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Paul J Donaldson, Mitchell Nye-Wood, Yadi Chen, Tom White, Ehsan Vaghefi; Inhibition of water and solute fluxes by oxidative stress in a hyperbaric oxygen (HBO) model of lens ageing. Invest. Ophthalmol. Vis. Sci. 2021;62(8):2096.
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© ARVO (1962-2015); The Authors (2016-present)
To determine how water and solute fluxes are affected in a bovine hyperbaric oxygen (HBO) model of lens ageing that has previously been shown to induce an age-dependent hyperopic shift in lens power clinically observed in human lens.
All experiments were performed on bovine lenses that had been first exposed to either 100% nitrogen (HBN) (pressure control group) or 100% oxygen (HBO) at a pressure of 100atm for 15hr in a Cell Disruption Vessel. A pico-injector/microelectrode based pressure measurement system was utilised to measure the intracellular hydrostatic pressure gradient that drives water efflux. T1 based MRI imaging was used to map free water content and to visualise the delivery of the MRI contrast agent FeraSpin XS to the lens core. Western blotting of dissected lens fractions with Cx46 antibodies was used to assess gap junction protein degradation in the different areas of the lens.
HBO exposure significantly increased the free water content in the inner cortex and core of the bovine lens and this change was associated with an increase in the hydrostatic pressure gradient relative to the HBN control. These effects of HBO were deemed to be associated with an inhibition of microcirculation system as the delivery of the FeraSpin XS to the core of the lens was abolished following HBO exposure but was unaffected by incubation in HBN. HBO also induced the degradation of Cx46 in the outer and inner cortex.
Our results show that acute oxidative damage to the lens gap junctions traps water in the lens core causing an elevation of the hydrostatic pressure gradient and an inhibition of solute delivery to the lens core that is driven by the microcirculation system. We envisage that the age-related accumulation of oxidative damage to gap junctions may trigger similar changes in older human lenses, which may eventually contribute to the onset of lens cataract.
This is a 2021 ARVO Annual Meeting abstract.
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