Eryptosis-inducing activity of bisphenol A and its analogs in human red blood cells (in vitro study)

被引:98
作者
Macczak, Aneta [1 ]
Cyrkler, Monika [1 ]
Bukowska, Bozena [1 ]
Michalowicz, Jaromir [1 ]
机构
[1] Univ Lodz, Fac Biol & Environm Protect, Dept Environm Pollut Biophys, Pomorska 141-143 St, PL-90001 Lodz, Poland
关键词
Bisphenols; Erythrocytes; Eryptosis; Calpain activation; Caspase-3; activation; CYTOPLASMIC DOMAIN; EXPOSURE; DEATH; ERYTHROCYTES; APOPTOSIS; URINARY; ASSOCIATION; IMPAIRMENT; ACTIVATION; INDUCTION;
D O I
10.1016/j.jhazmat.2015.12.057
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Bisphenols are important chemicals that are widely used in the manufacturing of polycarbonates, epoxy resin and thermal paper, and thus the exposure of humans to these substances has been noted. The purpose of this study was to assess eryptotic changes in human erythrocytes exposed (in vitro) to bisphenol A (BPA) and its selected analogs, "i.e.,bisphenol F (BPF), bisphenol S (BPS) and bisphenol AF (BPAF). The erythrocytes were incubated with compounds studied at concentrations ranging from 1 to 250 mu g/mL for 4,12 or 24 h. The results showed that BPA and its analogs increased cytosolic calcium ions level with the strongest effect noted for BPAF. It has also been revealed that all bisphenols analyzed, and BPAF and BPF in particular increased phosphatidylserine translocation in red blood cells, which confirmed that they exhibited eryptotic potential in this cell type. Furthermore, it was shown that BPA and its analogs caused significant increase in calpain and caspase-3 activities, while the strongest effect was noted for BPAF. BPS, which is the main substituent of bisphenol A in polymers and thermal paper production exhibited similar eryptotic potential to BPA. Eryptotic changes in human erythrocytes were provoked by bisphenols at concentrations, which may influence the human body during occupational exposure or subacute poisoning with these compounds. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:328 / 335
页数:8
相关论文
共 56 条
[1]   Tannic Acid Induced Suicidal Erythrocyte Death [J].
Abed, Majed ;
Herrmann, Tabea ;
Alzoubi, Kousi ;
Pakladok, Tatsiana ;
Lang, Florian .
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2013, 32 (04) :1106-1116
[2]  
Ahmed W. M. S., 2015, Global Veterinaria, V14, P228
[3]   Bisphenol A Exposure during Pregnancy Disrupts Glucose Homeostasis in Mothers and Adult Male Offspring [J].
Alonso-Magdalena, Paloma ;
Vieira, Elaine ;
Soriano, Sergi ;
Menes, Lorena ;
Burks, Deborah ;
Quesada, Ivan ;
Nadal, Angel .
ENVIRONMENTAL HEALTH PERSPECTIVES, 2010, 118 (09) :1243-1250
[4]  
[Anonymous], GLOB BISPH A BPA MAR
[5]   Influences of Flavonoids on Erythrocyte Membrane and Metabolic Implication Through Anionic Exchange Modulation [J].
Barreca, Davide ;
Lagana, Giuseppina ;
Tellone, Ester ;
Ficarra, Silvana ;
Leuzzi, Ugo ;
Galtieri, Antonio ;
Bellocco, Ersilia .
JOURNAL OF MEMBRANE BIOLOGY, 2009, 230 (03) :163-171
[6]   In Vitro Sensitization of Erythrocytes to Programmed Cell Death Following Baicalein Treatment [J].
Bissinger, Rosi ;
Malik, Abaid ;
Honisch, Sabina ;
Warsi, Jamshed ;
Jilani, Kashif ;
Lang, Florian .
TOXINS, 2014, 6 (09) :2771-2786
[7]   Scientific Opinion on the risks to public health related to the presence of bisphenol A (BPA) in foodstuffs: Executive summary [J].
Bolognesi, Claudia ;
Castle, Laurence ;
Cravedi, Jean-Pierre ;
Engel, Karl -Heinz ;
Fowler, Paul ;
Franz, Roland ;
Grob, Konrad ;
Guertler, Rainer ;
Husoy, Trine ;
Mennes, Wim ;
Milana, Maria Rosaria ;
Penninks, Andre ;
Roland, Franz ;
Silano, Vittorio ;
Smith, Andrew ;
Pocas, Maria de Fatima Tavares ;
Tlustos, Christina ;
Toldra, Fidel ;
Woelfle, Detlef ;
Zorn, Holger .
EFSA JOURNAL, 2015, 13 (01)
[8]   Dynamic adhesion of eryptotic erythrocytes to endothelial cells via CXCL16/SR-PSOX [J].
Borst, Oliver ;
Abed, Majed ;
Alesutan, Ioana ;
Towhid, Syeda T. ;
Qadri, Syed M. ;
Foeller, Michael ;
Gawaz, Meinrad ;
Lang, Florian .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2012, 302 (04) :C644-C651
[9]   Programmed cell death in mature erythrocytes: a model for investigating death effector pathways operating in the absence of mitochondria [J].
Bratosin, D ;
Estaquier, J ;
Petit, F ;
Arnoult, D ;
Quatannens, B ;
Tissier, JP ;
Slomianny, C ;
Sartiaux, C ;
Alonso, C ;
Huart, JJ ;
Montreuil, J ;
Ameisen, JC .
CELL DEATH AND DIFFERENTIATION, 2001, 8 (12) :1143-1156
[10]  
Calafat AM, 2005, ENVIRON HEALTH PERSP, V113, P391, DOI 10.1289/ehp.7534