Polyelectrolyte stiffness on gold nanorods mediates cell membrane damage

Nanoscale ◽  
2020 ◽  
Vol 12 (26) ◽  
pp. 14021-14036
Author(s):  
Nurul ‘Ain Azman ◽  
Laurent Bekale ◽  
Thanh Xuan Nguyen ◽  
James Chen Yong Kah
Keyword(s):  
Cell Membrane ◽  
Lipid Bilayer ◽  
Gold Nanorods ◽  
Mechanical Stability ◽  
Membrane Damage ◽  
Hemolysis Assay ◽  
Cell Membrane Damage

CGMD showed that ligand mechanical stability which resulted in the exposure of the hydrophobic AuNR core, disrupted the lipid bilayer organization. The damage was confirmed using hemolysis assay whereby lipid bilayer disruption resulted in the release of hemoglobin.

Surface chemistry of gold nanorods: origin of cell membrane damage and cytotoxicity

Nanoscale ◽  
2013 ◽  
Vol 5 (18) ◽  
pp. 8384 ◽  
Author(s):  
Liming Wang ◽  
Xiumei Jiang ◽  
Yinglu Ji ◽  
Ru Bai ◽  
Yuliang Zhao ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Surface Chemistry ◽  
Gold Nanorods ◽  
Membrane Damage ◽  
Cell Membrane Damage

Particle Size of Drug Nanocarriers Defines the Fate of Spinal Cord Injury’s Recovery

2021 ◽  
Author(s):  
Delaram Poormoghadam ◽  
Bita Rasoulian Shiadeh ◽  
Fereshte Azedi ◽  
Hani Tavakol ◽  
Seyed Mahdi Rezayat ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Membrane ◽  
Muscular Atrophy ◽  
Muscle Tone ◽  
Membrane Damage ◽  
Definitive Treatment ◽  
Detrusor Muscle ◽  
Cell Membrane Damage ◽  
Fty 720 ◽  
Cord Injury

Abstract Spinal cord injury (SCI) is a debilitating condition for which no definitive treatment has yet been identified. Noteworthy, it influences other tissues through inflammatory reactions and metabolic disturbance. Therefore, fingolimod (FTY-720) as an FDA-approved inflammatory modulator would be promising. In the present study, nanocarriers at two distinct monodisperse particle sizes of 60 (nF60) and 190 (nF190) nm were prepared.The neural stem cell (NSC) viability and LDH release were studied in the face of the nanocarriers and free FTY-720. Results indicated that nanocarriers and free FTY-720 enhanced NSC viability than the control group.However, nF190 significantly induced less cell membrane damage than nF60. Nanocarriers and free FTY-720 enhanced motor neuron recovery in SCI rats, while body weight and return to bladder reflux by nF190 was significantly higher than nF60 groups. Return to bladder reflux might be due to the role of FTY-720 in regulation of detrusor muscle tone and preservation of the integrity of vessels by acting on endothelial cells. Moreover,nF190 gained higher soleus muscle weight than the free drugs;probably decreasing pro-inflammatory cytokines in soleus diminish muscular atrophy in SCI rats.To sum thing up, larger nanacarrirs with less cell membrane damage seems to be more efficient than smaller ones to manage SCI.

Surface chemistry modification of silica nanoparticles alters the activation of monocytes

2021 ◽  
Author(s):  
Romina Mitarotonda ◽  
Martín Saraceno ◽  
Marcos Todone ◽  
Exequiel Giorgi ◽  
Emilio L Malchiodi ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Immune System ◽  
Cell Membrane ◽  
Cell Activation ◽  
Membrane Damage ◽  
Living Cells ◽  
Cell Membrane Damage ◽  
Study Materials ◽  
Therapeutic Molecules ◽  
Pro Inflammatory Cytokines

Aim: Nanoparticles (NPs) interaction with immune system is a growing topic of study. Materials & methods: Bare and amine grafted silica NPs effects on monocytes/macrophages cells were analyzed by flow cytometry, MTT test and LIVE/DEAD® viability/cytotoxicity assay. Results: Bare silica NPs inhibited proliferation and induced monocyte/macrophages activation (increasing CD40/CD80 expression besides pro-inflammatory cytokines and nitrite secretion). Furthermore, silica NPs increased cell membrane damage and reduced the number of living cells. In contrast, amine grafted silica NPs did not alter these parameters. Conclusion: Cell activation properties of bare silica NPs could be hindered after grafting with amine moieties. This strategy is useful to tune the immune system stimulation by NPs or to design NPs suitable to transport therapeutic molecules.

