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PubMed1997

Cooperative inhibition of acetylcholinesterase activities by hexachlorophene in human erythrocytes.

Hexachlorophene (HCP), pentachlorophenol (PCP), 2,4,5-trichlorophenol (2,4,5-TCP) and 2,4,6-trichlorophenol (2,4,6-TCP) all hemolyzed washed human erythrocytes and inhibited acetylcholinesterase (AchE) activities in erythrocyte membrane. HCP was much more potent in either effect than any other compound examined. The inhibition of AchE activities by HCP was reversed on adding albumin. The dose-response curves by HCP and PCP were sigmoidal, indicating cooperative inhibition, while those by 2,4,5-TCP and 2,4,6-TCP were not. Furthermore, the cooperativity of the inhibition by HCP was greater than by PCP. Differing from that by PCP, the cooperativity of inhibition increased depending on the temperature (13, 25, 37 degrees C) and decreased when the membrane was treated with Triton X-100. The cooperativity was also decreased in the presence of albumin. On a Scatchard plot analysis, erythrocyte membranes appeared to have multiple binding sites of different affinities for HCP; binding of HCP to the low affinity site [dissociation constant (Kd) 4.7 x 10(-5) M] seemed to be responsible for the observed cooperative inhibition of AchE activities. Neither neostigmine nor fenitrothion altered the cooperativity. HCP seems to be the most potent cooperative inhibitor of AchE in human erythrocyte membranes known to date. HCP may be useful to examine AchE and milieu in human erythrocyte membranes.

Adult↗

PubMed1975

Biochemical and pathological studies of myelin in hexachlorophene intoxication.

Adult female rats were fed a diet containing 500 ppm hexachlorophene (HCP). Morphological study of brains from these animals showed vacuolation of the myelin sheaths due to separation of myelin lamellae at the minor dense line. However, myelin could be isolated from the brains of these animals in normal yield. The myelin isolated from HCP-fed animals had normal lipid and protein compositions as shown by analyses of the individual lipids and by disc gel electrophoresis of the proteins. Assay of the myelin-specific enzyme, 2',3'-cyclic nucleotide-3'-phosphohydrolase, showed normal specific activity in myelin obtained from HCP-fed rats. Brains of HCP-fed rats showed an increase in wet weight and a decrease in dry weight, with the chloroform-methanol insoluble fraction showing the greatest weight loss. During isolation of myelin from HCP-fed rats material was found floating over 0.32 M sucrose. This "floating fraction" contained a higher ratio of lipid to protein but the same relative proportions of the individual lipids as are found in myelin. The yield of "floating fraction" from each HCP-fed rat was less than 10 percent of the yield of myelin. Disc gel electrophoresis demonstrated the presence of the usual myelin proteins in this fraction, but with a slight increase in the relative amount of the low molecular weight basic protein. The data were compared to reports on the biochemistry of triethyltin poisoning, and it was concluded that vacuolation of myelin in HCP poisoning is probably due to increased permeability of myelin lamellae to water and electrolytes.

Animals↗

PubMed1979

Effect of organotin compounds and hexachlorophene on brain adenosine cyclic 3',5'-monophosphate metabolism.

The effect of triethyltin (TET), triphenyltin (TPT), hexachlorophene (HCP) and cuprizone on adenosine cyclic 3',5'-monophosphate (cyclic AMP) production in rat brain was examined both in vitro and in vivo. TET and TPT inhibited basal adenylate cyclase activity of brain homogenate at a concentration as low as 1 microM in vitro but these compounds had no effect on norepinephrine (NE) and dopamine(DA)-stimluated enzyme activity. HCP and cuprizone failed to inhibit adenylate cyclase activity. In vivo TET given intravenously at a dose rate of 10 mg/kg decreased the cyclic AMP content of cerebrum, but not of medulla. TPT and HCP give intravenously and intraperitoneally respectively failed to decrease the cyclic AMP content of the cerebrum. In the case of TET the reduction in cyclic AMP content of the cerebrum was prevented by maintaining the rats normothermic after treatment. On the basis of these results the inhibition of adenylate cyclase produced by TET in brain homogenates in vitro would not appear to be involved in the development of nervous changes associated with acute TET toxicity, or in the production of progressive brain oedema caused by TET, HCP and cuprizone.

