The Extract of Acacia sieberiana (DC.) Leaf Prevents Blood REDOX Status, Oxidative Lipid and DNA Damage Complications in DMH-induced Pre-Malignant Colon Cancer in Male Rat
doi.org/10.26538/tjnpr/v5i8.25
Keywords:
Oxidative stress, 8-OHdG, A. sieberiana, Lipid profiles, MDAAbstract
Alkaloids are important plant phytochemical reported to have diverse pharmacological significance most especially for cancer treatment. This study sought to evaluate protective effects of alkaloid-rich extract of Acacia sieberiana leaf on blood reduction and oxidation (REDOX) status, oxidative lipid and DNA damage complications in DMH-induced pre-malignant colon cancer in male rat. Pre-malignant colon cancer was induced using 1, 2- dimethylhydrazine (DMH) in male Wistar rats through intraperitoneal injection. Alkaloid-rich leaf extract of Acacia sieberiana (50, 100 and 150 mg/kg) and 2 mg/kg doxorubicin (standard drug) were simultaneously administered with DMH intraperitoneally to the animals once per week for 22 weeks. The haematological indices, liver and kidney function tests, serum lipid profile and serum REDOX status were assessed. Serum lipid and DNA oxidative damage biomarkers, and induction of the colon aberrant foci crypt were evaluated. The results indicated that administration of the extract significantly (p<0.05) prevented the DMH-induced reduction of packed cell volume (PCV), haemoglobin (Hb), red blood cells (RBC), superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT). The extract significantly (p<0.05) reversed in a dose dependent manner the increased white blood cells (WBC), platelet (PLT), alanine amino transferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin (TBIL), malondialdehyde (MDA) and 8-hydroxyl-2-deoxyguanosine (8-OHdG) occasioned by DMH. Induction of colon cancer aberrant foci by DMH was not observed in the groups exposed to the extract. The study revealed that the alkaloid extract of the plant has potential to prevent the complications in tissues arising from chemical-induced pre-malignant colon cancer incidence.
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