Elsevier

Toxicology Reports

Volume 2, 2015, Pages 624-637
Toxicology Reports

Mitochondrial toxicity of triclosan on mammalian cells

https://doi.org/10.1016/j.toxrep.2015.03.012Get rights and content
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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.

Abstract

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.

Abbreviations

EC50
concentration that diminishes the respective vitality parameter by ≥50%
ΔΨ
electric transmembrane potential
ΔΨp
membrane potential of the plasma membrane
ΔΨm
membrane potential of the mitochondrial membrane
BCF
bioconcentration factor
PBMC
monocyte-enriched peripheral blood mononuclear cells
HaCaT
a spontaneously immortalized (non-neoplastic) keratinocyte cell line
PK-15
a porcine kidney tubular epithelial cell line
MNA
a murine neuroblastoma cells
MIN-6
a murine pancreatic beta cell line
TPP+
tetraphenylphosphonium
JC-1
5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolyl-carbocyanine iodide
MIC
minimal inhibitory concentration
PI
propidium iodide
RLM
rat liver mitochondria
PN
pyridine nucleotides

Keywords

Sperm motility
Oxidative phosphorylation
Uncoupler
Glycolysis
Acidosis
Electric transmembrane potential

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1

These authors contributed equally to the work.