Authors :
Okechukwu Anyigor-Ogah; Chijioke Stanley Anyigor-Ogah; Albert N. Eteudo; Clinton O. Njoku; Idika Mba Idika; Chukwuemeka Otakpo; Agatha Nkechinyere Ekechi; Ndudim O. Okezie
Volume/Issue :
Volume 10 - 2025, Issue 8 - August
Google Scholar :
https://tinyurl.com/yx8asj7b
Scribd :
https://tinyurl.com/3kbkzhet
DOI :
https://doi.org/10.38124/ijisrt/25aug264
Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.
Note : Google Scholar may take 30 to 40 days to display the article.
Abstract :
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.
Keywords :
Cadmium, Extract, Oxidative Stress, Toxicity, Hippocampus.
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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.
Keywords :
Cadmium, Extract, Oxidative Stress, Toxicity, Hippocampus.