Asian Journal of Research and Reports in Neurology

Background and Objectives: Cadmium is a potent neurotoxic heavy metal known to induce oxidative stress, apoptosis, and neurotransmitter dysfunction, leading to neurodegenerative effects. Turmeric (Curcuma longa) has gained attention as a natural antioxidant with potential neuroprotective properties. This study evaluates the neuroprotective effects of turmeric against cadmium chloride-induced neurotoxicity in male Wistar rats by assessing oxidative stress and cholinergic function.

Method: Twenty-four male Wistar rats (150–180 g) were divided into four groups (n = 6): Group I (Control), Group II (Turmeric only: 500 mg/kg BW orally), Group III (Cadmium only: 120 mg/kg BW subcutaneously), and Group IV (Cadmium + Turmeric). Turmeric was administered daily for four weeks. Superoxide dismutase (SOD) and acetylcholinesterase (AChE) activities were measured using standard spectrophotometric methods. Data were analyzed using one-way ANOVA and Tukey’s test, with p < 0.05 as the significance threshold.

Results: Cadmium exposure significantly reduced SOD activity (3.77 ± 0.19 U/mg protein) and AChE levels (11.0 ± 4.36 U/L) compared to the control group (6.22 ± 0.11 U/mg and 28.0 ± 0.52 U/L, respectively; p < 0.05). Turmeric co-administration markedly improved SOD (7.12 ± 0.12 U/mg) and AChE (32.0 ± 1.42 U/L) levels, demonstrating restoration of antioxidant and cholinergic function. Interestingly, turmeric alone elevated both SOD (6.50 ± 0.09 U/mg) and AChE (46.0 ± 0.48 U/L) beyond control values.

Conclusion: Turmeric mitigates cadmium-induced neurotoxicity by significantly enhancing antioxidant defenses and cholinergic neurotransmission. These findings support its potential as a dietary supplement or therapeutic agent in managing neurodegenerative conditions related to heavy metal toxicity. Further studies incorporating behavioral and histopathological assessments are recommended to validate its cognitive benefits.