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PubMed1981

Hexachlorophene and the central nervous system. Toxic effects in mice and baboons.

A study on hexachlorophene encephalopathy in mice and baboons is reported. By light microscopy, a severe spongiform lesion of the central nervous system (CNS) was localized in the white matter, without myelin breakdown or cellular reaction. By electron microscopy, the myelin alteration was characterized by wide intralamellar spaces or "splitting" developed in the intraperiod line of compact sheaths. The acute changes described were induced by administration of the drug by the digestive or cutaneous routes at various dosage levels in an aqueous solution or in talcum powder. The toxic effects depended on the age of the animals, the survival times and the concentrations of hexachlorophene, i.e., 6%, 3%, and 0.5%. The findings are compared with previous reports on the neurotoxicity of hexachlorophene and other chemicals in human and experimental animals. Hexachlorophene cannot be recommended for use in young infants because of its neurotoxicity in very low doses as demonstrated in the present report.

Age Factors↗

PubMed1975

Investigation of hexachlorophene for dominant lethal effects in the mouse.

Hexachlorophene (HCP) was studied for mutagenic effects in the dominant lethal test on mice. Groups of male mice were treated with either 2.5 or 5.0 mg hexachlorophene per kg body weight as a single intraperitoneal injection. Control animals were treated with the propylene glycol vehicle. Each male was mated with 3 untreated females for each of 8 consecutive weeks with the uterus of the females examined at mid-pregnancy for signs of early embryonic death. Treatment did not alter mating capacity and fertility of the males. The administration of hexachlorophene had no influence on pre- or post-implantation losses. An increase in early resorptions among female mice bred to males treated with the reference compound, methyl methanesulfonate (MMS) given a single i.p. injection of 100 mg/kg, indicated the susceptibility of the mouse strain used to a known mutagen. It is concluded that hexachlorophene at maximally tolerated doses is not mutagenic in the dominant lethal test in mice.

Animals↗

PubMed2000

Inhibition of the Staphylococcus aureus NADPH-dependent enoyl-acyl carrier protein reductase by triclosan and hexachlorophene.

Enoyl-acyl carrier protein reductase (FabI) plays a determinant role in completing cycles of elongation in type II fatty acid synthase systems and is an important target for antibacterial drugs. The FabI component of Staphylococcus aureus (saFabI) was identified, and its properties were compared with Escherichia coli FabI (ecFabI). ecFabI and saFabI had similar specific activities, and saFabI expression complemented the E. coli fabI(Ts) mutant, illustrating that the Gram-positive FabI was interchangeable with the Gram-negative FabI enzyme. However, ecFabI was specific for NADH, whereas saFabI exhibited specific and positive cooperative binding of NADPH. Triclosan and hexachlorophene inhibited both ecFabI and saFabI. The triclosan-resistant ecFabI(G93V) protein was also refractory to hexachlorophene inhibition, illustrating that both drugs bind at the FabI active site. Both the introduction of a plasmid expressing the safabI gene or a missense mutation in the chromosomal safabI gene led to triclosan resistance in S. aureus; however, these strains did not exhibit cross-resistance to hexachlorophene. The replacement of the ether linkage in triclosan by a carbon bridge in hexachlorophene prevented the formation of a stable FabI-NAD(P)(+)-drug ternary complex. Thus, the formation of this ternary complex is a key determinant of the antibacterial activity of FabI inhibitors.

Amino Acid Sequence↗

PubMed2006

Hexachlorophene inhibits Wnt/beta-catenin pathway by promoting Siah-mediated beta-catenin degradation.

Aberrant activation of Wnt/beta-catenin signaling and subsequent up-regulation of beta-catenin response transcription (CRT) is a critical event in the development of human colon cancer. Thus, Wnt/beta-catenin signaling is an attractive target for the development of anticancer therapeutics. In this study, we identified hexachlorophene as an inhibitor of Wnt/beta-catenin signaling from cell-based small-molecule screening. Hexachlorophene antagonized CRT that was stimulated by Wnt3a-conditioned medium by promoting the degradation of beta-catenin. This degradation pathway is Siah-1 and adenomatous polyposis colidependent, but glycogen synthase kinase-3beta and F-box beta-transducin repeat-containing protein-independent. In addition, hexachlorophene represses the expression of cyclin D1, which is a known beta-catenin target gene, and inhibits the growth of colon cancer cells. Our findings suggest that hexachlorophene attenuates Wnt/beta-catenin signaling through the Siah-1-mediated beta-catenin degradation.

