PMID: 16617294Apr 18, 2006Paper

Estradiol attenuates mitochondrial depolarization in polyol-stressed lens epithelial cells

Molecular Vision
James M Flynn, P R Cammarata

Abstract

This study examined the state of mitochondrial physiology subsequent to exposing lens epithelium to high ambient galactose (Gal), which upon conversion to galactitol (GalOH) and resultant intracellular accumulation thereof, leads to profound destabilization of mitochondrial membrane potential (Deltapsim). Further, we determined whether the aldose reductase (AR) inhibitor, Sorbinil, or estrogen (17beta-E2, and its isomer, 17alpha-E2, which exhibits marginal binding affinity for estrogen receptor), administered prior to and concomitant with Gal exposure might prevent or delay mitochondrial membrane depolarization. Secondary cultures of bovine lens epithelial cells (BLECs), as well as a virally-transformed human lens epithelial cell line (HLE-B3), were maintained in 40 mM galactose (Gal) for up to seven days in the presence and absence of Sorbinil, 17beta-E2 or 17alpha-E2. Endogenous accumulation of reactive oxygen species (ROS) was assessed by loading cells with H2DCF-DA, which upon oxidation in the presence of ROS transitions to the fluorescent compound, DCF. To assess Deltapsim, confocal microscopy was employed in conjunction with the potentiometric dye, JC-1. Intracellular polyol content was determined by gas chromatography. C...Continue Reading

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