The oral toxicity profile of the crude aqueous stem bark extract of Pausinystalia yohimbe was studied in adult albino rats. The Up and Down method (AOT425statPgm version 1.0) for acute oral toxicity was carried out using a starting dose of 175 mg/kg body weight via the oral route. For the sub chronic study, 40 male albino rats weighing between 150-200 g, were grouped into three treatment groups and a control group with 10 rats in each group. A repeat dose oral toxicity study was conducted by daily oral dosing of 600 mg/kg body weight, 150 mg/kg body weight of extract dissolved in 1ml of 0.9% saline to groups 1 and 2, respectively and 30% powdered stem bark mixed with 70% rat chow (w/w) to group 3 and 1ml of 0.9% saline was administered to rats in the control group for 28 days. On day 29, blood samples for bioassay were collected by cardiac puncture under diethyl ether anesthesia. The LD50 estimate of the extract was calculated to be greater than 2000mg/kg body weight/oral route. The extract did not cause any significant difference in the body weight of the rats. Platelet count and White Blood Cell count (WBC) were significantly elevated across the treatment groups p<0.05. Total bilirubin was significantly higher p<0.05 in the 600 and 150mg treatment groups, while conjugated bilirubin was significantly higher in the 600 mg treatment group. Total protein was significantly lower p<0.05 in the 600mg treatment group. Aspartate Transaminase was significantly higher in all the treatment groups, while Alkaline phosphatase was significantly higher in the 600 and 150mg treatment groups, p<0.05, respectively. Alanine transaminase was significantly higher in 600 mg treatment group. Na + was elevated significantly, p<0.05. These results suggest incipient toxicity of the extract and indicate need for morphometric toxicity study.
Earlier reports showed that neural stem cell microenvironment can become so complex making neurogenesis to be associated with stem cells transformation to radial glial cells and that the complexity of this microenvironment increases due to the presence of neuronal progenitors, differentiated cells and extracellular signaling molecules see review by
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