WISTAR RATS

Exposure to neurotoxic substances like nickel chloride poses significant risks to neurological health. Vinpocetine, a synthetic derivative of the alkaloid vincamine acts as a phosphodiesterase- 1 inhibitor, modulating intracellular signaling and enhancing cerebral metabolism. It improves cerebral blood flow and supports synaptic plasticity, by increasing cyclic GMP and reducing neuroinflammation and neurodegenerative damage by reducing oxidative stress. Accordingly, this study was aimed at investigating the possible neuroprotective activity of vinpocetine on Nickel Chloride-induced neurotoxicity in adult Wistar rats. In this study, Fourty-two (42) Wistar rats was randomly divided into six (6) groups (n=7). Group A rats served as the control group to be given 1ml of distilled water. Group B rats was administered Nickel Chloride only at a dose of 5mg/kg body weight. Group C rats was administered 2.5mg/kg body weight of Vinpocetine and 5mg/kg body weight of Nickel Chloride. Group D rats was administered 5mg/Kg body weight of Vinpocetine and 5mg/kg body weight of Nickel Chloride. Group E rats was administered with 2.5mg/Kg body weight of Vinpocetine only and group F rats was administered with 5mg/Kg body weight of vinpocetine. Neurobehavioral activities were assessed 24 hours before the last administration, and at the end of the experimental period, the rats were weighed and sacrificed, and the body and brain weight changes, antioxidant enzymes activity, as well as histological assessment of the cerebrum. Results indicate that nickel chloride administration led to significant decrease on body weight, brain weight, neurobehavioral activity, and antioxidant enzymes levels, while increasing lipid peroxidation. However, pretreated rats with Vinpocetine mitigated these detrimental effects induced by nickel chloride. Vinpocetine supplementation was associated with improved body and brain weight, enhanced neurobehavioral performance, elevated antioxidant enzyme levels. This study sheds light on vinpocetine's potential as a neuroprotective agent against nickel chloride-induced neurotoxicity, suggesting its importance in preventing or mitigating neurological disorder caused by nickel chloride.

This study evaluates the hematoprotective effects of ethanol leaf extract of Acalypha wilkesiana on Wistar rats exposed to 1,2-dimethylhydrazine (DMH), a carcinogen. The experiment involved nine groups of rats with varying treatments: normal control, positive control with DMH and Xeloda (Capecitabine), and several groups receiving different doses of Acalypha wilkesiana extract both before and after DMH exposure. Hematological parameters analyzed included Mean Corpuscular Volume (MCV), Mean Corpuscular Hemoglobin (MCH), and Mean Corpuscular Hemoglobin Concentration (MCHC). Results demonstrated significant changes in these parameters among treated groups. Rats treated with Acalypha wilkesiana extract exhibited increased MCV, MCH, and MCHC levels compared to controls, indicating potential hematoprotective properties. Specifically, groups receiving the extract showed improvement in red blood cell indices affected by DMH, suggesting its efficacy in mitigating DMH-induced hematological damage. These findings highlight the potential therapeutic application of Acalypha wilkesiana in managing hematological disorders caused by carcinogenic agents. Further research is necessary to elucidate the mechanisms of action and optimize dosage for clinical use. Overall, this research opens promising avenues for utilizing natural remedies to enhance patient well- being and combat hematological abnormalities

The disruption of cardiovascular and renal function by environmental toxicants remains a major concern in toxicological research, particularly when such agents interfere with biochemical markers essential for assessing organ integrity. Among these toxic agents, exposure to sodium
arsenite poses a serious threat due to its ability to induce acute myocardial injury and impair renal filtration processes. This study evaluated the potential of vitamin E to counteract these toxic effects in male Wistar rats, focusing exclusively on validated clinical biomarkers of cardiac
and renal injury. Rats exposed to sodium arsenite (Group C) showed a pronounced rise in cardiac troponin (59.24 ± 3.8 pg/mL) and CK-MB (62.30 ± 2.1 U/L), indicating significant myocardial cell damage relative to the control group. The nephrotoxic impact was equally evident, as reflected by elevated serum urea (24.49 ± 1.8 mg/dL) and creatinine (1.98 ± 0.1 mg/dL), demonstrating impaired glomerular filtration and reduced renal functional capacity. Administration of vitamin E showed a clear dose-dependent protective effect. Rats receiving 25 mg/kg (Group D) and 50 mg/kg (Group E) of vitamin E along with sodium arsenite experienced significant reductions in cardiac troponin (48.65 ± 2.2 and 40.04 ± 2.9 pg/mL) and CK-MB
(41.17 ± 2.9 and 31.02 ± 1.2 U/L), indicating decreased myocardial damage. Renal biomarkers also improved, with urea decreasing to 16.08 ± 1.6 and 10.20 ± 1.7 mg/dL, and creatinine dropping to 1.08 ± 0.1 and 0.88 ± 0.1 mg/dL in Groups D and E, respectively. These results highlight vitamin E’s ability to protect both cardiac and renal functions despite ongoing toxic exposure. Overall, this study shows that vitamin E provides significant cardioprotective and
nephroprotective effects, mainly by normalizing key biomarkers of myocardial and renal dysfunction in rats exposed to sodium arsenite.