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At least 19 recordsLinked to original sources
PubMed1982

Hexachlorophene. Secondary microorganism resistance to hexachlorophene. Conjugative transfer inhibition by the R-plasmid-coded resistance by hexachlorophene.

Strain resistance of the genus Escherichia, Salmonella, and Pseudomonas to hexachlorophene is inducible. Secondary resistance of the Gram-negative microorganisms to hexachlorophene is an inherited property of these strains. There are not any explicit differences of primary sensitivity to hexachlorophene between sensitive strains and those resistant to antibiotics. The secondary resistance level of Gram-negative microorganisms to hexachlorophene is also not dependent on the natural resistance (or sensitivity) of strains to antibiotics. Hexachlorophene, in concentration of 10 micrograms/ml of conjugation mixture, causes 100% inhibition of the conjugation transfer of the resistance determinants to antibiotics from tested strains with conjugative R-plasmid. The indirect secondary resistance conjugation transfer to hexachlorophene was verified in two cases. The resistance to hexachlorophene was transferred, coupled with resistance to chloramphenicol, tetracycline, and streptomycin, from the Escherichia coli strains (No. 8) and Salmonella typhimurium (No. 4) to the recipient Escherichia coli strain K 12, SZK-Ec-329/74 (No. 2).

Anti-Bacterial Agents↗
PubMedDate not supplied

Hexachlorophene retinopathy in suckling rats. A light- and electron-microscopic study of short-term and long-term effect of hexachlorophene intoxication on the retina of young rats.

Hexachlorophene (HCP) in very large doses has a toxic effect on the retina of adult rats. The present study examined the sensitivity of the developing retina to smaller doses and its ability to recover from neurotoxic damage. Suckling rats were intoxicated with HCP added to the mothers' diet. The retinae of the pups were examined by light and electron microscopy for early and late effects. All dose levels above 100 ppm caused vacuolar degeneration of the outer segments of photoreceptor cells within 14 days of intoxication, followed by degeneration of the inner segments after 28 days. The cell bodies of photoreceptor cells and all other retinal layers remained normal. Suckling intoxicated with HCP (100 - 500 ppm) added to the mothers' diet for 28 days and then withdrawn, showed no recovery of the outer or inner segments o photoreceptors when examined up to 150 days later. In addition, extensive degeneration and loss of photoreceptor cell occurred after withdrawal of HCP and the degenerative process extended to involve the inner nuclear layer. The rate of appearance of pathological changes was proportional to the total amount of ingested HCP. This study showed that photoreceptor cells in newborn rats are highly sensitive to HCP. The retinal lesions were irreversibly an continued to progress by continued trans-synaptic degeneration after withdrawal of the toxic agents.

Animals↗
PubMed2001

Enoyl-ACP reductase (FabI) of Haemophilus influenzae: steady-state kinetic mechanism and inhibition by triclosan and hexachlorophene.

