Mitochondrial toxicity of triclosan on mammalian cells

Charmaine Ajao, Maria Andersson, Vera V Teplova, Szabolcs Nagy, Carl G. Gahmberg, Leif C. Andersson, Maria Hautaniemi, Balazs Kakasi, Merja Roivainen, Mirja Sinikka Salkinoja-Salonen

Research output: Contribution to journalArticleScientificpeer-review

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) paralysed 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.
Original languageEnglish
JournalToxicology reports
Volume2
Pages (from-to)624-637
Number of pages14
ISSN2214-7500
DOIs
Publication statusPublished - 7 Apr 2015
MoE publication typeA1 Journal article-refereed

Fields of Science

  • 317 Pharmacy
  • 3111 Biomedicine
  • 119 Other natural sciences
  • triclosan
  • MITOCHONDRIA
  • MITOCHONDRIAL DYSFUNCTION
  • Insulin
  • beta cells
  • PBMC
  • keratinocytes
  • HaCaT
  • MIN cells
  • spermatozoa
  • metabolic acidosis
  • aerobic glycolysis
  • MNA cells
  • sperm motility
  • motility inhibition
  • PK-15 cells
  • mitochondrial depolarization
  • respiration control

Cite this

Ajao, Charmaine ; Andersson, Maria ; Teplova, Vera V ; Nagy, Szabolcs ; Gahmberg, Carl G. ; Andersson, Leif C. ; Hautaniemi, Maria ; Kakasi, Balazs ; Roivainen, Merja ; Salkinoja-Salonen, Mirja Sinikka. / Mitochondrial toxicity of triclosan on mammalian cells. In: Toxicology reports . 2015 ; Vol. 2. pp. 624-637.
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title = "Mitochondrial toxicity of triclosan on mammalian 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) paralysed 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 withisolated 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.",
keywords = "317 Pharmacy, 3111 Biomedicine, 119 Other natural sciences, triclosan, MITOCHONDRIA, MITOCHONDRIAL DYSFUNCTION, Insulin , beta cells, PBMC, keratinocytes, HaCaT, MIN cells, spermatozoa, metabolic acidosis, aerobic glycolysis, MNA cells, sperm motility, motility inhibition, PK-15 cells, mitochondrial depolarization, respiration control",
author = "Charmaine Ajao and Maria Andersson and Teplova, {Vera V} and Szabolcs Nagy and Gahmberg, {Carl G.} and Andersson, {Leif C.} and Maria Hautaniemi and Balazs Kakasi and Merja Roivainen and Salkinoja-Salonen, {Mirja Sinikka}",
year = "2015",
month = "4",
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language = "English",
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Mitochondrial toxicity of triclosan on mammalian cells. / Ajao, Charmaine; Andersson, Maria; Teplova, Vera V; Nagy, Szabolcs; Gahmberg, Carl G.; Andersson, Leif C.; Hautaniemi, Maria; Kakasi, Balazs; Roivainen, Merja; Salkinoja-Salonen, Mirja Sinikka.

In: Toxicology reports , Vol. 2, 07.04.2015, p. 624-637.

Research output: Contribution to journalArticleScientificpeer-review

TY - JOUR

T1 - Mitochondrial toxicity of triclosan on mammalian cells

AU - Ajao, Charmaine

AU - Andersson, Maria

AU - Teplova, Vera V

AU - Nagy, Szabolcs

AU - Gahmberg, Carl G.

AU - Andersson, Leif C.

AU - Hautaniemi, Maria

AU - Kakasi, Balazs

AU - Roivainen, Merja

AU - Salkinoja-Salonen, Mirja Sinikka

PY - 2015/4/7

Y1 - 2015/4/7

N2 - 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) paralysed 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 withisolated 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.

AB - 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) paralysed 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 withisolated 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.

KW - 317 Pharmacy

KW - 3111 Biomedicine

KW - 119 Other natural sciences

KW - triclosan

KW - MITOCHONDRIA

KW - MITOCHONDRIAL DYSFUNCTION

KW - Insulin

KW - beta cells

KW - PBMC

KW - keratinocytes

KW - HaCaT

KW - MIN cells

KW - spermatozoa

KW - metabolic acidosis

KW - aerobic glycolysis

KW - MNA cells

KW - sperm motility

KW - motility inhibition

KW - PK-15 cells

KW - mitochondrial depolarization

KW - respiration control

U2 - 10.1016/j.toxrep.2015.03.012

DO - 10.1016/j.toxrep.2015.03.012

M3 - Article

VL - 2

SP - 624

EP - 637

JO - Toxicology reports

JF - Toxicology reports

SN - 2214-7500

ER -