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Hypoestes rosea (family: Acanthacea), has been harnessed and utilized for treatment of several ailments. However, there is the paucity of available data on nephrotoxicity associated with this herb. Here, we investigated the phytochemical profile and toxicological effect of H. rosea on Wistar Rats. Twenty rats (weight range: 75–100 g) were assigned into five study groups, viz; (a) control (without treatment) (b) treatment group 1, orally administered with 50 mg/kg (c) treatment group 2, orally administered with 100 mg/kg (d) treatment group 3, orally administered with 250 mg/kg, and (e) treatment group 4, orally administered with 300 mg/kg of H. rosea, respectively for 28 days of four rats per group. The rats were made unconscious by using oral administration of chloroform. Cardiac punctures were made, and blood samples collected into 10 ml labeled plain container, allowed to clot and spun to harvest serum for determination of sodium, potassium, chloride, bicarbonate, urea and creatinine using colorimetric, back-titrimetric, Urease-Berthelot and Jaffe's reaction methods respectively. Kidneys of rats were harvested, weighed and immediately fixed in 10% neutral buffered formalin for histological analysis. Mean serum sodium (p = 0.049), potassium (p = 0.007), and urea (p < 0.001) levels were significantly higher among the treatment groups compared to controls. Histopathological findings of kidney sections revealed mild glomerular infiltration in treatment groups 2–4. Additionally, sclerosis was observed in groups 3–4. Phytochemical analysis of H. rosea revealed presence of alkaloids, flavonoids, saponins, tannins, terpenoids, steroids and reducing sugars. From the findings in this study, H. rosea leaf extract causes significant damage to the kidneys of Wistar rats at higher doses. Of which, the damages were dose-dependent in direct proportionality manner. To better determine the safe dosage and ideal duration of consumption, there is the need for further studies on H. rosea. [ABSTRACT FROM AUTHOR]

Cigarette smoking has been linked to atherosclerosis, coronary artery disease, peripheral vascular disorders and various malignancies. However, the mechanism by which smoking increases the risk of cardiovascular diseases is still controversial. One hundred and forty one apparently healthy male cigarette smokers and sixty apparently healthy non-smokers aged 18 to 65 years were enrolled into the study. The smokers were sub-divided into light (<8 pack years), moderate (8-30 pack years) and heavy (>30 pack years) smokers. Anthropometric indices and blood pressure were measured. Fasting plasma glucose, total cholesterol (TC), triglycerides and High density lipoprotein-cholesterol (HDL-C) were estimated using colorimetric test methods while low density lipoproteincholesterol (LDL-C) and very low density lipoprotein were calculated using Friedewald's equation. Serum insulin was estimated using ELISA. Data was analyzed using SPSS version 20.0; level of significance was set at p<0.05. The smokers had significantly higher diastolic BP (p=0.0001), TC (p= 0.008) and LDL-C (p = 0.0001) and significantly lower HDL-C (p = 0.0001) compared to the non-smokers. There was a significant higher fasting plasma glucose in the light smokers (p=0.001) than in the moderate and heavy smokers whereas, serum TC and LDL-C levels were significantly increased in heavy smokers (p=0.001) than in the light and moderate smokers. There was a negative correlation between BMI and smoking pack years. Dyslipidaemia was observed to be the most prevalent cardiovascular disease risk factor. It is concluded that the alterations in lipid profile and blood pressure observed in this study may contribute to higher risk of cardiovascular disease. [ABSTRACT FROM AUTHOR]