Abstract
Lead (Pb) is a toxic, environmental heavy metal that induces serious clinical defects in all organs, with the nervous system being its primary target. Curcumin is the main active constituent of turmeric rhizome (Curcuma longa) with strong antioxidant and anti-inflammatory properties. This study is aimed at evaluating the therapeutic potentials of curcumin on Pb-induced neurotoxicity. Thirty-six male Sprague Dawley rats were randomly assigned into five groups with 12 rats in the control (normal saline) and 6 rats in each of groups, i.e., the lead-treated group (LTG) (50 mg/kg lead acetate for four weeks), recovery group (RC) (50 mg/kg lead acetate for four weeks), treatment group 1 (Cur100) (50 mg/kg lead acetate for four weeks, followed by 100 mg/kg curcumin for four weeks) and treatment group 2 (Cur200) (50 mg/kg lead acetate for four weeks, followed by 200 mg/kg curcumin for four weeks). All experimental groups received oral treatment via orogastric tube on alternate days. Motor function was assessed using a horizontal bar method. The cerebellar concentration of Pb was evaluated using ICP-MS technique. Pb-administered rats showed a significant decrease in motor scores and Superoxide Dismutase (SOD) activity with increased Malondialdehyde (MDA) levels. In addition, a marked increase in cerebellar Pb concentration and alterations in the histological architecture of the cerebellar cortex layers were recorded. However, treatment with curcumin improved the motor score, reduced Pb concentration in the cerebellum, and ameliorated the markers of oxidative stress, as well as restored the histological architecture of the cerebellum. The results of this study suggest that curcumin attenuates Pb-induced neurotoxicity via inhibition of oxidative stress and chelating activity.
Highlights
Lead (Pb) is a ubiquitous environmental neurotoxin that induces several physiological, behavioral, and biochemical abnormalities in humans and animals [1]
This study revealed that withdrawal of Pb acetate alone was not enough to restore the damage inflicted by Pb toxicity on rats of the recovery group (RC) group
In consideration of the results obtained from this study, Pb toxicity resulted in decreased motor function, increased oxidative stress, aberrations in the histological structure of the cerebellum, and accumulation of Pb in the cerebellums of affected rats
Summary
Lead (Pb) is a ubiquitous environmental neurotoxin that induces several physiological, behavioral, and biochemical abnormalities in humans and animals [1]. Program indicate a significant decrease in the incidence of blood lead levels (BLLs) among adult industrial workers, occupational exposure to Pb remains a public health concern, accounting for about. Occupational exposure to Pb is linked to several health consequences, such as cognitive impairment, reproductive disorders, hypertension, motor dysfunction, cancer, hepatotoxicity, nephrotoxicity, and mortality [4,5]. Pb toxicity has long been linked with impaired motor function, deficits in visuomotor coordination among adult industrial workers and children exposed to Pb [7]. When treated with Pb, animal models display increased oxidative stress, cognitive impairments, degeneration of neurons, deficits in motor coordination, and mortality [9,10,11]
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