Abstract

The Impact of Senile Cataract Maturity on Blood Oxidative Stress Markers and Glutathione-Dependent Antioxidants: Relations with Lens VariablesOxidative stress is implicated in senile cataract (SC) genesis, although the impact of SC maturity on blood oxidative stress markers is unclear. Total hydroperoxides, malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) were measured in the blood and lens samples of patients having either immature (n=31) or mature SC (n=50), and in 22 blood samples from noncataract controls. Compared to controls, SC patients had higher plasma MDA and serum GST, and decreased plasma GR and GSH levels. Plasma GPx as well as hydroperoxides differed from control values only in patients with mature SC. The multivariate logistic regression analysis showed that the fall of plasma GR activity (OR 5.14; CI 1.82-14.51;p=0.0020), as well as serum GST activity (OR 3.84; CI 1.36-10.83;p=0.0108) were independently associated with the maturity of SC. Lens hydroperoxides, MDA and GST, showed no correlation with correspondent blood values, in contrast to GPx (r=0.715; p<0.001) and GR (r=0.703; p<0.001). This study showed that the severity of SC is associated with increased systemic oxidative stress, which could be due to the fall of GSH-dependent antioxidant enzymes activities.

Highlights

  • An increasing body of evidence suggests that ocular oxidative stress, defined as an imbalance between oxidants and antioxidants, is the key pathophysiological mechanism of senile cataract (SC) genesis [1,2,3,4,5]

  • Summary: Oxidative stress is implicated in senile cataract (SC) genesis, the impact of SC maturity on blood oxidative stress markers is unclear

  • Plasma glutathione peroxidase (GPx) as well as hydroperoxides differed from control values only in patients with mature SC

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Summary

Introduction

An increasing body of evidence suggests that ocular oxidative stress, defined as an imbalance between oxidants and antioxidants, is the key pathophysiological mechanism of senile cataract (SC) genesis [1,2,3,4,5]. The avascular lens contains an unusually high concentration of GSH which spontaneously, or as a cofactor of GPx and GST, reduces a variety of intracellular oxidizing species. Organic peroxides present in the circulation are, converted to correspondent alcohols, mainly by the plasma GPx-3 isoenzyme, a seleno-glycoprotein secreted to the blood by renal proximal tubules, and expressed within the lens [12, 13]. Oxidized vitamin C is uptaken in cells and reduced back to ascorbate by GSH, which acts either directly or as a cofactor of glutaredoxin and erythrocyte membrane cytochrome b561 [16]. This prevents the formation of irreversible, completely oxidized diketogulonic acid and its loss from the body

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