ABSTRACT
The use of medicinal plant extracts to maintain health, prevent or cure various diseases is known since ancient times. However, most times, there is little or no knowledge of the associated possible toxic injuries on vital organs morphology or functions from the use of such plants in whole or parts. Randia nilotica had long been known and used traditionally for various diseases, with no information on its toxicity profile. This study aims at evaluating the ethanolic stem bark extract of the plant for acute, sub-chronic and chronic toxicities. Three groups of animals were treated with extract (250, 500 and 1000 mg/kg daily) and a fourth one with distilled water for 28 and 90 days. Blood samples were collected at the end of treatment periods and used for biochemical and haematological analysis. The brain, heart, kidney, liver and spleen of all the rats in each group were also isolated and weighed prior to fixing in 10% buffered formalin and Bouin‟s fluid (brain only) for histopathological examinations. The extract was found to contain saponins, carbohydrates, cardiac glycosides, triterpenes, flavonoids and tannins, while alkaloids, steroids, cardenolides and anthraquinones were absent. The LD50 was greater than 5000 mg/kg body weight, since no mortality was found at this dose level. 1000 mg/kg extract significantly (p ≤ 0.05) decreased the PCV level following 28 days oral administration, while for the 90 days daily oral administration, both the 500 and 1000 mg/kg doses caused significant (p ≤ 0.05) decrease in PCV, Hb and RBC counts. The mean cell volume (MCV) was also significantly (p ≤ 0.05) decreased, but only at 1000 mg/kg following 90 days daily oral administration. The 28 days oral administration caused no alteration in blood urea nitrogen, creatinine and calcium levels at all dose levels, but the 90 days treatment caused significant (p ≤ 0.05) increase in blood urea nitrogen. No significant (p ≤ 0.05) increases and decreases were observed in the liver enzymes, total protein, albumin, total cholesterol, triglycerides and high density lipoprotein for the 28 days treatment, but the 90 days administration showed significant (p ≤ 0.05) increase of high density lipoprotein (HDL) level only at the 250 mg/kg dose. Significant (p ≤ 0.05) decrease in brain weight was observed following 90 days daily oral administration. The histopathology of the organs showed both dose and duration- dependent alterations. The 28 day oral administration showed neuronal degeneration and congested blood vessels of the brain, the heart showed myocardial congestion, infiltration of inflammatory cells and myocardial haemorrhage. The kidney showed atrophy of glomeruli, haemorrhage, tubular necrosis, cellular infiltration, hyper cellular glomeruli and adhesion of the parietal surface with Bowman‟s capsule. The alterations on the spleen were congestion of blood vessels and depletion of lymphocytes while the liver had congestion of blood vessels, perivascular infiltration of inflammatory cells and necrosis of hepatocytes. The 90 days treatment further revealed cerebral congestion in the brain, fragmentation of the heart‟s muscle fibres and oedema. Effects on the kidney were vacuolation of glomeruli, infiltration of inflammatory cells and congestion of glomeruli. The alterations on the spleen were congestion of blood vessels and depletion of lymphocytes, while the liver had congestion of blood vessels, perivascular infiltration of inflammatory cells and necrosis of hepatocytes. The major inference that could be drawn from the above work is in the fact that the stem bark extract of Randia nilotica is toxic to the organs at the doses tested, over prolonged period. It is therefore concluded that, while it could have pharmacological utility, Randia nilotica merits further attention with respect to toxicity
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