scholarly journals Salt Stress-induced Injury is Associated with Hormonal Alteration in Kentucky Bluegrass

HortScience ◽  
2018 ◽  
Vol 53 (1) ◽  
pp. 97-101 ◽  
Author(s):  
Xunzhong Zhang ◽  
Wenli Wu ◽  
Erik H. Ervin ◽  
Chao Shang ◽  
Kim Harich
Keyword(s):  
Salt Stress ◽  
Cell Membrane ◽  
Poa Pratensis ◽  
Membrane Damage ◽  
Kentucky Bluegrass ◽  
Zeatin Riboside ◽  
Cool Season ◽  
Cell Membrane Damage ◽  
Turf Quality ◽  
Isopentenyl Adenosine

Plant hormones play an important role in plant adaptation to abiotic stress, but hormonal responses of cool-season turfgrass species to salt stress are not well documented. This study was carried out to investigate the responses of hormones to salt stress and examine if salt stress-induced injury was associated with hormonal alteration in kentucky bluegrass (KBG, Poa pratensis L.). The grass was grown in a growth chamber for 6 weeks and then subjected to salt stress (170 mm NaCl) for 28 days. Salt stress caused cell membrane damage, resulting in photosynthetic rate (Pn), chlorophyll (Chl), and turf quality decline in KBG. Salt stress increased leaf abscisic acid (ABA) and ABA/cytokinin (CK) ratio; reduced trans-zeatin riboside (ZR), isopentenyl adenosine (iPA), and indole-3-acetic acid (IAA), but did not affect gibberellin A4 (GA4). On average, salt stress reduced ZR by 67.4% and IAA by 58.6%, whereas it increased ABA by 398.5%. At the end of the experiment (day 28), turf quality, Pn, and stomatal conductance (gs) were negatively correlated with ABA and ABA/CK ratio, but positively correlated with ZR, iPA, and IAA. Electrolyte leakage (EL) was positively correlated with ABA and ABA/CK and negatively correlated with ZR, iPA, IAA, and GA4. GA4 was also positively correlated with turf quality and gs. The results of this study suggest that salt stress-induced injury of the cell membrane and photosynthetic function may be associated with hormonal alteration and imbalance in KBG.

Acquired haemolytic anaemia

2020 ◽  
pp. 5479-5489
Author(s):  
Amy Powers ◽  
Leslie Silberstein
Keyword(s):  
Cell Membrane ◽  
Haemolytic Anaemia ◽  
Membrane Damage ◽  
Autoimmune Haemolytic Anaemia ◽  
Red Cell ◽  
Drug Induced ◽  
Red Cell Membrane ◽  
Cell Membrane Damage ◽  
Drug Dependent ◽  
Transfusion Reactions

Premature destruction of red cells occurs through two primary mechanisms: (1) decreased erythrocyte deformability that leads to red cell sequestration and extravascular haemolysis in the spleen and other components of the reticuloendothelial system—may be caused by membrane defects, metabolic abnormalities, exogenous oxidizing agents, or pathological antibodies; and (2) red cell membrane damage and intravascular haemolysis—may be caused by exposure to pathological antibodies, activated complement, mechanical forces, chemicals, and infectious agents. Congenital haemolytic anaemias—congenital disorders resulting in a haemolytic anaemia include (1) disorders of the red cell membrane such as hereditary spherocytosis and hereditary elliptocytosis; (2) disorders of red cell enzymes such as glucose-6-phosphate dehydrogenase deficiency and pyruvate kinase deficiency; and (3) disorders of globin structure. Acquired immune haemolytic anaemias—immune haemolysis may occur when IgG, IgM, or IgA antibodies and/or complement bind to the erythrocyte surface. Autoimmune haemolytic anaemias—these are best classified according to the temperature at which the antibody optimally binds to the erythrocyte: warm autoimmune haemolytic anaemia, cold agglutinin-mediated autoimmune haemolytic anaemia, paroxysmal cold haemoglobinuria, and mixed type autoimmune haemolytic anaemia. Drug-induced haemolytic anaemia—haemolysis can be caused by drugs that induce a positive DAT. Drug-induced antibodies may be drug dependent or drug independent depending on whether the presence of the drug is required for their detection. Alloimmune haemolytic anaemias—these include acute haemolytic transfusion reactions and other conditions such as delayed haemolytic transfusion reactions, passenger lymphocyte haemolysis, and haemolytic disease of the newborn. Acquired nonimmune haemolytic anaemias and microangiopathic haemolytic anaemia are also discussed in this chapter.

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