(s):  
G. S. PREMACHANDRA ◽  
HIROHUMI SANEOKA ◽  
MUNEAKI KANAYA ◽  
SHOITSU OGATA

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Sung-Chih Hsieh ◽  
Jeng-Ting Tsao ◽  
Wei-Zhen Lew ◽  
Ya-Hui Chan ◽  
Lin-Wen Lee ◽  
...  

One of the causes of dental pulpitis is lipopolysaccharide- (LPS-) induced inflammatory response. Following pulp tissue inflammation, odontoblasts, dental pulp cells (DPCs), and dental pulp stem cells (DPSCs) will activate and repair damaged tissue to maintain homeostasis. However, when LPS infection is too serious, dental repair is impossible and disease may progress to irreversible pulpitis. Therefore, the aim of this study was to examine whether static magnetic field (SMF) can attenuate inflammatory response of dental pulp cells challenged with LPS. In methodology, dental pulp cells were isolated from extracted teeth. The population of DPSCs in the cultured DPCs was identified by phenotypes and multilineage differentiation. The effects of 0.4 T SMF on DPCs were observed through MTT assay and fluorescent anisotropy assay. Our results showed that the SMF exposure had no effect on surface markers or multilineage differentiation capability. However, SMF exposure increases cell viability by 15%. In addition, SMF increased cell membrane rigidity which is directly related to higher fluorescent anisotropy. In the LPS-challenged condition, DPCs treated with SMF demonstrated a higher tolerance to LPS-induced inflammatory response when compared to untreated controls. According to these results, we suggest that 0.4 T SMF attenuates LPS-induced inflammatory response to DPCs by changing cell membrane stability.


Author(s):  
Jun Yin ◽  
Yong Huang

Process-induced damage to cells is of significant importance and must be mitigated for safe and reproducible cell direct writing. The objective of this study is to investigate the cell membrane stability under the external normal pressure. This investigation is performed by studying the dipalmitoylphosphatidylcholine bilayer behavior under different normal pressures using molecular dynamics. As the normal pressure increases, the force necessary to rupture the bilayer structure decreases, which indicates cell membrane instability under high normal pressure. This phenomenon can also be explained by the change of free energy difference before and after rupture under different normal pressures. The effect of the pulling speed on the rupture force is also investigated, showing that the rupture force increases almost linearly with the pulling speed.


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