Anti-Infective Agents, Local↗

PubMed1971

Antimicrobial actions of hexachlorophene: cytological manifestations.

Hexachlorophene is a soap-compatible bisphenol that has been widely used as an antiseptic, yet its mechanism of action is undefined. The relative threshold concentration for bactericidal effect on a susceptible test organism, Bacillus megaterium, was established to be about 10 mug/mg of cell dry weight. At this or at high (>/=100 mug/mg) concentration, adsorptive uptake by cells displayed saturation kinetics. At about 30 mug/mg, the time course of adsorption occurred in three distinct stages. The triphasic pattern was interpreted to represent successive penetration of and adsorption by the cell wall, the protoplast membrane, and the cytoplasm. This interpretation was substantiated by determinations of hexachlorophene adsorption by isolated cell components. Electron microscopy disclosed cytopathology, evidenced as gaps or discontinuities, in the protoplast membrane (but not in the cell wall or cytoplasm) at > 30 mug of hexachlorophene per mg of cell dry weight. Similarly, treatment with > 30 mug/mg allowed a fluorescigenic dye (tolyl-peri acid) to penetrate into the protoplast. However, no detectable cytological manifestations were discerned at the minimum lethal concentration of 10 mug/mg. Apparently, hexachlorophene is physically disruptive at intermediate or high relative concentrations but acts in a more subtle fashion at the minimal lethal concentration.

Adsorption↗

PubMed1971

Antimicrobial actions of hexachlorophene: lysis and fixation of bacterial protoplasts.

Hexachlorophene was found to be both a lytic and a fixative agent for protoplasts isolated from Bacillus megaterium. Concentrations of 50 to 100 mug of drug per mg of original cell dry weight were required to lyse 4.4 x 10(9) protoplasts (2 mg of original cell dry weight). At higher drug concentrations, protoplasts became fixed against osmotic stress and reduced in sensitivity to disruption by n-butanol. Lower drug concentrations caused proportionate lysis in the protoplast population. Intact cells lost the ability to become plasmolyzed at these same hexachlorophene concentrations. Nonplasmolyzed, drug-treated cells were resistant to the action of lysozyme, whereas plasmolyzed, drug-treated cells were sensitive. But the sensitivity of isolated cell walls to lysozyme digestion was not markedly altered by hexachlorophene treatment. These effects appeared to be secondary in the killing of cells by hexachlorophene because they occurred at concentrations higher than the minimum lethal concentration.

Alcohols↗

PubMed1975

Serial hexachlorophene blood levels in the premature infant.

The concentration of hexachlorophene was determined in serial blood samples taken from seven premature infants washed with pHisoHex. Results indicated that after a single wash with 5ml of pHisoHex, blood concentrations reached a maximum of 0.75-1.20mug/ml two to four days after application. The results obtained in this study confirm that the dermal absorption of hexachlorophene is greater in premature than in full-term infants. Use of hexachlorophene for infants. Use of hexachlorophene for infants of birth weight less than 2kg has now been discontinued at Queen Mary Hospital and the amount of pHisoHex used in the initial toileting of infants with birth weight more than 2kg has been limited to a single application of 5ml.

Birth Weight↗

PubMed1978

Bioassay of hexachlorophene for possible carcinogenicity.

A bioassay of hexachlorophene for possible carcinogenicity was conducted by administering the test chemical in feed to Fischer 344 rats. Groups of 24 rats of each sex were administered hexachlorophene at one of three doses, either 17, 50, or 150 ppm, for 105-106 weeks. Higher doses of 200-600 ppm, used in 8-week subchronic studies, induced neuronal necrosis of the brain and clinical signs of toxicity. Matched-control groups consisted of 24 untreated rats of each sex. All surviving animals were killed at 105-106 weeks. Mean body weights of the rats were unaffected by the hexachlorophene, and no clinical signs of toxicity were recorded. Survival also was unaffected, and adequate numbers of animals survived, permitting meaningful evaluation of the incidences of late-appearing tumors. No tumors were present in a statistically significant incidence at any site in the treated rats. It is concluded that under the conditions of this bioassay, hexachlorophene did not induce malignant or benign tumors in Fischer 344 rats.

