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,

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.

Cadmium (Cd) is a heavy metal that is deleterious to brain development as it increases brain aging. Trévo is a multi-herbal supplement that provides various health benefits, including boosting the immune system and detoxification. In this study, we investigated the neuroprotective effects of Trévo against the neurotoxic effects of cadmium chloride (CdCl₂). Thirty male Wistar rats were equally divided into three groups: Group I (normal control), Group II (administered CdCl₂), and Group III (administered Trévo and CdCl₂), and were used in the experiments. Animals were pretreated with 2 mL/kg of Trévo for five days and injected with Cd intraperitoneally 3 h later. Cd significantly increased the production of malondialdehyde (MDA), amyloidogenesis, activation of caspase 3 and 9, and the production of p53 and glutamate. It also inhibited the activity of Na⁺/K⁺ ATPase, glutamate dehydrogenase, catalase, superoxide dismutase, and glutathione-S-transferase. The administration of Trévo revealed its antioxidant, anti-amyloidogenic, anti-excitotoxicity, and anticholinesterase properties as it prevented the biochemical changes induced by Cd toxicity in the brain of male Wistar rats. Our results supported the reported health benefits of Trévo as a good dietary supplement in preventing the toxic effects of poisonous substances, such as cadmium.

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.