Adenylyl Cyclases↗

PubMed1991

Persistent light reaction to hexachlorophene.

The first patient with what appears to be persistent light reaction caused by hexachlorophene alone is reported. Persistent light reaction may occur in patients with milder degrees of photosensitivity, and appropriate photopatch testing should be performed.

Female↗

PubMed1988

Effect of short-term exposure to hexachlorophene on rat brain cell specific marker enzymes.

Seven cell specific marker enzymes in brain and optic nerve and morphological evaluation by light microscopy were used to characterize the neurotoxicity associated with exposure of rats to hexachlorophene (HCP; 40 mg/kg/day, po, for 9 days). In vitro exposure to HCP at concentrations up to 100 microM had no direct inhibitory effect on the marker enzymes, validating their use in evaluating brain function in vivo. Rats exhibited a reduction in body weight gain, weakness, and ataxia of the hind limbs by the ninth day of HCP exposure. At 24 hr following the last day of exposure to HCP, the activities of the three neuron specific enzymes, glutamic acid decarboxylase, tyrosine hydroxylase, and choline acetyltransferase, in rat brain were unchanged from those of the vehicle-treated control group. Of the two astroglial enzyme markers measured, a small but significant increase was observed in the activity of nonneuronal enolase in the cerebellum and glutamine synthetase in the hippocampus of HCP-treated rats. The optic nerve appeared to be the most sensitive tissue in that the activity of both the astroglial marker, nonneuronal enolase, and the myelin marker, 2',3'-cyclic nucleotide phosphohydrolase, was significantly decreased following HCP exposure. This decrease in enzyme activity is consistent with the histological observations demonstrating extensive vacuolization and edema in the optic nerve after exposure to HCP.

Animals↗

PubMed1984

Protection with butylated hydroxytoluene and other compounds against intoxication and mortality caused by hexachlorophene.

The antioxidants butylated hydroxytoluene (BHT) and ethoxyquin protected rats against intoxication and mortality normally produced by hexachlorophene (HCP, 100 mg/kg). BHT also prevented the elevation of cerebrospinal fluid pressure, a central nervous system effect of HCP poisoning. In addition, both phenobarbital and SKF-525A protected against HCP poisoning, with the barbiturate also offering significant protection against triethyltin. L-Ascorbic acid, vitamin E, N,N-diphenyl-p-phenylenediamine and reduced and oxidized glutathione over a range of doses were ineffective in preventing HCP lethality. The protective effect of phenobarbital against HCP and triethyltin intoxication further supports existing evidence of a common or similar mechanism of toxic action for these two structurally dissimilar compounds.

Animals↗

PubMed1978

Effect of hexachlorophene intoxication on learning in rats.

Neurotoxicity in the form of hindlimb paralysis is known to be associated with brain lesions characterized by vacuolation of the white matter following hexachlorophene (HCP) intoxication; these paralytic and histopathological effects are reversible with time after discontinuance of HCP exposure. The rates of acquiring a bar-pressing escape and avoidance behavior were measured in female rats after recovery from paralysis following daily oral dosing with HCP (25 mg/kg). Learning deficits were seen as a delay in reaching a 90% escape performance level, as an increase in the number of sessions required to reach a 50% avoidance criterion, as an increase in training time needed to transfer from escape to avoidance responding, and by an increase in the number of sessions needed to reach a maximum level of avoidance behavior over a 35-session period. Peak responding eventually reached a level comparable to controls only after prolonged periods. Brain lesions seen 2-3 months after HCP intoxiciation correlated with the lag in learning ability but not with the maximum avoidance acquisition before sacrifice. These results indicate a long-lasting behavioral deficiency following neurotoxicity which is slowly reversible.

Animals↗

PubMed1978

Vaginal absorption of hexachlorophene in the rat.

