Humans can be exposed to cyanide through inhalation from fire incidents or ingestion of cyanide containing food or drinks. 1,2 Apart from these two major routes of exposures, humans working close to industries that utilize cyanide as part of the chemicals, such as plastic and foam making industries are also exposed. 3,4 Symptoms of cyanide poison include depression in breathing control, pulseless electrical activity, arrhythmia, and hypotension. 5 Some of the cardiac symptoms of cyanide poisoning includes; dysrhythmia, impaired repolarization, and cardiorespiratory arrest. 6 The sensitivity of the heart to cyanide poison is due to its dependence on ATP, which is majorly produced in the mitochondria through the electron transport system. Cyanide inhibits cytochrome C oxidase, a complex IV enzyme of the mitochondria respiratory system. Inhibition of this enzyme prevents the mitochondria from producing ATP, required by the heart to perform its function effectively, leading to the early symptoms observed in patients exposed to cyanide poison. Also, cyanide induces oxidative stress, which further damages the cardiac system. Approved drugs for treating cyanide poisoning include; hydroxycobalamin, 7 sodium thiosulfate, 1 cobinamide sulfite, 8 and sulfanegen. 9 Some of the mechanisms of action of these drugs includes; redox homeostasis,
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 (P<0.05), while diazepam had no significant effect on AST, ALT (P>0.05), 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.
Lead exposure has been linked to health challenges involving multiple organ failure. More than fifty percent of lead present in the human body is accumulated in the liver causing hepatic injury. A major mechanism of lead toxicity is oxidative stress. TrévoTM is a nutritional supplement with numerous bioactive natural products with detoxifying and antioxidant properties. This study was designed to investigate the hepatoprotective effects of TrévoTM dietary supplements against lead-hepatotoxicity in male Wistar rats. Thirty-five healthy animals were divided into five groups of seven each as follows: Group I=control; II=15 mg/kg of lead acetate (PbA); III= 2 mL/kg of TrévoTM + PbA; IV= 5 mL/kg of TrévoTM + PbA;V=5 mL/kg of TrévoTM . Animals were orally treated with TrévoTM for two days before co-administration with PbA intraperitoneally for 12 consecutive days. Animals were sacrificed 24 h after the last administration and blood were collected via cardiac puncture and processed for hematological parameters and assessment of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin (ALB). The liver was excised and processed for markers of oxidative stress and histopathological examination. Intraperitoneal administration of 15 mg/kg of PbA caused a significant increase in serum concentration of AST, ALT, while the concentration of ALB was significantly decreased (P<0.001). PbA caused a significant reduction in packed cell volume, hemoglobin while the total white blood cell count, neutrophils, lymphocytes, monocytes, eosinophils, and basophils were increased. Oxidative stress was significantly pronounced in the liver of rats exposed to PbA as observed in the high concentration of malonedialdehyde, decreased concentration of glutathione, the activity of catalase, superoxide dismutase, and glutathione-S-transferase. Pretreatment with TrévoTM was able to significantly prevent the anemic, oxidative damage, and hepatic injury initiated by PbA. Histological examination also corroborated the biochemical results. In conclusion, the study reveals that TrévoTM is effective in attenuating PbA-induced hepatotoxicity in male Wistar rats.
Background: Exposure to lead has been linked to biochemical changes similar to those patients suffering from Alzheimer’s disease. Trévo is a phytonutrient-rich product with antiaging and antioxidant properties. Purpose: To investigate the neuroprotective activity of trévo against lead-induced biochemical changes in male Wistar rats. Methods: The study involves 35 animals that were randomly divided into five groups of seven rats each. Group I (Control): Orally administered distilled water; Group II (Induced): Administered 15 mg/kg of lead acetate (PbA) intraperitoneally; Group III (Treatment group): Orally administered 2 mL/kg of trévo for two days before co-administration with PbA for 12 consecutive days; Group IV (Treatment group): Orally administered 5 mL/kg of trévo for two days prior to coadministration with PbA for 12 consecutive days; Group V: Orally administered 5 mL/kg of trévo for 14 consecutive days. Animals were anesthetized with diether and the brain excised and processed for the following biochemical assays: Malonedialdehyde (MDA), glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GT), acetylcholinesterase (AChE), beta-amyloid, glutamate, Na+/K+ ATPase, and glutamate dehydrogenase (GD). Results: PbA caused significant oxidative stress (increased MDA concentration, decreased GSH concentration, suppressed the activity of CAT, SOD), decreased GT activity, increased activity of AChE, increased the concentration of beta-amyloid, and caused glutamate excitotoxicity (increased concentration of glutamate, decreased activity of Na+/K+ ATPase, and GD) in rat brains. Treatment with trévo at the two different doses significantly prevented oxidative damage, beta-amyloid aggregation, glutamate excitotoxicity, and acetylcholine breakdown induced by lead acetate. Conclusion: Our findings added to the reported pharmacological activity of trévo and supported the antiaging potential of trévo.
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.
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