Journal Article↗

PubMed1984

Interaction of hexachlorophene and other compounds with spin-labeled brain membranes.

Experiments reported here demonstrate that hexachlorophene influences oxidation-reduction events inside the brain membrane, possibly via a free radical mechanism. This was shown by nitroxide spin label quenching inside the rat cerebellum membrane bilayer due to the interaction between hexachlorophene and peroxidase-hydrogen peroxide system. Prior addition of antioxidants, e.g., vitamin E or butylated hydroxytoluene, prevented such membrane-bound fatty acid spin label reduction, presumably due to their free radical scavenging abilities. The 5-doxyl stearic acid spin probe attached to the brain membranes did not exhibit any detectable changes in their ESR spectra nor, consequently, in the microviscosity of the membranes when exposed to up to 40 mM hexachlorophene.

Animals↗

PubMed1975

Neurotoxicity of hexachlorophene: new pathological and biochemical observations.

Twenty female rats with nursing litters were fed a diet containing 500 p.p.m. of hexachlorophene (HCP). The blood concentrations of hexachlorophene in mother rats were 4.7-6.0 mug/ml and in infant rats 2.0-2.5 mug/ml. Fifty percent of mother rats and 75% of infant rats died. Most of the surviving animals were asymptomatic apart from imparied visual function. Ten adult and 20 infant rats were killed by perfusion. Light- and electron-microscopic studies showed vacuolation of myelin in the central and peripheral nervous system and axonal degeneration which was especially severe in the optic nerves. After withdrawal of HCP hydrocephalus ex vacuo was present in the chronically intoxicated infant rats and the optic nerves showed marked atrophy and gliosis. Studies with liver mitochondria prepared from lactating hexachlorophene-fed rats showed a 50-75% inhibition of respiration with succinate as substrate.

Animals↗

PubMed1985

In vitro inhibition of Giardia lamblia and Trichomonas vaginalis growth by bithionol, dichlorophene, and hexachlorophene.

Bithionol, dichlorophene, and hexachlorophene, which are used in treating some helminthic infections, killed trophozoites of Giardia lamblia and Trichomonas vaginalis in modified BI-S-33 and Asami media, respectively. Virtually all G. lamblia and T. vaginalis cells were killed within 24 h with a 0.42 mM concentration of these compounds, except that 0.93 mM dichlorophene was required for sterilizing T. vaginalis in the same period. In modified BI-S-33 and Asami media from which bovine and human sera were omitted, respectively, the inhibitory actions of the compounds against in vitro growth of these protozoa were significantly enhanced. Trophozoites of G. lamblia and T. vaginalis could be killed in shorter than 10 min with 0.074 mM dichlorophene and 0.0025 mM hexachlorophene, respectively, in serum-free media. G. lamblia, which was incubated in the complete medium containing dichlorophene, showed a characteristic swelling of the ventral side which led to disruption of the parasite, whereas bithionol caused a thin crack in the cytoplasm of T. vaginalis incubated in Asami medium. The crack appeared to enlarge and result in vacuolization of T. vaginalis. These observations suggest that bithionol, dichlorophene, and hexachlorophene merit further evaluation to ascertain whether they are useful for treatment of giardiasis and trichomoniasis.

Animals↗

PubMed1990

Hexachlorophene toxicosis in a litter of Doberman pinschers.

A litter of 5-week-old Doberman Pinschers with pustular dermatitis was treated dermally with a hexachlorophene-containing emulsion. Shortly after a second treatment, all of the puppies developed neurologic signs consisting of muscle tremors, ataxia, and apparent muscle weakness. The clinical history and signs, histologic lesions within the central nervous system, and measurement of hexachlorophene in liver and kidney tissue confirmed a diagnosis of hexachlorophene toxicosis.

Animals↗

PubMed1975

Hexachlorophene retinopathy in rats.

The primary effect of hexachlorophene on rat retina is disruption of the disc membranes of photoreceptor outer segments and irreversible destruction of their cell bodies. The neurons of the ganglion cell layer of the retina also become affected, probably secondary to optic nerve lesions present in hexachlorophene intoxication. The early and probably reversible changes of the discs are vacuolation and vesiculotubular degeneration. Vacuolation in the discs results from separation of their inner aspects. This lesion is analogous to the separation of myelin lamellae at the intraperiod line, also produced by hexachlorophene.

