Bisphenol A and its analogs exhibit different apoptotic potential in peripheral blood mononuclear cells (in vitro study).
There are only a few studies that have assessed the effect of bisphenol A (BPA) on human blood cells and no study has been conducted to analyze the impact of BPA analogs on human leucocytes. In this study, we have investigated the effect of BPA and its analogs like bisphenol F (BPF), bisphenol S (BPS) and bisphenol AF (BPAF) on apoptosis induction in human peripheral blood mononuclear cells (PBMCs). In order to clarify the mechanism of bisphenols-induced programmed cell death, changes in various signaling molecules of this process have been assessed. We observed an increase in cytosolic calcium ions (Ca(2+)) level and reduction of transmembrane mitochondrial potential (ΔΨm) in PBMCs incubated with all compounds examined, and particularly BPA and BPAF. All compounds studied changed PBMCs membrane permeability, activated caspase-8, -9, -3 and induced PARP-1 cleavage and chromatin condensation, which confirmed that they were capable of inducing apoptosis both via intrinsic and extrinsic pathway. Moreover, we have found that modus operandi of bisphenols studied was different. We noticed that BPAF and BPS caused mainly necrotic and apoptotic changes, respectively, whereas BPA induced comparable apoptotic and necrotic effects in the incubated cells.
Department of Environmental Pollution Biophysics, Faculty of Biology and Environmental Protection, University of Łódź, Pomorska 141/143 St., 90-001 Łódź, Poland.
Katarzyna
K
Mokra
Department of Environmental Pollution Biophysics, Faculty of Biology and Environmental Protection, University of Łódź, Pomorska 141/143 St., 90-001 Łódź, Poland.
Magdalena
M
Kocia
Department of Environmental Pollution Biophysics, Faculty of Biology and Environmental Protection, University of Łódź, Pomorska 141/143 St., 90-001 Łódź, Poland. Electronic address: michalow@biol.uni.lodz.pl.
Jaromir
J
Michałowicz
D001559:Benzhydryl Compounds / Q000494:pharmacology*; D001771:Blood Banks; D020013:Calcium Signaling / Q000187:drug effects; D002274:Carcinogens, Environmental / Q000737:chemistry / Q000494:pharmacology*; D053148:Caspase 3 / Q000737:chemistry / Q000378:metabolism; D053181:Caspase 8 / Q000737:chemistry / Q000378:metabolism; D053453:Caspase 9 / Q000737:chemistry / Q000378:metabolism; D002463:Cell Membrane Permeability / Q000187:drug effects; D002478:Cells, Cultured; D042002:Chromatin Assembly and Disassembly / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D004968:Estrogens, Non-Steroidal / Q000494:pharmacology*; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D009336:Necrosis; D010636:Phenols / Q000494:pharmacology*; D000071137:Poly (ADP-Ribose) Polymerase-1; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D059748:Proteolysis / Q000187:drug effects; D013450:Sulfones / Q000494:pharmacology; D000098831:Bisphenol S Compounds; D000098826:Bisphenol A Compounds; D005466:Fluorocarbons; D000098833:Bisphenol F Compounds
D001559:Benzhydryl Compounds; D002274:Carcinogens, Environmental; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9; D004968:Estrogens, Non-Steroidal; D010636:Phenols; D000071137:Poly (ADP-Ribose) Polymerase-1; D011065:Poly(ADP-ribose) Polymerases; D013450:Sulfones; C543008:bisphenol S; D000098831:Bisphenol S Compounds; C499320:PARP1 protein, human; C505407:CASP3 protein, human; C505530:CASP8 protein, human; C506433:CASP9 protein, human; C006780:bisphenol A; D000098826:Bisphenol A Compounds; C583074:bisphenol AF; D005466:Fluorocarbons; C008745:4,4'-bisphenol F; D000098833:Bisphenol F Compounds
Apoptosis; Bisphenols; Caspase activation; Cytosolic calcium ions level; PARP-1 cleavage; Peripheral blood mononuclear cells