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PubMed1989

The inhibition of granulocyte phagocytosis by various components of nasal drops.

The effect of two decongestive substances and two preservatives used in nasal drops on phagocytosis by human granulocytes was studied. The vasoactive substances oxymetazoline chloride and zylometazoline chloride incubated with human granulocytes during 20 min. gave a reduction of phagocytosis to almost zero when using concentrations found in commercially used nasal drops (500 mg/l respectively 1000 mg/l). However, a dilution of 1:100 was consistent with an almost normal phagocytic function. The preservatives benzalkonium chloride and thiomersal gave a dose related reduction of phagocytosis down to zero. A dilution of 1:100 of the benzalkonium chloride solution used commercially (200 mg/l) and a dilution of 1:10 of the thiomersal solution used commercially (24 mg/l) were needed to get an almost normal phagocytic function. These results together with previous studies indicate that the addition of preservatives in nasal drops should be questioned, excluded or replaced with other less harmful substances.

Administration, Intranasal↗
PubMed1993

Inhibition of human neutrophil actin polymerization, phagocytosis and oxidative burst by components of decongestive nosedrops.

Human neutrophil functions have been examined after exposure of leukocytes to components of decongestive nosedrops in vitro. Both the vasoactive components oxymethazoline chloride and xylomethazoline chloride, as well as the preservative benzalkonium chloride, showed a concentration- and time-dependent deleterious effect on neutrophil actin polymerization, phagocytosis and oxidative burst. The most toxic of the drug components was benzalkonium chloride, which in the commercial nosedrops tested was present in concentrations about 20 times higher than that compatible with intact neutrophil functions. These findings suggest possible inhibition of mucosal neutrophil activity following exposure to nosedrops in vivo, and support earlier reports that have questioned the use of preservatives in decongestive nosedrops.

Actins↗
PubMed1995

The effect of a benzalkonium chloride-containing nasal spray on human respiratory mucosa in vitro as a function of concentration and time of action.

Human respiratory mucosa was exposed to oxymetazoline nasal spray in varying concentrations and for varying periods of time in vitro. The drug destroyed the tissue in a concentration- and time-dependent manner. In the experiments with various concentrations of the spray, some tissue fragments retained their viability throughout the experiment. This number increased parallel to a decrease in concentrations of the test substance. All the tissue fragments exposed to undiluted nose spray underwent severe destructive alterations during the exposure period. These alterations appeared first and were most extensive in those exposed for the longest periods of time. It has previously been demonstrated that the toxic effect of oxymetazoline nasal spray in vitro is probably due to the preservative benzalkonium chloride. The apparent lack of consistency between the toxic effects of benzalkonium chloride in vitro and in vivo is discussed, with special reference to protective systems absent in vitro but present in vivo.

Adenoids↗
PubMed1997

Actions of spermicidal and virucidal agents on electrogenic ion transfer across human vaginal epithelium in vitro.

Human ectocervical tissue was removed at operation over the menstrual cycle mounted as a sheet in vitro in an Ussing-style chamber and incubated in bicarbonate saline. The net electrogenic ion transport was measured as the short-circuit current (Isc in muamps/cm2) and was characterised as mainly (60-86%) an amiloride-sensitive electrogenic Na+ transport (lumen to serosa). Serosal application of amiloride had no effect. Serosal application of ouabain, a selective Na(+)-pump inhibitor, reduced the Isc to near zero but neither theophylline (10 mM) nor furosemide (1 mM) had any action. The data are compatible with a model ectocervical vaginal cell having an amiloride-sensitive Na+ entry mechanism at the lumenal membrane and a Na(+)-pump at the basolateral membrane removing the ion from the cell. The effects of the putative virucides, chlorhexidine and benzalkonium chloride, were tested on the preparation. Mucosally added chlorhexidine (2 mg/ml) had no effect on the Isc or tissue resistance but benzalkonium chloride, at concentrations between 0.06-1.2%, caused a rapid fall in the Isc. At the highest concentration this was only partly reversible even after two washes with fresh buffer. At the lowest concentration (0.03%) benzalkonium chloride sometimes caused an initial increase in the Isc which then fell to zero. In all the tissues even after the Isc was reduced to near zero, nigrosin left in contact with the tissue for 5 min. did not enter and stain the cells, indicating the detergent had a selective membrane action rather than causing a non-specific increase in permeability. The preparation allows objective measurements to be made of the initial acute membrane actions of putative spermicides and virucides on human vaginal ectocervical epithelial cells and offers a new approach of assessing their pharmacological/toxicological actions.

Adult↗
PubMed1975

Permeability of rabbit corneal epithelium to horseradish peroxidase after the influence of benzalkonium chloride.

