Disease relevance of Heinz Bodies

• 1 During 6-month oral toxicity studies of dipyrone in rats and dogs, there was an increase in the number of reticulocytes and Heinz bodies at the highest dose, and a slight haemosiderosis was induced [1].

High impact information on Heinz Bodies

• Binding of Heinz bodies to the inner surface of the sickle cell membrane promotes clustering and colocalization of the membrane protein band 3, outer surface-bound autologous IgG and, to some extent, the membrane proteins glycophorin and ankyrin [2].
• However, the EKLF-/- colonies were poorly hemoglobinized and enucleated erythrocytes in these colonies contained numerous Heinz bodies [3].
• Moreover, exposure of intact RBC to 20 mmol/L APH induced depletion of procalpain activity for which the time course was inversely related to formation of Heinz bodies [4].
• With 100 mg/dL phenylhydrazine, when the entire membrane was coated with Heinz bodies, RBC filterability and membrane deformability were drastically reduced [5].
• These studies indicate that the erythrocytes of premature infants are uniquely sensitive to the development of Heinz bodies after exposure to sodium ascorbate [6].

Biological context of Heinz Bodies

• Mice appeared to be more sensitive than rats to the formation of Heinz bodies and the development of anemia that was characterized by a decrease in hemoglobin, hematocrit, and erythrocyte count [7].
• Erythrocytes exposed to tBHP also show an increase in mean corpuscular volume and a remarkable formation of methemoglobin (met-Hb) without any appearance of hemichromes that form Heinz bodies [8].

Anatomical context of Heinz Bodies

• Percent Heinz bodies in diabetic cats directly correlated with plasma beta-hydroxy-butyrate concentration (r = .622; P = .0002), as well as with serum chloride concentration (r = -0.576; P = 0.0009) and the number of monocytes (r = .536; P = .0023) [9].

Associations of Heinz Bodies with chemical compounds

• Methylene blue potentiated the oxidative denaturation of haemoglobin by aniline as judged by the size and number of Heinz bodies and their turbidity in haemolysate [10].
• Dapsone and Heinz bodies [11].
• Heinz bodies induced by acetylphenylhydrazine in intact cells or in the presence of membrane remained attached to membrane when separated by a sucrose gradient [12].
• The decrease in deformability starts even before Heinz body formation is recognized and is enhanced with PHZ as Heinz bodies are attached on the inner surface of the membrane, but remains at a low level in MMH-treated cells in which Heinz bodies are formed mostly away from the membrane surface [13].
• Irreversible haemoglobin oxidation also occurred in these cells, shown by the formation of Heinz bodies; purified haemoglobin likewise suffered oxidative damage when incubated with sporidesmin in the presence of glutathione [14].

Gene context of Heinz Bodies

• When exposed to acetylphenylhydrazine, erythrocytes from the G6PD-deficient colt produced more and smaller Heinz bodies than did erythrocytes from normal horses [15].
• There was no correlation between amount of Heinz bodies and the concentrations of blood methaemoglobin, serum haptoglobin or serum hemopexin [16].
• They demonstrated methaemoglobinaemia, Heinz bodies and reduction in plasma haptoglobin indicating Hb oxidation [17].
• Addition of catalase to suspensions of erythrocytes in the presence and absence of superoxide dismutase inhibited the formation of Heinz bodies [18].

Analytical, diagnostic and therapeutic context of Heinz Bodies

• With phenylhydrazine concentrations below 30 mg/dL, even in the presence of multiple Heinz bodies, the RBC deformability measured by filtration through 2.6-, 4.5-, and 6.8-microns pores and the membrane deformability determined by a filter aspiration technique were not altered [5].
• In contrast, Heinz bodies were not identified on scanning electron microscopy of intact erythrocytes of the remaining 2 cats even though Heinz bodies were found on their blood films stained with brilliant cresyl blue [19].

References