ANTIOXIDANT – MEDIATED HEINZ BODIES LEVELS OF GLUCOSE – 6 – PHOSPHATE DEHYDROGENASE – DEFICIENT ERYTHROCYTES EXPOSED TO ACETYLPHENYLHYDRAZINE.
Aloh, G. S, *Obeagu, Emmanuel Ifeanyi, Okoroiwu, I.L., Odo, Christian Emeka, Odo Matthew Chibunna, Kanu,S.N, Elemchukwu, Q., Okpara,K.E., Ugwu, Getrude Uzoma,
ABSTRACT
The effects of two antioxidants, ascorbic acid and α-tocopherol, on the
levels of Heinz bodies (Hzbs) induced with acetylphenylhydrazine
(APHZ), a classical inducer of oxidative stress, were studied in
glucose-6-phosphate dehydrogenase (G6PD)-deficient erythrocytes. In
both the control and G6PD- deficient erythrocytes, no Hzbs were
present pre-APHZ treatment but post – APHZ, the Hzbs levels rose
significantly (p<0.05) to 2.40+ 0.05% and 62.50+ 2.99% in the control
and G6PD-deficient red cells respectively. Upon treatment with
ascorbic acid, their respective Hzbs levels were significantly reduced to 1.60+0.05% and
48.60+4.35%, while α-tocopherol was more effective as it reduced the post-APHZ Hzbs
levels to 0.98+0.02% and 41.80+ 5.83% respectively. It was concluded that the red cells did
not bear Hzbs pre- APHZ treatment most probably because of an efficient system of removal
of those offending inclusions (Hzbs) in the absence of exogenous oxidant challenge, but upon exposure to APHZ, both erythrocyte types formed significant levels of Hzbs, although more
in G6PD-deficient cells. Both ascorbic acid and α-tocopherol (antioxidants), tested in this
study could reduce the post-APHZ Hzbs levels significantly but the latter was more effective.
None of the two antioxidants tested could reduce the Hbzs of the erythrocytes to their pre-
APHZ treatment levels in both the control and G6PD-deficient erythrocytes. In spite of this, it
is advisable to co-administer, or follow, oxidant drugs with an antioxidant, especially α-
tocopherol which, in this study,was found to be very effective in counteracting APHZinduced
Heinz bodies formation.
Keywords: Antioxidants, Heinz bodies, acatylphenylhydrazine, glucose -6- phosphate dehydrogenase.
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