Animals↗

PubMed1975

Recurrence of skin disease in a nursery: ineffectuality of hexachlorophene bathing.

An outbreak of streptococcal and staphylococcal skin disease was discovered in a full-term nursery after the discontinuation of bathing infants with hexachlorophene. The epidemic was only temporarily controlled by conventional means and recurred despite reinstitution of hexachlorophene bathing. Measures that decreased infants' exposure to visitors and hospital personnel and enforced aseptic techniques in the nursery were more important than use of hexachlorophene soap in achieving and maintaining control.

Anti-Bacterial Agents↗

PubMed1979

Suspected link between exposure to hexachlorophene and malformed infants.

Retrospective studies, performed in 6 hospitals in Sweden, demonstrated that severe congenital malformations occurred more frequently in neonates born to mothers who used hexachlorophene soaps, 10--60 times a day by handwashing and hand-creams during at least the first trimester of pregnancy (25 severe malformations in 460 neonates), when compared to neonates born to similarly employed mothers who did not use hexachlorophene soaps (0 severe malformations in 233 neonates). Minor congenital anomalies were also more commonly noted in the hexachlorophene-exposed group when contrasted with controls. Other known adverse influences, such as age, infections during pregnancy, other drug usage, or smoking habits did not appear different in the two groups.

Abnormalities, Drug-Induced↗

PubMed1983

Comparative activity of benzoyl peroxide and hexachlorophene. In vivo studies against propionibacterium acnes in humans.

The bactericidal effects of benzoyl peroxide (5% lotion) and hexachlorophene (3% colloidal suspension) against Propionibacterium acnes were compared in nine healthy college students who had the microbiological and skin lipid characteristics typical of acne vulgaris, but no active lesions. Each of the two medications was applied twice daily, to opposite sides of the face, for four consecutive weeks. Hexachlorophene was effective against surface aerobes but only slightly active against P acnes. It marginally reduced free fatty acid concentrations in surface lipids and in follicular porphyrin fluorescence. Conversely, benzoyl peroxide virtually eliminated P acnes and aerobes and induced substantially decreased free fatty acid concentrations and follicular fluorescence. We conclude that benzoyl peroxide exerts its antimicrobial action in the follicles and inhibits P acnes, while the antimicrobial effectiveness of hexachlorophene is limited to the skin surface.

Acne Vulgaris↗

PubMed1984

[Caustic diaper dermatitis and encephalitis secondary to the application of talcum contaminated with hexachlorophene].

Five observations of infants with transcutaneous intoxication by 6,3 p. 100 hexachlorophene contaminated talcum powder are reported. The diaper dermatitis is particular because of its topography (red pants shape), of its sudden occurring, of its papyraceous aspect evoking caustic origin, and of its association with severe encephalopathy. The neurological signs start with epileptic fits leading rapidly to coma. Prognosis is serious leading either to death or to paraplegia. Enquiry on that epidemic shows that mortality raised up to 18 p. 100. The neurological signs with oedematous degeneration of myelin are characteristic of hexachlorophene toxicity. Plasma levels of toxics range up to 15,94 mg/ml i.e. 30 times more than the rates observed by Curley in a premature washed with a commercial solution containing 3 p. 100 hexachlorophene. During a toxic neurological syndrome, the existence of diaper dermatitis with red plants shape must lead to an aetiological diagnosis of the possibility of transcutaneous intoxication even if the product seems as harmless as talcum powder.

Animals↗

PubMed1978

Cell binding and growth inhibition by hexachlorophene of decanoate and their reversibility.

More than 80% of the hexachlorophene added to a Bacillus subtilis culture binds to the cells. Complete growth inhibition requires 6 x 10(5) molecules bound per cell. In contrast, more than 99% decanoate remains in solution and 3.8 x 10(7) molecules bound per cell are needed to inhibit growth. Centrifugation and resuspension of cells in growth medium removes only decanoate, whereas the addition of 1% bovine serum albumin to the growth medium removes both inhibitors from their binding sites on the cells. The addition of untreated cells to a hexachlorophene-treated culture enables the hexachlorophene molecules to redistribute among all the cells with the result that the inhibited cells can resume growth.

Bacillus subtilis↗