Attempts to validate a possible predictive animal model for human erythrocyte G‐6‐PD deficiency

Abstract

The use of Dorset sheep erythrocytes as a model for human G‐6‐PD deficient erythrocytes was investigated. Seven Pharmaceuticals were examined for oxidant Stressor effects using a liver microsomal enzyme system to generate metabolites of the drugs. The Pharmaceuticals examined were salicylic acid, dapsone, naphthalene, B‐naphthol, p‐aminobenzoic acid, sulfanilamide and sulfapyridine. The test compounds were incubated with Dorset sheep erythrocytes and oxidant Stressor effects were measured through reduced qlutathione (GSH) levels and methemoglobin formation. The response of the Dorset sheep erythrocytes to the seven agents was compared to previous studies revealing the response of human G‐6‐PD deficient erythrocytes to these agents.

The results indicated that metabolites of the Pharmaceuticals, B‐naphthol, dapsone, and sulfanilamide, are oxidant. Stressor agents towards sheep G‐6‐PD deficient erythrocytes. These results agreed with studies on the response of human G‐6‐PD deficient erythrocytes. The metabolized naphthalene and sulfapyridine did not cause oxidant stress in the sheep erythrocvtes, despite the fact that these two agents caused oxidizing effects in human G‐6‐PD deficient erythrocytes in previous studies. None of the non‐metabolized parent compounds caused oxidant stress in the sheep erythrocytes, which agreed with the responses of human G‐6‐PD deficient erythrocytes.

Key words:

• G‐6‐PD Deficiency
• Dorset Sheep
• Pharmaceuticals
• Metabolization
• Erythrocytes
• Oxidant Stress