289.5), trivial names triclosan and irgasan, was introduced to commerce in 1964, in products of health care industry in 1972 and is since then in wide spread world-wide use in personal care products, textiles, food contact materials. The antibacterial preservative 5-chloro-2′-(2,4-dichlorophenoxy) phenol (mol. The mitochondriotoxic mechanism of triclosan differs from that of valinomycin, cereulide and the enniatins by not involving potassium ionophoric activity. These exposure concentrations are 100–1000 fold lower that those permitted in consumer goods.

Experiments with isolated rat liver mitochondria showed that triclosan impaired oxidative phosphorylation, downshifted ATP synthesis, uncoupled respiration and provoked excessive oxygen uptake. 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). Triclosan induced a regression of insulin producing pancreatic islets into tiny pycnotic cells and necrotic death. 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. 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.

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