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Kuiyi Xing, Min Wei, Y Fan, Marjorie F. Lou; Damage of Thiol Repair Systems in the Human Cataractous Lenses. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1551.
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To investigate the thiol repair systems of thioltransferase (TTase) and thioredoxin (TRx), and the oxidatively damaged proteins in the human cataractous lenses.
Human cataractous lenses (57-85 yrs) were classified into cortical, nuclear, mixed, mature and hypermature cataracts by LOCSIII system and obtained through extracapsular cataract extraction (ECCE) procedure. Cortical and nuclear cataractous lenses were also grouped according to decreasing order of visual acuity: optical chart reading (R), counting fingers (CF), hand motion (HM), and light perception (LP). Homogenate of ECCE lenses was used to determine free GSH level and enzyme activities of TTase, glutathione reductase (GR), TRx and thioredoxin reductase (TR). Cortical and nuclear cataractous lenses (8 of each) with visual acuity better than HM were also dissected into cortical and nuclear portions to examine the activity of glyceraldehyde 3-phosphate dehydrogenase (G3PD), a marker for oxidation damage. Clear lenses (8 of 49-71 yrs) were dissected into cortical and nuclear portions and used as controls.
Compared with the control, all cataractous lenses lost more than 80% GSH, 70% activity of GR, TR and TRx, and 40-70% of TTase activity, and the loss in GSH pool and enzyme activities corroborated with the status of visual acuity. Furthermore, in the cataracts with visual acuity of R and CF, the cortical cataract lost more G3PD activity (18% of control) in the cortical region than that of the nuclear cataract (50% of control). However, the loss in GSH pool and TTase activity was similar in the cortex of both types of cataracts.
The thiol repair systems were damaged in all types of cataracts. Cortical cataract and nuclear cataract showed different degree of G3PD inactivation in the cortex, implying this two type of cataracts may be formed through different mechanisms.
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