Background: Cadmium (Cd) is a heavy metal with very high toxicity, whose prolonged contact is linked to neurodegenerative disorders due to its ability to induce oxidative stress, neuro-inflammation, and apoptosis in critical brain regions such as the hippocampus and prefrontal cortex. Objectives: This study evaluated the effects of Daucus carota ethanolic leaf extract in cadmium-induced toxicity on the oxidative stress markers in the hippocampus and prefrontal cortex of adult wistar rats. Methods: Thirty adults male Wistar rats (weighing 150–180 g) were randomly assigned into five groups (6 per group). Group 1 (normal control) received water, Group 2 (Cd-only) was administered cadmium chloride (5 mg/kg) to induce neurotoxicity. Group 3 received only CLE (400 mg/kg). Groups 4 and 5 were received cadmium chloride and CLE at doses of 200 mg/kg and 400 mg/kg, respectively. All treatments were administered orally for 28 days. At the end of the experiment, brain tissues were harvested for biochemical analysis of oxidative stress markers (MDA, ROS and 4-HNE) and anti-oxidant enzyme (SOD, CAT, GSH) activities. Data were analyzed using GraphPad Prism version 8 and presented as Mean ± SEM. Statistical comparisons were made using one-way ANOVA followed by Tukey’s post hoc test, with significance set at p < 0.05. Results: Cadmium exposure significantly increased oxidative stress, and triggered neuro-inflammation, as evidenced by elevated MDA, ROS and 4-HNE levels and reduced antioxidant enzyme activity (SOD, CAT, GSH). However, CLE treatment ameliorated these changes in a dose-dependent manner. The Cd + CLE (200 mg/kg) and Cd + CLE (400 mg/kg) groups exhibited significant improvements compared to the Cd-only group, showing reduced oxidative damage. The highest dose (400 mg/kg) demonstrated the most pronounced neuroprotective effects, with biochemical parameters approaching those of the control group. Conclusion: This study provides compelling evidence that Daucus carota ethanolic leaf extract exhibits potent neuroprotective properties against cadmium-induced neurotoxicity. The observed anti-oxidative effects suggest that CLE could serve as a promising natural intervention for mitigating heavy metal-induced cognitive and neuronal impairments.
Anyigor-Ogah et al. (Fri,) studied this question.
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