title: Loss of thiol repair systems in human cataractous lenses.
abstract: OBJECTIVE
  The purpose of this study was to investigate the thiol repair systems of thioltransferase (TTase) and thioredoxin (Trx) and oxidation-damaged proteins in human cataractous lenses.
  
  
  METHODS
  Cataractous lenses in humans (57-85 years of age) were classified into cortical, nuclear, mixed, mature, and hypermature cataract types by using a lens opacity classification system, and were obtained by extracapsular cataract extraction (ECCE) procedure. Cortical and nuclear cataracts were grouped by decreasing order of visual acuity into optical chart reading (R), counting fingers (CF), hand motion (HM), and light perception (LP). ECCE lens homogenate was analyzed for glutathione (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 each dissected into cortical and nuclear portions for measurement of glyceraldehyde 3-phosphate dehydrogenase (G3PD) activity. Clear lenses (in humans 49-71 years of age) were used as control.
  
  
  RESULTS
  Compared with control, all cataractous lenses lost more than 80% GSH and 70% GR; TR and Trx activity; and 40% to 70% TTase activity, corroborated with the loss in visual acuity. Among cataracts with R and CF visual acuity, cortical cataract lost more cortical G3PD activity (18% of control) than that of nuclear cataract (50% of control), whereas GSH depletion and TTase inactivation were similar in both cataracts.
  
  
  CONCLUSIONS
  Thiol repair systems were damaged in all types of cataracts. Cortical and nuclear cataracts showed differential G3PD inactivation in the cortex, implying those 2 type of cataracts might be formed through different mechanisms.
authors.affiliation: Department of Ophthalmology, Sichuan Provincial People's Hospital, Chengdu, China School of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Nebraska, United States.
authors.forename: Min
authors.initials: M
authors.lastname: Wei
authors.affiliation: School of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Nebraska, United States Redox Biology Center, University of Nebraska-Lincoln, Lincoln, Nebraska, United States.
authors.forename: Kui-Yi
authors.initials: KY
authors.lastname: Xing
authors.affiliation: Department of Ophthalmology, Sichuan Provincial People's Hospital, Chengdu, China.
authors.forename: Yin-Chuan
authors.initials: YC
authors.lastname: Fan
authors.affiliation: Second University Eye Department, the Second University, Naples, Italy.
authors.forename: Teodosio
authors.initials: T
authors.lastname: Libondi
authors.affiliation: School of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Nebraska, United States Redox Biology Center, University of Nebraska-Lincoln, Lincoln, Nebraska, United States Department of Ophthalmology, University of Nebraska Medical Center, Omaha, Nebraska, United States.
authors.forename: Marjorie F
authors.initials: MF
authors.lastname: Lou
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000378:metabolism*; D002386:Cataract / Q000378:metabolism* / Q000473:pathology; D005260:Female; D054477:Glutaredoxins / Q000378:metabolism*; D006801:Humans; D015151:Immunoblotting; D007908:Lens, Crystalline / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D013879:Thioredoxins / Q000378:metabolism*
chemical_list: D054477:Glutaredoxins; D013879:Thioredoxins
keywords: PSSG; PSSP; glyceraldehyde 3-phosphodehydrogenase; human cataract; oxidative stress; redox regulation; thiol oxidation damage repair; thioltransferase system; thioredoxin system