Relation between reduced glutathione content and Heinz body formation in sheep erythrocytes

Ikuo Goto From the Department of Veterinary Internal Medicine, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan (Goto, Maede), and Department of Physiology, University of New England, Armidale, NSW, Australia (Agar).

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N. S. Agar From the Department of Veterinary Internal Medicine, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan (Goto, Maede), and Department of Physiology, University of New England, Armidale, NSW, Australia (Agar).

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Yoshimitsu Maede From the Department of Veterinary Internal Medicine, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan (Goto, Maede), and Department of Physiology, University of New England, Armidale, NSW, Australia (Agar).

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Summary

To clarify the oxidant defense functions of reduced glutathione (gsh) in erythrocytes, the effect of gsh deficiency on in vitro oxidant defense was studied, using gsh-deficient sheep erythrocytes (low-gsh cells). The formation of Heinz bodies in low-gsh cells was higher than that in high-gsh cells when the cells were incubated with an oxidant drug, acetylphenylhydrazine (aph). Artificial depletion of gsh by 1-chloro-2,4-dinitrobenzene in high-gsh cells resulted in increased Heinz body formation in these cells incubated with aph. Furthermore, high negative correlation was observed between Heinz body formation and gsh content in sheep erythrocytes exposed to aph. These results clearly indicate that erythrocyte gsh is indispensable for erythrocyte defense against oxidative damage induced by aph, and support the previous observations that sheep with low-gsh erythrocytes were more susceptible to oxidative agents than were sheep with high-gsh erythrocytes.

Summary

To clarify the oxidant defense functions of reduced glutathione (gsh) in erythrocytes, the effect of gsh deficiency on in vitro oxidant defense was studied, using gsh-deficient sheep erythrocytes (low-gsh cells). The formation of Heinz bodies in low-gsh cells was higher than that in high-gsh cells when the cells were incubated with an oxidant drug, acetylphenylhydrazine (aph). Artificial depletion of gsh by 1-chloro-2,4-dinitrobenzene in high-gsh cells resulted in increased Heinz body formation in these cells incubated with aph. Furthermore, high negative correlation was observed between Heinz body formation and gsh content in sheep erythrocytes exposed to aph. These results clearly indicate that erythrocyte gsh is indispensable for erythrocyte defense against oxidative damage induced by aph, and support the previous observations that sheep with low-gsh erythrocytes were more susceptible to oxidative agents than were sheep with high-gsh erythrocytes.

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