Abstract

Background: Cyclophosphamide use is often limited by associated hematotoxicity. This study investigated the effects of melatonin on haematological indices in cyclophosphamide-induced hematotoxicity in mice. Methods: Ninety mice weighing between 20-25 gm were randomly divided equally into nine groups (A-I). Group A (saline control) received 2 ml/kg intraperitoneal (i.p.) normal saline with 10 ml/kg distilled water orally, groups B, C and D (melatonin control) received i.p. normal saline with melatonin at 5, 10 and 20 mg/kg orally, respectively. Group E (cyclophosphamide control) received 150 mg/kg/day i.p. cyclophosphamide with 10 ml/kg distilled water orally, while group F received 150 mg/kg/day cyclophosphamide with standard drug, (erythropoietin control) at 100 IU/kg. Group G, H and I (treatment groups) received 150 mg/kg/day cyclophosphamide with melatonin at 5, 10 and 20 mg/kg/day orally. Cyclophosphamide was administered on days 1 and 2 only, oral administrations occur once daily for 14 days. On day 15, animals were sacrificed and blood collected by cardiac puncture for assessment of haematological parameters; white blood cell count (WBC), red blood cell count (RBC) and platelets (PLT). Results: The results showed a significant increase in WBC in groups C D, G and H (melatonin control; 10 mg/kg. 20 mg/kg and melatonin treatment; 5 mg/kg and 10 mg/kg) and a significant (p=0.001) decrease in group E (cyclophosphamide control) compared to A (saline control). RBC increased significantly in groups B and D (melatonin control; 5 mg/kg and 20 mg/kg) and significantly decreased in group E (cyclophosphamide control) compared to group A (saline control). Compared to group E (cyclophosphamide control), RBC increased significantly in groups F-I (erythropoietin standard, melatonin treatment). PLT increased significantly in groups B, C, (melatonin control; 5mg/kg and 10 mg/kg) G, H and I (melatonin treatment) compared with groups A (saline control) and E (cyclophosphamide control) (p=0.001). Conclusions: Melatonin has potential to attenuate cyclophosphamide-induced hematotoxicity in mice.

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