Mitochondrial toxicity of triclosan on mammalian cells
| Autor: | Maria A. Andersson, Carl G. Gahmberg, Maria Hautaniemi, Szabolcs Nagy, Merja Roivainen, Mirja Salkinoja-Salonen, Balázs Kakasi, Vera V. Teplova, Charmaine Ajao, Leif C. Andersson |
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| Přispěvatelé: | Department of Food and Nutrition, Biosciences, Biochemistry and Biotechnology, Medicum, Department of Pathology |
| Rok vydání: | 2015 |
| Předmět: |
metabolic acidosis
triclosan Health Toxicology and Mutagenesis PK-15 cells Mitochondrion ΔΨm membrane potential of the mitochondrial membrane Toxicology respiration control chemistry.chemical_compound MITOCHONDRIA EC50 concentration that diminishes the respective vitality parameter by ≥50% Insulin MIN cells Glycolysis HaCaT a spontaneously immortalized (non-neoplastic) keratinocyte cell line Sperm motility MNA cells Electric transmembrane potential ATP synthase MNA a murine neuroblastoma cells 3. Good health medicine.anatomical_structure Biochemistry 317 Pharmacy Acidosis JC-1 5 5′ 6 6′-tetrachloro-1 1′ 3 3′-tetraethylbenzimidazolyl-carbocyanine iodide keratinocytes endocrine system PN pyridine nucleotides MITOCHONDRIAL DYSFUNCTION BCF bioconcentration factor mitochondrial depolarization 119 Other natural sciences Oxidative phosphorylation Biology PK-15 a porcine kidney tubular epithelial cell line Article PI propidium iodide ΔΨp membrane potential of the plasma membrane lcsh:RA1190-1270 spermatozoa MIN-6 a murine pancreatic beta cell line medicine MIC minimal inhibitory concentration sperm motility RLM rat liver mitochondria aerobic glycolysis PBMC monocyte-enriched peripheral blood mononuclear cells lcsh:Toxicology. Poisons Pancreatic islets HaCaT fungi PBMC motility inhibition Molecular biology Triclosan ΔΨ electric transmembrane potential beta cells TPP+ tetraphenylphosphonium chemistry Uncoupler biology.protein 3111 Biomedicine |
| Zdroj: | Toxicology Reports, Vol 2, Iss C, Pp 624-637 (2015) Toxicology Reports |
| ISSN: | 2214-7500 |
| DOI: | 10.1016/j.toxrep.2015.03.012 |
| Popis: | Highlights • We show (sub)cellular toxicity of triclosan (TCS) on six types of mammalian cells. • 1–5 μg ml−1 TCS induced metabolic acidification and uncoupled respiration. • TCS ceased progressive boar sperm motility at 1 μg ml−1. • TCS uncouples ATP synthetase complex V in mitochondrion. • TCS caused regression of pancreatic islets to pycnotic cells. Effects of triclosan (5-chloro-2′-(2,4-dichlorophenoxy)phenol) on mammalian cells were investigated using human peripheral blood mono nuclear cells (PBMC), keratinocytes (HaCaT), porcine spermatozoa and kidney tubular epithelial cells (PK-15), murine pancreatic islets (MIN-6) and neuroblastoma cells (MNA) as targets. We show that triclosan (1–10 μg ml−1) depolarised the mitochondria, upshifted the rate of glucose consumption in PMBC, HaCaT, PK-15 and MNA, and subsequently induced metabolic acidosis. Triclosan induced a regression of insulin producing pancreatic islets into tiny pycnotic cells and necrotic death. Short exposure to low concentrations of triclosan (30 min, ≤1 μg/ml) paralyzed the high amplitude tail beating and progressive motility of spermatozoa, within 30 min exposure, depolarized the spermatozoan mitochondria and hyperpolarised the acrosome region of the sperm head and the flagellar fibrous sheath (distal part of the flagellum). Experiments with isolated rat liver mitochondria showed that triclosan impaired oxidative phosphorylation, downshifted ATP synthesis, uncoupled respiration and provoked excessive oxygen uptake. These exposure concentrations are 100–1000 fold lower that those permitted in consumer goods. The mitochondriotoxic mechanism of triclosan differs from that of valinomycin, cereulide and the enniatins by not involving potassium ionophoric activity. |
| Databáze: | OpenAIRE |
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