The Effects of Surfactants on the Potential, Short‐circuit Current, and Ion Fluxes Across the Isolated Frog Skin

Webb, G. A.

doi:10.1111/j.1748-1716.1965.tb04077.x

Cited by 14 publications

(6 citation statements)

References 14 publications

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“…They did note an increased initial oxygen uptake of the tissue following detergent treatment, at a time which corresponds to the electrophysiological changes observed by ourselves. Schoeffeniels et al (1962) and Webb (1965) observed an initial hyperpolarization of the isolated frog skin with surfactants. The hyperpolarization was thought to be caused by disruption of cellular integrity through interactions of the surfactant with calcium in the membrane.…”

Section: Discussionmentioning

confidence: 97%

The Effect of Benzalkonium Chloride on the Electropotential of the Rabbit Cornea

Green¹,

Tønjum²

1975

Acta Ophthalmologica

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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.

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Section: Discussionmentioning

confidence: 97%

The Effect of Benzalkonium Chloride on the Electropotential of the Rabbit Cornea

Green¹,

Tønjum²

1975

Acta Ophthalmologica

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“…The mechanisms, whereby the surface-active alkyltrimethylammonium bromides decrease axonal conduction and depress muscle conctraction, is apparently related to the ability of these agents to alter the permeability of the cell membrane. An increased permeability in cells and tissues following a treatment with these surface-active agents has been observed by several authors (Taylor 1963;Webb 1965;Sund 1975;Isomaa 1979). The alteration in permeability is probably a consequence of a burial of the surfactant molecules within the lipid bilayer of the cell membrane.…”

Section: Discussionmentioning

confidence: 88%

“…In experimental studies with isolated preparations, C16 has been found to produce an irreversible block of axonal conduction (Walsh & Lee 1962;Kishimoto & Adelman 1964) and to depolarize frog skin (Webb 1965). In a previous study (Isomaa & Ahlroth 1979) it was found that CIO-C~O depress spontaneous and induced contractions of isolated rat jejunum.…”

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confidence: 96%

Toxicity and Pharmacological Properties of Surface‐active Alkyltrimethylammonium Bromides in the Rat

Isomaa

Bjondahl

1980

Acta Pharmacologica et Toxicologica

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Acute intravenous toxicity and pharmacological properties ofsurface-activealkyltrimethylammonium bromides (CIO-C~O) were studied in female rats. The acute toxicity of the surfactants decreased with an increasing length of the alkyl chain up to a chain length of 16 carbon atoms. Death appeared to be due to respiratory failure. The twitch responses of sciatic nerve-gastrocnemius muscle preparations were reversibly depressed at direct and indirect stimulation following intravenous injections of sublethal doses of C1~-C14. Doses blocking the twitch responses of indirectly stimulated gastrocnemius corresponded to about half the LD50, and at these doses CIO-CIJ caused a transient decrease in respiratory rate. The C16 homologue caused respiratory arrest without affecting the twitch responses of gastrocnemius at relative low intravenous doses. Sublethal intravenous doses of CI~-CZO caused, apparently due to vasodilatation, a tarnsient fall in arterial blood pressure. The depressor response increased and the twitch response decreased with an increase in the length of the alkyl chain up to a chain length of 16 carbon atoms. Both the depression of skeletal muscle contraction and the vasodilatation is suggested to originate from a non-specific effect of the surfactants on muscle cells.

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“…The effects of CPC on translens and intrafibrillar lens potentials are under study. CPC, CTAB, and sodium lauryl sulfate depolarized nerve, muscle membrane, urinary bladder and toad skin [20,24]. Webb [24], working with isolated frog skin, found that at the higher concentrations (2 mmol or more) CPC increased Na+ per meability in addition to inhibiting the Na+ pump.…”

Section: Discussionmentioning

confidence: 99%

“…CPC, CTAB, and sodium lauryl sulfate depolarized nerve, muscle membrane, urinary bladder and toad skin [20,24]. Webb [24], working with isolated frog skin, found that at the higher concentrations (2 mmol or more) CPC increased Na+ per meability in addition to inhibiting the Na+ pump. The epithelium of the lens has a primary role and the cortical fibers a secondary role in maintaining normal K+, Na+ and water lens levels, the capsule allows free diffusion and the lens nucleus functions as a 'sink'.…”

Section: Discussionmentioning

confidence: 99%

Effects of Cetylpyridinium Chloride on the Membranes of the Lens Fibers and on Lens Permeability, Hydration and <sup>22</sup>Na and <sup>86</sup>Rb Transport

Cotlier¹,

Sanders²,

Wyhinny³

1974

Ophthalmic Res

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Cetylpyridinium chloride (CPC) lysed the membranes of the lens fibers without damaging the lens capsule. Swelling of lens fibers preceded their rupture. The following chemical changes were found in lenses incubated in Tyrode’s media containing CPC: gain of Na⁺ ions and water with loss of K⁺ ions, increase in the total Na⁺ + K⁺ ions concentrations (osmolarity), (c) a 10-fold increase in the ²²Na space and 2.6-time increase in the ¹⁴C inulin space (4 h in vitro), (d) marked increases in ⁸⁶Rb and ²²Na lens permeability, (e) inactivation of the ²²Na and ⁸⁶Rb ‘pumps’. CPC exposure resulted in selective lysis of fibers (posterior lens surface) or fibers and epithelial cells (anterior lens surface). At the 0.1-percent CPC concentration, damage to the posterior lens surface increased ⁸⁶Rb permeability and stimulated the ⁸⁶Rb ‘pump’. When the anterior surface was damaged by CPC, the lens permeability to K⁺, Na⁺ or water was greater than when the posterior surface was damaged. Lactate formation in vitro was decreased only when the anterior surface of the lens was exposed to CPC. Na⁺ and K⁺ ions were distributed asymmetrically in the normal rabbit lens. CPC-induced cataracts, with Na⁺ ion gains and K⁺ ion losses were localized to the posterior lens cortex of the rabbit. Circumferential (along fibers) and translenticular movement of Na⁺ or K⁺ ions were present in the cataracts. Na⁺–K⁺ pump-leak by the lens involved systems which were differentiated at the individual fiber or regional level as well as the lens as a whole.

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The Effects of Surfactants on the Potential, Short‐circuit Current, and Ion Fluxes Across the Isolated Frog Skin

Cited by 14 publications

References 14 publications

The Effect of Benzalkonium Chloride on the Electropotential of the Rabbit Cornea

The Effect of Benzalkonium Chloride on the Electropotential of the Rabbit Cornea

Toxicity and Pharmacological Properties of Surface‐active Alkyltrimethylammonium Bromides in the Rat

Effects of Cetylpyridinium Chloride on the Membranes of the Lens Fibers and on Lens Permeability, Hydration and <sup>22</sup>Na and <sup>86</sup>Rb Transport

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