Steady-state kinetics, equilibrium binding, and primary substrate kinetic isotope effect studies revealed that the reduction of crotonyl-CoA by NADH, catalyzed by Haemophilus influenzae enoyl-ACP reductase (FabI), follows a rapid equilibrium random kinetic mechanism with negative interaction among the substrates. Two biphenyl inhibitors, triclosan and hexachlorophene, were studied in the context of the kinetic mechanism. IC(50) values for triclosan in the presence and absence of NAD(+) were 0.1 +/- 0.02 and 2.4 +/- 0.02 microM, respectively, confirming previous observations that the E-NAD(+) complex binds triclosan more tightly than the free enzyme. Preincubation of the enzyme with triclosan and NADH suggested that the E-NADH complex is the active triclosan binding species as well. These results were reinforced by measurement of binding kinetic transients. Intrinsic protein fluorescence changes induced by binding of 20 microM triclosan to E, E-NADH, E-NAD(+), and E-crotonyl-CoA occur at rates of 0.0124 +/- 0.001, 0.0663 +/- 0.002, 0.412 +/- 0.01, and 0.0069 +/- 0.0001 s(-1), respectively. The rate of binding decreased with increasing crotonyl-CoA concentrations in the E-crotonyl-CoA complex, and the extrapolated rate at zero concentration of crotonyl-CoA corresponded to the rate observed for the binding to the free enzyme. This suggests that triclosan and the acyl substrate share a common binding site. Hexachlorophene inhibition, on the other hand, was NAD(+)- and time-independent; and the calculated IC(50) value was 2.5 +/- 0.4 microM. Steady-state inhibition patterns did not allow the mode of inhibition to be unambiguously determined, but binding kinetics suggested that free enzyme, E-NAD(+), and E-crotonyl-CoA have similar affinity for hexachlorophene, since the k(obs)s were in the same range of 20-24 s(-1). When the E-NADH complex was mixed with hexachlorophene ligand, concentration-independent fluorescence quenching at 480 nm was observed, suggesting at least partial competition between NADH and hexachlorophene for the same binding site. Mutual exclusivity studies, together with the above-discussed results, indicate that triclosan and hexachlorophene bind at different sites of H. influenzae FabI.

Binding Sites↗
PubMed1978

Endoneurial pressure in hexachlorophene neuropathy.

Increased endoneurial pressure of up to 17.0 cm H2O was recorded in the peripheral nerves of rats fed hexachlorophene in their laboratory diet. The pressure was measured using a micropressure transducer developed for recording pressure in the microcirculation. The results were correlated with morphologic findings. Teased nerve fibers and araldite-embedded specimens of hexachlorophene damaged sciatic nerve revealed the characteristic severe intramyelinic edema due to splits in the minor dense lines of compact myelin giving rise to wide interlamellar spaces as shown in previous studies. The endoneurial pressure of rats exposed to hexachlorophene for 11 days and subsequently fed a normal diet returned to normal (0.2-3.0 cm H2O) after 12 days, and morphologic examination showed few residual abnormalities. Prolonged exposure to hexachlorophene for up to 4 weeks caused widespread axonal degeneration in addition to intramyelinic edema. Animals treated with hexachlorophene for 21 days followed by a normal diet for 14 days showed degenerated axons, phagocytosis of myelin as well as interstitial edema and elevated endoneurial pressure. It is suggested that axonal degeneration in hexachlorophene neuropathy is caused by increased endoneurial pressure.

Animals↗
PubMed1983

Vaginal absorption of hexachlorophene during labor.

Surgical soap that contains hexachlorophene is used as an antiseptic lubricant for vaginal examinations during labor in some centers. Theoretically, hexachlorophene can be absorbed from the vaginal mucosa and be potentially toxic to the fetus and neonate. To evaluate vaginal absorption and placental transfer of hexachlorophene, we measured levels in mixed arterial/venous cord serum and postpartum maternal serum in 28 women whose vaginal examinations were lubricated with pHisoHex during labor. The serum of 12 women had detectable levels of hexachlorophene, with a high level of 942 ng/ml. Cord serum had detectable levels in nine neonates, with a high level of 617 ng/ml. The conclusion is that hexachlorophene from vaginal lubricants is variably absorbed from the vaginal mucosa, and appreciable amounts can be detected in maternal and cord serum. Because of the potential for neonatal hexachlorophene toxicity, we recommend the use of alternative lubricants for pelvic examinations during labor.

Absorption↗
PubMed1976

Hexachlorophene lesions in newborn infants.

Vacuolization of the white matter of the brain is produced by a number of disease entities and chemicals, including hexachlorophene. Brains of 135 stillborn infants and infants dying in the neonatal period were examined for vacuole formation in the white matter to determine if any hexachlorophene-like lesions could be found. A nonsignificant excess of vaculoes was found in infants bathed in hexachlorophene at birth compared with infants not bathed in it. Analysis of 11 brains for hexachlorophene showed that detectable levels were present in five, all of which showed vacuolization. None was detected in the remaining six, three of which also showed vacuolization. In two of these there was no hexachlorophene exposure.