A tight barrier against permeation of horseradish peroxidase into the corneal epithelium exists at the corneal surface adjacent to the tear film. The present light and transmission electron microscopic study reveals that the cationic surfactant, benzalkonium chloride, which is commonly added to eye drops as a preservative, breaks down this barrier. Lysis of the cell membranes was demonstrated, resulting in a leakage of the tracer into and underneath the superficial cells. The grade of cellular destruction caused by benzalkonium chloride was dependent upon the concentration and exposure time of the drug.

Animals↗
PubMed1975

The effect of benzalkonium chloride on the electropotential of the rabbit cornea.

The effect of benzalkonium chloride on the electropotenial of the cornea has been examined. The anterior surface of the in vivo or in vitro cornea was exposed to various concentrations of the surfactant, from 0.005% to 0.02%, for either 1 or 2 min. The initial effect is a hyperpolarization lasting up to 30 sec, followed by a rapid fall in potential difference with a subsequent recovery. The degree of potential difference decrease and the recovery rate was dependent upon both the concentration of the detergent, and the exposure time. There is excellent correlation between the previous anatomical and physiological studies on tracer penetration across the in vivo and in vitro cornea and our present work. The data indicate that benzalkonium chloride acts by breaking down the physiological and anatomical diffusion barrier to solute and solvent which is located in the outer layer of the epithelium.

Animals↗
PubMed1975

Effects of benzalkonium chloride upon the corneal epithelium studied with scanning electron microscopy.

The corneal surface of rabbits and vervet monkeys was studied by means of scanning electron microscopy after the influence of the cationic surfactant, benzalkonium chloride. The concentration of the drug was 0.02% or 0.01% and the exposure time was 2 or 4 min. The corneas treated with the drug had characteristic changes with small holes or more extensive lesions of the superficial cell membranes, and loss of microvilli or microplicae. The damage was considered to be due to the lytic effect of benzalkonium chloride upon the plasma membranes.

Animals↗
PubMed1977

Effects of ophthalmic vehicles on the stability of the precorneal film.

The break up time (B.U.T.) of the precorneal film has been studied before and after application of 34 different vehicles. The material examined comprised 646 eyes. Maximum increase of the B.U.T. was obtained with 2% methyl cellulose (four times) and 10% polyvinyl alchohol (seven times). These vehicles in the usually employed concentrations, fat-free ointment (polyethylene glycol), acetyl cysteine and polysaccharide (dextran) affected a less pronounced prolongation. The B.U.T. was reduced four or five times by fatty, anhydrous ointments and by silicone oil, about two or three times by emulsions and oils, and twice by 0.01% benzalkonium chloride. The clinical significance of the B.U.T. alterations is discussed.

Acetylcysteine↗
PubMed1982

The effect of ophthalmic preservatives on the shape of corneal endothelial cells.

The mean area (293.6 +/- 53.6 micrometers 2) and perimeter (65.5 +/- 5.8 micrometers) of individual cells were determined from the photographed endothelium of a total of 54 guinea pig corneas, after staining with silver nitrate and removal of the epithelium and stroma. In addition a quantitative assessment of cell shape S (= P2/A) was calculated. The mean cell density (3406 +/- 619 cells per mm2) was similar to that for young humans, and the S value (14.76 +/- 0.73) was as expected for slightly irregular hexagonal and pentagonal shapes. Incubation of the corneas in glutathione-bicarbonate-Ringer solution for periods up to 4 h resulted in only slight changes in the endothelial cell shape (S = 15.21 +/- 0.89). However, incubation with thimerosal (0.01%) for 2 h (S = 16.78 +/- 1.79) or with disodium ethylenediaminetetraacetate (Na2EDTA) (0.2%) for 1 h (S = 17.20 +/- 2.36) gave a marked increase in the tortuosity of the cell 'outlines'. Longer periods of contact with Na2EDTA resulted in a rounding up and separation of endothelial cells.

Animals↗
PubMed1986

Ultrastructural changes to corneal stromal cells due to ophthalmic preservatives.

Normal and keratectomised rabbit corneas received drops containing preservatives over a two day period. All preservatives investigated caused some change in the morphology of the stromal keratocytes, particularly in the absence of the anterior epithelial barrier. Thimerosal (0.004%) or disodium ethylenediaminetetraacetate (0.1% Na2EDTA) produced only minimum change. Chlorbutanol (0.5%) applied to intact corneas resulted in swelling of the cytoplasm and occasionally breaks in the external cell membrane, whilst in the keratectomised corneas some mitochondria showed swelling and distortion of cristae. In the normal cornea, benzalkonium chloride (0.02% or 0.01% with 0.1% Na2EDTA) resulted in intra and extracellular oedema and contraction of keratocytes. On removal of the superficial layers, there was extensive disruption of mitochondria, other organelles and outer cell membranes resulting in total destruction of some cells. Benzalkonium chloride should not be used on corneas with abnormalities of the epithelium.

Animals↗