We studied the effects of visible (400-750 nm), infrared (750-1100 nm), and ultraviolet (300-400 nm) radiation on the breakdown of the blood-aqueous barrier (BAB) in albino rabbit eyes using ...fluorophotometry and fluorescein-bound albumin. There was no evidence of BAB breakdown following exposure to visible (158 J cm-2) or infrared (106 J cm-2) radiation. Fluorescence was detected in the anterior chamber 15 min following ultraviolet (UV) (300-400 nm; 37 J cm-2 and 73 J cm-2) and ultraviolet-A (UV-A) (320-400 nm; 45 J cm-2 and 90 J cm-2) irradiation. This fluorescence peaked at 2 hr after irradiation. Reestablishment of the BAB, indicated by no detectable fluorescence, occurred in all animals after 24 hr. There was a significant increase in fluorescence with increasing UV-irradiation dosage in all groups (P less than 0.05). Comparison of BAB breakdown following exposure to ultraviolet 320-400 nm and 300-400 nm in the same dosage (45 J cm-2) indicated that the inclusion of shorter wavelength UV exposure produced a significantly higher degree of BAB breakdown (P less than 0.001).
125I-Labeled choleragen was bound to liposomes containing galactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl)-galactosylglucosylce ramide (GM1), but not in large amounts to ganglioside-free ...liposomes nor to those containing N-acetylneuraminylgalactosylglucosylceramide (GM3), N - acetylgalactosaminyl - (N - acetylneuraminyl) - galactosylglucosylceramide (GM2), or N-acetylneuraminylgalactosyl-N-acetylgalactosaminyl-(N- acetylneuraminyl)-galactosylglucosylceramide (GD1a
). Choleragen released trapped glucose only from GM1-liposomes. This choleragen-induced glucose release from GM1-liposomes was relatively rapid for the first few minutes, then continued more slowly. The amount of glucose released from liposomes in 30 min was dependent on both the GM1content and choleragen concentration. Prior incubation of GM1-liposomes with anti-GM1antiserum prevented the choleragen-dependent release of trapped glucose. After incubation of GM1-liposomes with choleragen, addition of anticholeragen antibodies and complement led to more extensive glucose release. Under these latter conditions a much smaller glucose release was observed also from liposomes containing GM1or N-acetylneuraminylgalactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl)-ga lactosylglucosylceramide in the absence of choleragen. These releases were attributed to naturally-occurring antiganglioside antibodies in the antiserum and complement. Ganglioside-free liposomes did not release glucose in response to anticholeragen and complement. It appears that choleragen in the absence of other proteins binds specifically to liposomes containing GM1and can induce permeability changes.
We studied the effects of the Nd:YAG laser on the blood-aqueous barrier following photodisruption of the anterior capsule, posterior capsule, and mid-vitreous of the albino rabbit eye with ...fluorophotometric techniques using albumin-bound fluorescein. After photo-disruption of the anterior capsule, fluorescence appeared in the anterior chamber at 30 minutes, peaked at two hours, and decreased almost to baseline values by 24 hours. No fluorescence was noted at any time in contralateral control eyes or in eyes receiving photo-disruption of the posterior capsule or mid-vitreous.
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