摘要:

We have hypothesized that the cholesterol synthesis inhibitor, U18666A, induces nuclear cataracts in the rat by restricting the sterol content of the lens plasma membrane and, therefore, disrupting the structure of gap junctions. In order to directly examine this hypothesis, we isolated total plasma membrane and plasma membrane enriched in gap junctions from the cortical and nuclear regions of lenses from control and U18666A-treated rats. The protein, phospholipid and sterol compositions of the membrane fractions were determined and compared.U18666A treatment resulted in decreased sterol concentrations of both membrane fractions isolated from both the cortical and nuclear regions. The sterol content of total plasma membrane from the cortex and from the nucleus was decreased by 57%, and 36% respectively. The sterol content of the gap junctional membrane (membrane domain enriched in gap junctions) from the cortex and from the nucleus was decreased by 71% and 43% respectively. The observation of a selective decrease in the total sterol content of the cortical gap junctional membrane was reinforced by finding a 50% decrease in the sterol/phospholipid molar ratio of this fraction. The corresponding decrease in the sterol/phospholipid ratio of cortical total plasma membrane was only 22%. The sterol/phospholipid ratio of nuclear total plasma membrane was slightly increased (16%), and the sterol/phospholipid ratio of nuclear gap junctional membrane was decreased by only 8%.These data suggest to us that inhibition of cholesterol synthesis in the rat lens by U18666A results in a specific restriction of cholesterol availability for the synthesis of gap junctional membrane. Alteration of the sterol environment of these plasma membrane organelles may be the first step in the cataractogenesis induced by U18666A.

ISSN:0271-3683    

DOI:10.3109/02713688809015150

出版商:Taylor&Francis    

年代:1988

数据来源: Taylor

摘要:

Intravitreal injection of purified human chorionic gonadotropin (hCG) in rabbits decreased intraocular pressure (IOP). A dose-dependent decrease in IOP was observed with intravitreal hCG concentrations at 30 nM and 100 nM. The onset of this effect was later than 10 hr following the injection and it lasted for more than 24 hrs. The purified beta-subunit of hCG caused a similar decrease in IOP with a short duration. The threshold intravitreal concentration was 10 nM. Unlike the intact hCG, the hCG beta-subunit was inactive as a gonadotropic agent to activate the adenylate cyclase in the rat testis. Intravitreal injection of rabbit luteinizing hormone, which was active as a gonadotropic agent, had no effect on IOP in 4 intravitreal concentrations ranging from 1 nM to 30 nM. These observations indicate that the mechanism of IOP decrease by intravitreal hCG is not related to its gonadotropic action. The IOP decrease in rabbits due to intravitreal hCG or its beta-subunit is probably related to a contaminant or an immune reaction.

ISSN:0271-3683    

DOI:10.3109/02713688809015151

出版商:Taylor&Francis    

年代:1988

数据来源: Taylor