title: Increased glutathione conjugate transport: a possible compensatory protection mechanism against oxidative stress in obesity?
abstract: OBJECTIVE
  To compare glutathione S-conjugate transport in obese and nonobese persons, and how glutathione S-conjugates are involved in the antioxidant status in obesity.
  
  
  METHODS
  The efflux of glutathione conjugates and malondialdehyde (MDA) levels were measured in erythrocytes of obese (N = 33) and nonobese (N = 28) persons at every 30 min during a 120 min incubation time in vitro. 2,4-dinitrophenyl-S-glutathione (DNP-SG) represented the glutathione S-conjugate.
  
  
  RESULTS
  The efflux of conjugate in erythrocytes from obese subjects (708 +/- 147 DNP-SG efflux nmol/ml erythrocytes/h) was significantly higher than that of control group (490 +/- 105 DNP-SG efflux nmol/ml erythrocytes/h) (P < 0.05). At all time points measured (30-120 min), there was an increase in DNP-SG efflux in obese group (P < 0.05). This is manifested by a decrease in cellular DNP-SG levels. The susceptibility of erythrocytes to in vitro 1-chloro-2,4-dinitrobenzene (CDNB)-induced oxidative stress were greater for cells of control group (P < 0.05), although hemolysis sensitivity of these cells are not different between both groups (P > 0.05). Following CDNB pretreatment, incubation of erythrocyte with vanadate, a DNP-SG transport inhibitor, resulted in an increase of MDA in both groups. However, in this case, the difference in susceptibility was not related to obesity. On the other hand, while erythrocyte glutathione level was lower in obese subjects (79% of control) than in controls (P < 0.05), the adenosine 5'-triphosphate (ATP) levels, the enzyme activities of glutathione S-transferase (GST) and the conjugation capacities of the erythrocytes were not different between groups (P>0.05).
  
  
  CONCLUSIONS
  Obesity may increase erythrocyte glutathione conjugate transport independent from ATP and GST activity that may protect against MDA formation in vitro.
authors.affiliation: Division of Medical Biology, Cerrahpasa Medical Faculty, Istanbul University, Turkey.
authors.forename: A
authors.initials: A
authors.lastname: Ozaydin
authors.forename: I
authors.initials: I
authors.lastname: Onaran
authors.forename: T E
authors.initials: TE
authors.lastname: Yeşim
authors.forename: H
authors.initials: H
authors.lastname: Sargin
authors.forename: K
authors.initials: K
authors.lastname: Avşar
authors.forename: G
authors.initials: G
authors.lastname: Sultuybek
mesh_terms: D000255:Adenosine Triphosphate / Q000097:blood; D000328:Adult; D001692:Biological Transport; D002478:Cells, Cultured; D004137:Dinitrochlorobenzene / Q000494:pharmacology; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D005978:Glutathione / Q000031:analogs & derivatives* / Q000097:blood; D005982:Glutathione Transferase / Q000097:blood; D006461:Hemolysis; D006801:Humans; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D009765:Obesity / Q000097:blood* / Q000503:physiopathology; D018384:Oxidative Stress
chemical_list: D004137:Dinitrochlorobenzene; C030190:S-(2,4-dinitrophenyl)glutathione; D008315:Malondialdehyde; D000255:Adenosine Triphosphate; D005982:Glutathione Transferase; D005978:Glutathione