Effect of classic soft drink Coca-Cola as a solvent in the administration of tramadol and diazepam on biochemical and histological changes in liver and kidney

The objective of this study was to determine the biochemical and morphological changes in the liver and kidney as a result of the acute administration of tramadol and diazepam with classic soft drink Coca-Cola (Coke ). Method: Thirty-six (36) adult male Wistar rats were divided into six groups: Group A-control (distilled water), Group B (Coke ), Group C (tramadol, 50 mg/kg), Group D (tramadol dissolved in Coke, 50 mg/kg), Group E (diazepam, 10 mg/kg) and Group F (diazepam dissolved in Coke 10 mg/kg). All administrations were done intraperitoneal. Twenty-four hours after administration, blood samples were collected via cardiac puncture for evaluation of the liver (Aspartate aminotransferase [AST] and Alanine aminotransferase [ALT]), kidney (urea and creatinine [CREA]) function and the organs were excised and processed for histopathological examination. Result: A significantly increased in AST, creatinine and urea concentrations was observed in  Tramadol and Coke Groups compared to control (P0.05), though it caused a significant increase in urea and CREA (P<0.05). Dissolving the tramadol in Coke aggravated its hepatotoxicity and nephrotoxicity, while Coke had no significant effect on diazepam. Histological examination also corroborated the biochemical result. Conclusion: The results showed that mixing drugs with Coke does not improve the toxicity of tramadol and has no significant effect on diazepam

Reversal effect of Solanum dasyphyllum against rotenone-induced neurotoxicity

We earlier reported the protective effect of Solanum dasyphyllum against cyanide neurotoxicity. In furtherance to this, we investigated the protective effect of S. dasyphyllum against rotenone, a chemical toxin that causes brain-related diseases. Mitochondria fraction obtained from the brain of male Wistar rats was incubated with various solvents (hexane, dichloromethane, ethylacetate, and methanol) extracts of S. dasyphyllum before rotenone exposure. Mitochondria respiratory enzymes (MRE) were evaluated along with markers of oxidative stress. The inhibition of MRE by rotenone was reversed by treatment with various fractions of S. dasyphyllum. The oxidative stress induced by rotenone was also reversed by fractions of S. dasyphyllum. In addition, the ethylacetate fraction of S. dasyphyllum was most potent against rotenone-induced neurotoxicity. In conclusion, S. dasyphyllum is rich in active phytochemicals that can prevent some neurotoxic effects of rotenone exposure. Further study can be done in an in vivo model to substantiate our results