Original scientific paper
https://doi.org/10.2478/aiht-2021-72-3588
Ortho-substituted PCB 153: effects in CHO-K1 cells
Marina Miletić
; University of Zagreb Faculty of Food Technology and Biotechnology, Laboratory for Toxicology, Zagreb, Croatia
Teuta Murati
orcid.org/0000-0001-7157-400X
; University of Zagreb Faculty of Food Technology and Biotechnology, Laboratory for Toxicology, Zagreb, Croatia
Branimir Šimić
; University of Zagreb Faculty of Food Technology and Biotechnology, Laboratory for Toxicology, Zagreb, Croatia
Nina Bilandžić
; Croatian Veterinary Institute, Department of Veterinary Public Health, Laboratory for Residue Control, Zagreb, Croatia
Anamaria Brozović
; Ruđer Bošković Institute, Division of Molecular Biology, Laboratory for Cell Biology and Signalling, Zagreb, Croatia
Ivana Kmetič
orcid.org/0000-0001-5412-7128
; University of Zagreb Faculty of Food Technology and Biotechnology, Laboratory for Toxicology, Zagreb, Croatia
Abstract
Non-planar di-ortho-substituted PCB 153 (2,2’,4,4’,5,5’-hexachlorobiphenyl), one of the most abundant PCB congeners in the environment and in biological and human tissues, has been identified as potential endocrine disruptor affecting the reproductive and endocrine systems in rodents, wildlife, and humans. The aim of this study was to gain a deeper insight into its mode/mechanism of action in Chinese hamster ovary K1 cells (CHO-K1). PCB 153 (10–100 µmol/L) inhibited CHO-K1 cell proliferation, which was confirmed with four bioassays (Trypan Blue, Neutral Red, Kenacid Blue, and MTT), of which the MTT assay proved the most sensitive. PCB 153 also induced ROS formation in a dose-dependent manner. Apoptosis was seen after 6 h of exposure to PCB 153 doses ≥50 µmol/L, while prolonged exposure resulted in the activation of the necrotic pathway. PCB153-induced disturbances in normal cell cycle progression were time-dependent, with the most significant effects occurring after 72 h.
Keywords
ell cycle progression; cell death; cytotoxicity; polychlorinated biphenyls; ROS
Hrčak ID:
268093
URI
Publication date:
23.12.2021.
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