We have investigated the resistance of erythrocytes from diabetics and non‐diabetics to glutathione depletion caused by p‐benzoquinone, 1‐chloro‐2,4‐dinitrobenzene (CDNB), diethyl maleate and 4‐aminophenol. Incubation of erythrocytes with 4‐aminophenol (2mm) caused a precipitous reduction (>80%) in cellular glutathione levels although there was no significant difference between 4‐aminophenol‐mediated glutathione depletion in the diabetic and non‐diabetic cells. p‐Benzoquinone and CDNB were both associated with a less severe initial reduction in glutathione levels (>50% at 30 min) although p‐benzoquinone caused greater depletion (P < 0.001) at 4.5 h (21.1 ± 3.1%, non‐diabetic; 20.0 ± 1.0%, diabetic) compared with CDNB (49.2± 2‐2%, non‐diabetic; 51.3 ± 1.1% diabetic). Although there was no significant difference between the two types of cell in terms of level of depletion, administration of diethyl maleate caused a significant reduction in glutathione levels at 30 min (P < 0.0005), 3.5h (P < 0.05) and 4.5h (P < 0.05) in erythrocytes from diabetic man compared with those from non‐diabetic man. Co‐administration of buthionine sulphoximine (20 mm) and 4‐aminophenol (l mm) also led to a significant reduction in glutathione levels in diabetic cells at 30 min (P < 0.05), 3.5h (P < 0.02) and 4.5h (P < 0.007) compared with those in non‐diabetic cells. The observations that diabetic red cells' resistance to depletion was similar to that of non‐diabetic cells for three of the four depletors, and that the combination of 4‐aminophenol and buthionine sulphoximine‐mediated inhibition of glutathione synthesis was required to illustrate differences suggests that diabetic complications might be a result of the long‐term effect of small deficiencies in oxidative self‐defence mechanisms such as glutathione.
Journal of Pharmacy and Pharmacology: An International Journal of Pharmaceutical Science – Wiley
Published: Jan 1, 1999
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