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This study evaluated the toxicity potential of platinum (Pt) nanoparticles in Wistar rats. Wistar rats weighing between 180 and 193 g were randomly assigned into four groups. Animals in group 1 served as the control and received distilled water. Those in groups 2, 3, and 4 were administered with 10, 50, and 100 mg/kg body weight of Pt nanoparticles, respectively. At the end of treatments, the rats were fasted for 24 h and sacrificed under mild anesthesia. The blood and vital organs were collected and used for the biochemical and histopathological examinations. Pt nanoparticles caused significant alterations to the rat organ weights relative to the control. Also, the Pt nanoparticles altered the rat level of lipid profile and significantly elevated the atherogenic index relative to the control. The total protein level was increased in the tissues while the albumin decreased following nanoparticle treatment. Also, the nanoparticles inconsistently altered the level of serum urea and creatinine while the serum bilirubin level was raised. The activities of aspartate transaminase and alkaline phosphatase were reduced by nanoparticle treatments. However, the level of alanine aminotransferase (ALT) was inconsistently altered in serum and tissues by nanoparticle treatment with a significant elevation in the liver. Furthermore, nanoparticle exposure in rats caused several morphological lesions including inflammation and cellular degeneration, all of which were conspicuously absent in the control group. We show evidence that Pt nanoparticles potentiated alteration of rat biochemical and morphological indices in manners reminiscent of early cellular injury.

This study was aimed at investigating the antihyperglycemic and antidyslipidemic activity of Musa paradisiaca‐based diets in alloxan‐induced diabetic mellitus rats. Diabetes was induced by a single intraperitoneal injection of alloxan (150 mg/kg b.w) in 48 randomly selected rats. The rats were randomly grouped into four as follows: normal rats fed Dioscorea rotundata‐based diet, diabetic control rats fed D. rotundata‐based diet, diabetic rats fed D. rotundata‐based diet and administered metformin (14.2 mg/kg body weight) orally per day, and diabetic rats fed M. paradisiaca‐based diet. Body weight and fasting blood glucose level were monitored, on 28th days the rats were sacrificed, liver was excised. Thereafter, the hyperglycemic and dyslipidemic statii of the induced diabetic animals were determined. The M. paradisiaca‐based diet significantly (p < .05) reversed the levels of fasting blood glucose, with significant (p < .05) increase in insulin and glycogen concentrations. The diet also increased the activity of hexokinase with significant reduction (p < .05) in glucose‐6‐phosphatase and fructose‐1‐6‐diphosphatase activities. M. paradisiaca‐based diet demonstrated significant reduction (p < .05) in cholesterol, triacylglycerol (TG), very low‐density lipoprotein (VLDL), low‐density lipoprotein (LDL), and significant increase (p < .05) in high‐density lipoprotein (HDL) compared with those of diabetic control group. Also, M. paradisiaca‐based diet significantly (p < .05) reversed the activities of aspartate aminotransferase and alanine aminotransferase when compared with diabetic control animals. The consumption of this diet may be useful in ameliorating hyperglycemia and dyslipidemia in diabetes mellitus patients.

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