Original Article

International Journal of Obesity (2006) 30, 134–140. doi:10.1038/sj.ijo.0803108; published online 4 October 2005

Increased glutathione conjugate transport: a possible compensatory protection mechanism against oxidative stress in obesity?

A Ozaydin1, I Onaran1, T E Yes cedilim2, H Sargi nodotn3, K Avs cedilar4 and G Sultuybek1

  1. 1Division of Medical Biology, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey
  2. 2Endocrinology and Metabolism Department of Internal Medicine, Haseki Education and Research Hospital, Istanbul, Turkey
  3. 3Endocrinology and Metabolism Department of Internal Medicine, Dr Lütfi Ki nodotrdar Kartal Education and Research Hospital, Istanbul, Turkey
  4. 4Department of Biochemistry, GATA Military Educational Hospital, Istanbul, Turkey

Correspondence: Dr I Onaran, Division of Medical Biology, Cerrahpasa Medical Faculty, Istanbul University, Ortaklar Cd. Butan Sk. No: 2, Mecidiyeköy, Istanbul 34394, Turkey. E-mail: ilonaran@istanbul.edu.tr

Received 30 November 2004; Revised 17 July 2005; Accepted 3 August 2005; Published online 4 October 2005.

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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.

Materials and 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 (708plusminus147 DNP-SG efflux nmol/ml erythrocytes/h) was significantly higher than that of control group (490plusminus105 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).

Conclusion:

 

Obesity may increase erythrocyte glutathione conjugate transport independent from ATP and GST activity that may protect against MDA formation in vitro.

Keywords:

erythrocyte, glutathione S-conjugate transport, oxidative stress

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