The pharmacokinetics of hexachlorophene (HCP) was studied in sexually mature virgin Wistar rats. [14C] HCP was injected either via the femoral vein, (ivn, 0.87 or 3.87 mg/kg in saline) or into the vaginal orifice (ivg, 0.87 mg/kg in corn oil). The disappearance of 14C from the blood after ivn administration followed the kinetics of a 2 compartment open model. The blood 14C profiles were superimposable, suggesting that the distribution and elimination rate constants for both doses were similar. After ivg application of [14C] HCP, 14C was detected in tail blood at 0.5 h, peaked between 2 and 4 h and disappeared slowly to 12 h but more rapidly thereafter. Less than 10% of the ivg dose of [14C] HCP remained in the vagina after 4 h. The cumulative recoveries of 14C in the faeces and urine 5 days after ivn administration were 85% and 4.6% of the dose, respectively. Comparable recoveries following ivg administration were 72% and 3.7%. The results suggest that HCP readily penetrates through the vaginal mucosa of the rat.

Absorption↗

PubMed1980

The effect of hexachlorophene on the optic nerve and visual faculty in Beagle dogs after prolonged dermal application.

In a systemic tolerance study in Beagle dogs the effect of an ointment, containing 1, 3 or 10% hexachlorophene (HCP), applied dermally, on the optic system over a period of 12 weeks was investigated. Besides an irreversible loss of visual faculty during treatment with 3 and 10% HCP, a permanent mydriasis, peripapillary exudations and other alterations of the ocular fundus were observed at the same dose levels, suggesting that HCP has a strong affinity to the optic nervous system in dogs without clear-cut correlations to HCP plasma levels.

Administration, Topical↗

PubMed1984

Catalytic potential of field mouse Mus booduga brain acetylcholinesterase during repeated hexachlorophene treatment.

The catalytic efficiency of the field mouse (Mus booduga) brain acetyl cholinesterase (AChE, EC 3.1.1.7) was significantly (P less than 0.001) decreased probably through the reduction in the active site density of the enzyme content and elevation in the activation energy (delta E) requirements during repeated hexachlorophene (HCP) treatment. Fall in the activity potential of AChE may account for the interference of HCP or its reactive metabolites with the acetylcholine (ACh)-AChE system and deserve consideration in contributing to the neurotoxicity.

Acetylcholinesterase↗

PubMed2000

Hexachlorophene-induced brain edema in rat observed by proton magnetic resonance.

Rat brain was examined with 4.7 T proton magnetic resonance (MR). On administering hexachlorophene (HCP) 30 mg/kg/day for 5 days, myelin-rich structures stood out in T2-weighted images. Apparent diffusion coefficient (ADC) was markedly suppressed in all regions examined except for cerebral cortex. Seven days after terminating the exposure to HCP, without enhancement in T2-weighted images, ADC was still decreased in corpus callosum, optic nerve and trigeminal nerve. Rat administered with HCP and followed with high magnetic field proton MR seems to provide a good model for cytotoxic brain edema, and it may also be useful to visualize heavily myelinated structures.

Animals↗

PubMed1980

Thin section and freeze-fracture studies of hexachlorophene induced alterations in the rat liver with special regard to intercellular junctions.

The ultrastructural changes in the liver cells of male Wistar rats induced by the oral and intraperitoneal application of hexachlorophene (HCP) were studied by using the freeze-fracture technique and by producing ultrathin sections. The rats were given the HCP once at a dose of 30 mg/kg body weight and were sacrificed 60 hours after treatment. The enlargement of bile canaliculi, the disorganization of tight junctions and the increase in number of gap junctions were the most prominent alterations observed in the liver cells. Furthermore, an increase in the smooth and rough endoplasmic reticulum and the microbodies were found. Pathological alterations in the mitochondria were also seen. In general, the effects of the intraperitoneal application on the liver were more pronounced than the effects of the oral application.

Animals↗

PubMed1977

Clinical pharmacology of hexachlorophene in newborn infants.

Bathing with soap containing hexachlorophene was instituted during two major staphylococcal epidemics in a Neonatal Intensive Care Unit. Infants who weighed less than 1,200 gm, those with a postconceptional age of less than 35 weeks, and those with large areas of abraded skin were at highest risk to achieve elevated blood HCP concentrations. T 1/2 of HCP ranged from 6.1 to 44.2 hours and appeared to follow first order kinetics. Time of peak blood concentrations of HCP following a bath ranged from 6 to 10 hours. One infant with liver disease achieved a concentration of HCP of 4,350 ng/ml after seven baths and developed clinical symptoms consistent with HCP toxicity.

Autopsy↗

PubMed1978

Lifespan carcinogenicity studies with hexachlorophene in mice and rats.

