<i>In vitro</i>effect of CTAB- and PEG-coated gold nanorods on the induction of eryptosis/erythroptosis in human erythrocytes

Lau, Irene; Chen, Huanjun; Wang, Jianfang; Ong, H. C.; Leung, Ken Cham‐Fai; Ho, Ho P.; Kong, Siu Kai

doi:10.3109/17435390.2011.625132

Cited by 202 publications

(161 citation statements)

References 34 publications

Supporting

Mentioning

160

Contrasting

Order By: Relevance

“…The characteristic absorbance spectrum was scanned for hemoglobin released from erythrocytes upon the treatments with different concentrations of C‐GNRs (Figure 1B, bottom panel). Based on the absorbance at 541 nm, the hemolysis ratio was quantitatively calculated and the results showed that the positively charged nanoparticles exerted higher hemolytic activity than the negatively charged ones, and the pure erythrocytes in PBS were more vulnerable to nanorod stimulation than those in whole blood (Figure 1C), which was similar to the previous finding 12. Additionally, hemolysis of erythrocytes induced by C‐GNR was instant (within 0.2 h), nevertheless exhibited in time‐dependent and concentration‐related manners (Figure 1D and Figure S2, Supporting Information).…”

Section: Resultssupporting

confidence: 86%

Hematological Effects of Gold Nanorods on Erythrocytes: Hemolysis and Hemoglobin Conformational and Functional Changes

et al. 2017

View full text Add to dashboard Cite

Gold nanorods (GNRs) are a unique class of metal nanostructures that have attractive potentials in biomedical applications, and the concern on their biological safety is concomitantly increasing. Hemocompatibility is extremely important as their contact with blood circulation is unavoidable during in vivo delivery. Herein, two kinds of GNRs coated with hexadecyltrimethylammonium bromide (C‐GNRs) or poly(sodium‐p‐styrenesulfonate) are used to test their potential toxicological effects in blood. C‐GNRs with positive surface charges efficiently induce hemolysis when encountering erythrocytes. Cellular internalization of C‐GNRs is found, and they subsequently bind with hemoglobin, forming bioconjugates. The interaction between hemoglobin and C‐GNR (stoichiometry 32.7:1) is regulated by electrostatic forces. Chromophores like tryptophan (Trp) are found to interact with C‐GNRs, causing enhancement in fluorescence intensity. The conformation of protein is partially altered, evidenced by decrease in α‐helical, increase in β‐sheet and random coil of hemoglobin. Although C‐GNRs do not essentially decrease oxygen binding capacity of hemoglobin, they hamper oxygen release from the protein. Heme, the oxygen binding unit, releases from hemoglobin upon C‐GNR treatment, which could contribute to C‐GNR‐induced hemolysis. This study demonstrates the hematological effects of GNRs, revealing their potential risk in biomedical applications.

show abstract

Section: Resultssupporting

confidence: 86%

Hematological Effects of Gold Nanorods on Erythrocytes: Hemolysis and Hemoglobin Conformational and Functional Changes

et al. 2017

View full text Add to dashboard Cite

show abstract

“…In analogy to apoptosis of nucleated cells, erythrocytes may enter eryptosis, the suicidal death of erythrocytes characterized by cell shrinkage [45] and cell membrane scrambling with phosphatidylserine exposure at the cell surface [46]. Cellular mechanisms involved in the triggering of eryptosis include increase in cytosolic Ca 2+ activity ( [Ca 2+ ] i ) [46], ceramide [47], oxidative stress [46], energy depletion [46] and activated caspases [46,48,49]. Eryptosis is further stimulated following activation of casein kinase 1a, Janus-activated kinase JAK3, protein kinase C and p38 kinase [46].…”