Abnormalities, Drug-Induced↗
PubMed1979

Translocation, distribution, and environmental degradation of hexachlorophene in tomatoes.

The translocation, distribution, metabolism and environmental degradation of hexachlorophene were investigated in tomato plants (Lycopersicon esculentum Mill cv. beefsteak). All plants were grown under standardized conditions and treated with leaf-applied 14C-ring-labeled hexachlorophene (HCP). Treatment time ranged from 0 to 70 days. Autoradiographic analyses were performed on all plants. Selected plant tissues were extracted and chromatographed, using thin layer (TLC) and gas liquid chromatography (GLC). Hexachlorophene was not translocated from the plant leaves. No metabolites of hexachlorophene was found. A slight, but statistically nonsignificant, amount of HCP was lost from the leaves and the inert controls. At the end of the 70-day treatment, based on TLC and regression analysis of thin layer chromatographic plates, averages of 89.5% and 75.9% of the applied HPC remained unaltered on the treated plants and controls, respectively. This indicated that 10.5% and 24.1%, respectively, of the original HCP had been altered. Differences between the treatments and controls were statistically significant after 28 days of exposure. Further analyses of the above data, using gas chromatographic methods, showed that as many as 14 peaks were found in the treated samples and the controls, including the parent material. Ultraviolet photolysis seemed to be the mechanism responsible for alteration of the hexachlorophene. Three extracted chlorinated compounds have been identified by GC-mass spectral (MS) analysis including 2,2'-dihydroxy-3,5',6,6'-tetrachlorodiphenylmethane, 2,2'-dihydroxy-3,5,5',6,6'-pentachlorodiphenylmethane, and 2,2'-dihydroxy-3,3',5,5',6,6'-hexachlorodiphenylmethane (parent HCP). Eleven other electrophylic compounds have been found in various treated plant or control extracts. Further analyses will be necessary to verify the identification of the other degradation products.

Biodegradation, Environmental↗
PubMed1998

Efficacy of glutamate receptor antagonists in the management of functional disorders in cytotoxic brain oedema induced by hexachlorophene.

The hexachlorophene-induced cytotoxic brain oedema is an experimental model of brain damage, suitable for testing cerebroprotective substances (Andreas 1993). In order to examine whether glutamate receptors are involved in mediating functional disorders due to neurotoxic brain damage, we have studied the protective effects of several competitive and non-competitive antagonists using adult male Wistar rats in a simple "ladder-test" for assessing coordinative motor behaviour. Hexachlorophene-induced brain damage was verified by histological examination of the cerebellum with vacuolation of white matter, astrocyte hypertrophy and astrocyte proliferation taken as signs of neurotoxic injury. The non-competitive N-methyl-D-aspartate (NMDA) antagonist dizocilpine maleate (MK-801) decreased the motor disturbance on the first and second day of the "ladder-test" when applied in the doses 0.1 mg/kg and 0.2 mg/kg intraperitoneally for 3 weeks during the hexachlorophene treatment. Acute MK-801 administration (0.1 mg/kg intraperitoneally) after 3 weeks hexachlorophene exposure improved the coordinative motor response only on the first day. When testing the competitive NMDA receptor antagonist 2-amino-5-phosphonopentanoic acid (AP-5) in the dose 1.0 mg/kg intraperitoneally the motor disturbance was lowered significantly earlier than in spontaneous remission. Similar effects were observed with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) in the dose of 0.8 mg/kg intraperitoneally, an antagonist interacting both with the strychnine-insensitive binding site for glycine within the NMDA receptor complex and with the kainate(+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor complex. Concurrent MK-801 administration decreased the vacuolation of white matter. The results suggest that NMDA receptors and non-NMDA receptors are involved in development of functional disorders induced by hexachlorophene.