Hexachlorophene (HCP) was tested for carcinogenicity in lifetime feeding studies in male Sprague--Dawley rats that were fed on a protein- and vitamin-deficient diet and in C57B1 and XVII/G mice that received the chemical incorporated into a complete diet. After 2 years, no significant carcinogenic effects were observed in these animals. In XVII/G mice injected subcutaneously at birth or receiving HCP via the mother's milk, the incidence of tumors was not statistically increased. No carcinogenic effect was observed in (C57B1 X C3H) F1 hybrid mice that received HCP transplacentally.

Administration, Oral↗

PubMed1988

Deviations in hepatic amino acid profiles of mouse following repeated hexachlorophene administration.

Effects of repeated administration of hexachlorophene (HCP) on the food consumption, body and liver weights, liver somatic indices and hepatic levels of the free amino acids and amino acid-enzyme activities have been studied. A dose-dependent reduction in body weights and food consumption and increased liver somatic indices suggested a progressive and on toward response to HCP. The concentrations of hepatic free amino acids: phenylalanine, tyrosine, leucine, isoleucine, valine, threonine, asparagine, glutamic acid and glutamine were significantly (p less than 0.001) increased while serine, glycine, taurine and alanine levels were unaffected. The aspartic acid levels showed a conspicuous decrement. The specific activity patterns of the amino acid-enzymes denoted reduced oxidation of amino acids in liver. The abnormal rise in branched chain and aromatic amino acids could be due to the reduced utilization because of the depletion of skeletal muscle mass and hepatic dysfunction in HCP intoxication. A pronounced reduction in aspartic acid levels may deserve consideration in the manifestation of hyperammonemia and neurologic symptoms in HCP intoxication.

Alanine Transaminase↗

PubMed1992

Hexachlorophene induced alterations in brain carbohydrate metabolism of Wistar rat.

Effect of repeated oral administration of hexachlorophene (HCP) on glycolytic and oxidative pathways was studied in the rat brain. The rats were divided into three batches of six in each batch. The first batch was treated with paralytic dose (60 mg.kg-1.day-1) of HCP for 7 days. The second batch of animals was treated with sublethal dose (18 mg.kg-1.day-1) for 7 days. The third batch of animals was served as the age matched controls which received vehicle (corn oil) only. The glycolytic and oxidative metabolism of carbohydrates was significantly inhibited in the brain of rat during HCP treatment and the inhibition was more pronounced in paralytic dose treatment as compared to sublethal dose treatment. The inhibition of NADP-isocitrate dehydrogenase coupled with glucose 6-phosphate dehydrogenase indicates reduced generation of NADPH2 and pentoses for the synthesis of fatty acids and nucleotides.

Administration, Oral↗

PubMed1982

Reduced nerve blood flow in hexachlorophene neuropathy: relationship to elevated endoneurial fluid pressure.

To test the hypothesis that increased endoneurial fluid pressure (EFP) causes a reduction in nerve blood flow (NBF) in the vasa nervorum, we adapted a noninvasive method for measurement of nerve blood flow which was originally developed for measurement of local cerebral blood flow. This technique measures tissue distribution to the radioisotope, 14C-iodoantipyrine, and was used to compare NBF in sciatic nerves of rats with increased EFP induced by feeding them hexachlorophene (HCP), a neurotoxin which causes edema exclusively to the nervous system and confined to the myelin sheath. Elevation of interstitial fluid pressure in peripheral nerves from control values of 2.0 +/- 1.0 cm H2O to over approximately 6 cm H2O was associated with a statistically significant reduction in nerve blood flow from 14.8 +/- 5.9 to 7.8 +/- 2.5 ml/100 g of tissue/minute (min). These results support the hypothesis that increased endoneurial fluid pressure exacerbates the neuropathy by diminishing local blood flow.

Animals↗

PubMed1976

Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps.

Twenty-six patients undergoing chemotherapy for acute leukemia on a protected environment-prophylactic antibiotic program were randomly assigned to bathe with either P-300 or a 3% hexachlorophene preparation. Both agents substantially reduced the microbial flora of the skin, but the latter preparation was slightly more effective. The bacteriostatic compounds in both preparations were absorbed through the skin but no toxic effects were observed.

Bacterial Infections↗