mentioning

confidence: 99%

Triggering of Suicidal Erythrocyte Death by the Antibiotic Ionophore Nigericin

Bissinger

Malik

Bouguerra

et al. 2015

Basic Clin Pharma Tox

View full text Add to dashboard Cite

The K + ,H + ionophore and antibiotic nigericin has been shown to trigger apoptosis and is thus considered for the treatment of malignancy. Cellular mechanisms involved include induction of oxidative stress, which is known to activate erythrocytic Ca 2+ -permeable unselective cation channels leading to Ca 2+ entry, increase in cytosolic Ca 2+ activity ([Ca 2+ ] i ) and subsequent stimulation of eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. This study explored whether and how nigericin induces eryptosis. Phosphatidylserine exposure at the cell surface was estimated from annexin V binding, cell volume from forward scatter, [Ca 2+ ] i from Fluo3 fluorescence, pH i from BCECF fluorescence, ceramide abundance utilizing antibodies and reactive oxygen species (ROS) formation from DCFDA-dependent fluorescence. A 48-hr exposure of human erythrocytes to nigericin significantly increased the percentage of annexin-V-binding cells (0.1-10 nM), significantly decreased forward scatter (0.1-1 nM), significantly decreased cytosolic pH (0.1-1 nM) and significantly increased Fluo3 fluorescence (0.1-10 nM). Nigericin (1 nM) slightly, but significantly, increased ROS, but did not significantly modify ceramide abundance. Materials and MethodsErythrocytes, solutions and chemicals. Li-heparin-anticoagulated fresh blood samples were kindly provided by the blood bank of the University of T€ ubingen. The study was approved by the ethics committee of the University of T€ ubingen (184/2003 V). The blood was centrifuged at 120 9 g for 20 min. at 21°C and the platelet-and leucocyte-containing supernatant were disposed. Erythrocytes were incubated in vitro at a haematocrit of 0.4% in Ringer solution containing (in mM) 125 NaCl, 5 KCl, 1 MgSO 4 , 32 N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid (HEPES; pH 7.4), 5 glucose and 1 CaCl 2 , at 37°C for 48 hr. Where indicated, erythrocytes were exposed to nigericin (Enzo Life Sciences, L€ orrach, Germany) at the indicated concentrations.Annexin V binding and forward scatter. After incubation under the respective experimental condition, a 150-ll cell suspension was centrifuged at 350 rcf for 3 min. and, after trashing the supernatant,

show abstract

“…Increased [Ca 2+ ] i further leads to phospholipid scrambling of the cell membrane with phosphatidylserine translocation to the erythrocyte surface [11]. Eryptosis is further stimulated by ceramide formation [13], caspase activation [14][15][16][17][18] and deranged activities of AMP-activated kinase AMPK [19], casein kinase 1a [20,21], cGMP-dependent protein kinase [15], Janus-activated kinase JAK3 [22], protein kinase C [23], p38 kinase [24], PAK2 kinase [25], sorafenibsensitive kinases [26] and sunitinib-sensitive kinases [27]. Eryptosis is elicited by a wide variety of xenobiotics [13,, including tannic acid [48], honokiol [62], gossypol [46], gambogic acid [63], tanshinone II A [47], apigenin [64], ursolic acid [65], thymoquinone [66], oridonin [67] and a-lipoic acid [14].…”

mentioning

confidence: 99%

Stimulation of Suicidal Erythrocyte Death by Sulforaphane

Alzoubi

Calabrò

Faggio

et al. 2014

Basic Clin Pharma Tox

View full text Add to dashboard Cite

Sulforaphane, an isothiocyanate from cruciferous vegetable, counteracts malignancy. The effect is at least in part due to the stimulation of suicidal death or apoptosis of tumour cells. Mechanisms invoked in sulforaphane-induced apoptosis include mitochondrial depolarization and altered gene expression. Despite the lack of mitochondria and nuclei, erythrocytes may, similar to apoptosis of nucleated cells, enter eryptosis, a suicidal cell death characterized by cell shrinkage and phosphatidylserine translocation to the erythrocyte surface. This study explored whether sulforaphane influences eryptosis. To this end, the effect of sulforaphane exposure on human erythrocyte [Ca 2+ ] i , cell volume and phosphatidylserine surface abundance was quantified by flow cytometry. Materials and MethodsErythrocytes, solutions and chemicals. Fresh Li-heparinanticoagulated blood samples were kindly provided by the blood bank of the University of T€ ubingen. The study was approved by the ethics committee of the University of T€ ubingen (184/2003 V). The blood was centrifuged at 125 9 g for 20 min. at 23°C, and the platelet-and leucocyte-containing supernatant was disposed. Erythrocytes were incubated in vitro at a haematocrit of 0.4% in Ringer solution containing (in mM) 125 NaCl, 5 KCl, 1 MgSO 4 , 32 N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid (HEPES), 5 glucose, 1 CaCl 2 ; pH 7.4 at 37°C for 48 hr. Where indicated, erythrocytes were exposed to sulforaphane (Sigma-Aldrich, Schnelldorf, Germany) at the indicated concentrations,

show abstract

In vitroeffect of CTAB- and PEG-coated gold nanorods on the induction of eryptosis/erythroptosis in human erythrocytes

Cited by 202 publications

References 34 publications

Hematological Effects of Gold Nanorods on Erythrocytes: Hemolysis and Hemoglobin Conformational and Functional Changes

Hematological Effects of Gold Nanorods on Erythrocytes: Hemolysis and Hemoglobin Conformational and Functional Changes

Triggering of Suicidal Erythrocyte Death by the Antibiotic Ionophore Nigericin

Stimulation of Suicidal Erythrocyte Death by Sulforaphane

Contact Info

Product

Resources

About