Nickel has bio-importance as a trace element but the biotoxic effect of many of them in mammalian biochemistry is of great concern. There is a need for a proper understanding of the condition such as hyperplasia, hypoplasia, and oxidation states which makes them harmful and that is how biotoxicity occurs. Therefore, we studied the effect of oral administration of nickel nitrate (Ni(NO3)2) at different doses calculated for acute and sub-acute days on the bone marrow (BM). The myeloid, erythroid, and megakaryocytes cells were distinguished, quantitated, and statistically analyzed. Myeloid/erythroid cell ratio was also taken into consideration. Significant (p<0.001) decline in eosinophilic myelocytes of myeloid series has been observed after acute (1 day) and subacute (7, 14, and 21 days) treatment, whereas the erythroid cells, the basophilic normoblasts in BM registered increase after both the treatments. Further, megakaryocyte cells in BM revealed enhancement after acute and sub-acute intoxication due to thrombopoietin which gets increased due to the consumption or destruction of platelets. Enhancement in erythroid cells depends upon erythropoietin which stimulates the proliferation of erythroid progenitors. Hematogenecity has been reflected in terms of significant myeloid hypoplasia besides significant erythroid and megakaryocyte hyperplasia. Ni (Nickel) thus exhibits a change in BM response which in turn modifies normal physiology. The hyperplasia so observed can be attributed to Ni(NO3)2 which probably alter physiochemical reactions which in turn bring about proliferation in both erythroid and myeloid series of cells. It is thus concluded that Ni(NO3)2 exerts profound variation in the hematopoietic system.

Keywords: Ni(NO3)2 (nickel nitrate), BM (bone marrow) Megakaryocytes, erythrocytes, and myeloid cells.