2-Amino-5-phosphonovalerate↗
PubMed1971

Antimicrobial actions of hexachlorophene: release of cytoplasmic materials.

Intracellular solutes were released from growing or resting cells of Bacillus megaterium as a consequence of hexachlorophene treatment. The effect was dose dependent, with the optimum at a concentration about sevenfold greater than the minimal lethal dose. The effects of pH and temperature on the leakage process also were inconsistent with the killing effects of the drug. The types of materials released appeared to be the same with or without hexachlorophene treatment. The released materials were small molecules which apparently derived from preexisting ribonucleic acid and protein, but not from deoxyribonucleic acid. Compared to the effects of other representative surface-active agents and other bis-phenols, hexachlorophene was superior in ability to cause leakage of intracellular materials. Different microorganisms varied in their susceptibility to hexachlorophene, with Pseudomonas aeruginosa and a paracolon isolate the most resistant of the vegetative cells examined. It was concluded that the release of intracellular solutes was an effect secondary to the lethal event and presumably arose from hexachlorophene-mediated stimulation of degradative enzymes.

Bacillus megaterium↗
PubMed1977

Micromethod for measuring hexachlorophene in whole blood by gas-liquid chromatography.

We describe a micromethod for measuring hexachlorophene by use of gas-liquid chromatography with a 63Ni electron capture detector. The procedure requires 100 micronl of blood for extractions of hexachlorophene, and dichlorophene is added as an internal standard. CV is 3.4% over the concentration range of 500 to 1300 microng of hexachlorophene per liter of whole blood. This procedure permits repeated measurements of hexachlorophene in newborns who are being washed with soap containing hexachlorophene.

Chromatography, Gas↗
PubMed1975

Neurotoxicity of hexachlorophene in humans. II. A clinicopathological study of 46 premature infants.

To assess neurotoxic effects of hexachlorophene in the human population previously shown to be most at risk, a blind clinicopathological analysis was made of all premature infants under 1,400 gm birth weight who survived at least four days and were examined by autopsy over a 7.5-year period. Repeated whole-body bathing of premature newborn infants in 3% hexachlorophene-bearing soap (undiluted pHisoHex) shows a significant statistical association with a vacuolar encephalopathy of the brain stem reticular formation. The prevalence of the vacuolar encephalopathy in premature infants on whom we have adequate brain stem histological information appears to be related to the number of exposures to hexachlorophene, the concentration of hexachlorophene, the thoroughness of rinsing, and other factors (including exposure to ultraviolet light).

Administration, Topical↗
PubMed1993

Efficacy of cerebroprotective substances in the management of functional disorders induced by the cytotoxic brain oedema-producing substance hexachlorophene.

The hexachlorophene-induced cytotoxic brain oedema is used as experimental model of brain damage, suitable for testing cerebroprotective substances. It has clinical importance since many brain injuries are accompanied by an oedema. The primary target of the neurotoxin, hexachlorophene, is the neuronal cell membrane, but it also causes secondary effects including a disruption of myelin lamellae, increases in water and sodium content, decreases of potassium content, and vacuolation in the white matter. Rats received orally hexachlorophene 240 mg/kg a day for three weeks by liquid diet. The disruption of coordinative motor response, observed in a specially developed test, was used to characterise hexachlorophene-induced injuries in studies designed to evaluate the potential of cerebroprotective substances. Because of their membranotropic efficacy some nootropic substances with different modes of action were examined. The disturbance of coordinative motor response was restored significantly earlier than in spontaneous remission following administration of piracetam, pyritinol, methyl glucamine orotate, naftidrofuryl, and also under the influence of the calcium antagonists cinnarizine, flunarizine and nifedipine. These results support the therapeutic use of nootropic substances in the management of neurotoxic injuries and brain oedema.

Animals↗