No abstract

This study was undertaken to investigate the toxic effect of Walterinnesia aegyptia venom on the ultrastructure of rat myocardium. Male albino rats were prepared for intraperitoneal injection of saline (control group) and saline solution of W.aegyptia venom (study group) at a dose of 0.04 mg animal-1. Biopsies from the left ventricle were prepared for electron microscopy after 1 h (D1 group), 2 h (D2 group), 18 h (D3 group) and 24 h (D4 group). Myocardial cells were in a state of partial to complete contraction. The D1 group showed some mitochondrial vacuoles; D2 group demonstrated more vacuolation and alterations in the form of disorganized cristae. Similar findings were depicted in D3 group. The D4 group demonstrated, in addition, dissolution of mitochondrial cristae. Myofilaments in D3 group experienced coalescence into ill-defined amorphous masses (foci of myolysis). These masses were characterized by the presence of multiple, parallel, Z-like dark bands with disorganization of the filamentous arrangement. In the D4 group, more myolytic foci were observed. This reaction was not limited to one myocyte but extended to the neighbouring ones. Mitochondrial vacuoles were mostly associated with electron dense deposits. Glycogen particles tended to decrease as the experiment proceeded from D1 to D4. These ultrastructural changes were time dependent. They would suggest a cardiotoxic action of W.aegyptia snake venom.

The in vitro effect of recombinant human granulocyte-macrophage colony stimulating factor (rh-GMCSF) and recombinant human granulocyte colony stimulating factor (rh-GCSF) on oxygen free radical (OFR) generation by human neutrophils and blood monocytes derived human macrophages stimulated with phorbol myristate acetate was investigated and compared. The production of OFR by neutrophils and macrophages was time dependent, and the maximum release of OFR by neutrophils and macrophages was measured 90 and 180 min after stimulation with phorbol myristate acetate, respectively. The priming effects or rh-GMCSF and rh-GCSF on OFR production by human neutrophils and macrophages was dose dependent. The maximum generation of OFR by neutrophils occurred when primed with 1,000 U/ml of rh-GMCSF and reached 2.383+0.191 nmol/l0⁵ neutrophils/90 min as compared with 1.072 ± 0.113 nmol/l0⁵ neutrophils/90 min in the unprimed controls. This represents a 122.20% increase in OFR generation (p < 0.001). However, the percentage of maximum increase in OFR production was 57.84 when neutrophils were primed with a concentration of 5,000 U of rh-GCSF/ml. In 72-hour-old human macrophages, much higher levels of OFR production as compared with neutrophils were measured following stimulation with phorbol myristate acetate. The maximum generation of OFR was measured in macrophages primed for 45 min with 500 U/ ml of rh-GMCSF. These cells produced 8.960 ± 2.075 nmol/5×10⁴ macrophage/180 min as compared with 4.563+1.773 nmol/5×10⁴ unprimed macrophages/180 min (p < 0.001). In macrophages primed with rh-GCSF, however, the maximum OFR production was induced by a dose of 5,000 U/ml and reached 6.902+1.463 nmol/5× 10⁴ macrophages/180 min as compared with 4.563 ± 1.773 nmol/5×10⁴ macrophages/180 min in the unprimed controls (p < 0.05). In conclusion, the priming effect of rh-GMCSF on OFR generation by human macrophages and neutrophils was more potent than that of rh-GCSF, both in the extent of augmentation and in the dose required to produce maximum OFR generation.