Ca2+-ATPase Activity and Lens Lipid Composition in Reconstituted Systems

Zeng, Junwen; Zhang, Z; Paterson, Christopher A.; Ferguson-Yankey, Stacey R.; Yappert, Marta C.; Borchman, Douglas

doi:10.1006/exer.1999.0703

Cited by 19 publications

(14 citation statements)

References 51 publications

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“…When the hydrocarbon chains of lipids are disordered (fl uid), cholesterol inhibited SERCA activity ( 96 ), especially when cholesterol was forced into the lipid annulus surrounding the protein ( 97 ). However, cholesterol had no effect on SERCA activity when the lipid matrix was composed of bovine ocular lens lipids that are highly ordered ( 42 ).…”

Section: Serca/pmca-lipid Interactionsmentioning

confidence: 93%

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Lipids and the ocular lens

Borchman

Yappert

2010

Journal of Lipid Research

141

133

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Section: Serca/pmca-lipid Interactionsmentioning

confidence: 93%

“…Conversely, the more fl uid and disordered natural environment of SERCA leads to greater activity. Therefore, the differences in the natural lipid environment of SERCA ( 42 ) and PMCA ( 40 ) contribute to the activity of these different enzymes in the lens and thus to calcium homeostasis.…”

Section: Serca/pmca-lipid Interactionsmentioning

confidence: 99%

Lipids and the ocular lens

Borchman

Yappert

2010

Journal of Lipid Research

141

133

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“…For example, cortisol added to red blood cells rapidly intercalated into the polar head group region of membrane phospholipids and decreased Na ϩ /K ϩ -ATPase activity by 24% (48). Hydrocarbon chain ordering has also been shown to influence the function of lens membranes by decreasing the activity of the Ca-ATPase pumps (49). We have shown that ordered membranes scatter twice as much light as disordered membranes (50).…”

Section: Discussionmentioning

confidence: 78%

Direct perturbation of lens membrane structure may contribute to cataracts caused by U18666A, an oxidosqualene cyclase inhibitor

Cenedella

Jacob²,

Borchman

et al. 2004

Journal of Lipid Research

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Induction of cataracts in experimental animals is a common toxic feature of oxidosqualene cyclase (OSC) inhibitors. U18666A has been shown to produce irreversible lens damage within a few weeks of treatment. Drug actions, besides reducing the availability of cholesterol, could contribute to cataract formation. Cholesterol added to cultures of lens epithelial cells could only partially overcome the growth-inhibiting effects of U18666A. In view of this finding and the fact that U18666A and other OSC inhibitors are highly lipophilic cationic tertiary amines, we tested the hypothesis that the cataractogenic effect of U18666A is related to direct perturbation of lens membrane structure and function. Based on changes in the anisotropy of fluorescent probes, U18666A incorporated into bovine lens lipid model membranes increased membrane structural order and, using small-angle x-ray diffraction, U18666A was shown to intercalate into the lens lipid model membranes and produce a broad condensing effect on membrane structure. Also, exposure of cultured lens epithelial cells and intact rat lenses to U18666A induced apoptosis. Induction of apoptosis may begin by intercalation of U18666A into cell membranes. By increasing membrane structural order, U18666A may also increase light scatter, thus directly contributing to lens opacification. -Cenedella, R.

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“…Such alterations have been well documented [144,145] . Of particular relevance to the lens, the decrease in membrane fl uidity that presumably accompanies changes in the lipid composition may have an impact on membrane 'pores' such as the connexins and AQP0, and consequently on diffusion.…”

Section: Transport Within the Lensmentioning

confidence: 95%

Presbyopia: The First Stage of Nuclear Cataract?

McGinty

Truscott²

2006

Ophthalmic Res

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Presbyopia, the inability to accommodate, affects almost everyone at middle age. Recently, it has been shown that there is a massive increase in the stiffness¹ of the lens with age and, since the shape of the lens must change during accommodation, this could provide an explanation for presbyopia. In this review, we propose that presbyopia may be the earliest observable symptom of age-related nuclear (ARN) cataract. ARN cataract is a major cause of world blindness. The genesis of ARN cataract can be traced to the onset of a barrier within the lens at middle age. This barrier restricts the ability of small molecules, such as antioxidants, to penetrate into the centre of the lens leaving the proteins in this region susceptible to oxidation and post-translational modification. Major protein oxidation and colouration are the hallmarks of ARN cataract. We postulate that the onset of the barrier, and the hardening of the nucleus, are intimately linked. Specifically, we propose that progressive age-dependent hardening of the lens nucleus may be responsible for both presbyopia and ARN cataract.

show abstract

Ca2+-ATPase Activity and Lens Lipid Composition in Reconstituted Systems

Cited by 19 publications

References 51 publications

Lipids and the ocular lens

Lipids and the ocular lens

Direct perturbation of lens membrane structure may contribute to cataracts caused by U18666A, an oxidosqualene cyclase inhibitor

Presbyopia: The First Stage of Nuclear Cataract?

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