Neuroprotective effect of Costus afer on low dose heavy metal mixture (lead, cadmium and mercury) induced neurotoxicity via antioxidant, anti-inflammatory activities

Abstract

Humans are constantly exposed to heavy metals due to their ubiquity in the environment. Hence, this study investigated the possible protective effect of Costus afer aqueous leaf extract (CALE) against low dose heavy metal mixture (LDHMM)-induced neurotoxicity. Male albino rats were divided into 6 equal groups. Group 1 served as the normal control receiving only deionized water. Group 2 served as the toxic control receiving on metal mixture (20 mg/kg PbCl2, 1.61 mg/kg CdCl2 and 0.40 mg/kg HgCl2), groups 3, 4 and 5 were co-treated with metal mixture and CALE (750, 1500 and 2250 mg/kg body weight, respectively) and group 6 was treated with metal mixture and ZnCl2. All treatments were administered through oral gavage for 90days. Oxidative stress biomarkers [malondialdehyde (MDA), superoxide dismutase (SOD), glutathione content (GSH) and catalase (CAT)], inflammatory cytokines [interlukin-6 (IL-6) and interlukin-10 (IL-10)], histopathological changes and heavy metal concentration were determined in brain of rats. Results indicated that LDHMM significantly increased (p < 0.05) the lipid peroxidation marker (MDA) and the pro-inflammatory cytokine (IL-6), while lowered levels of the oxidative biomarkers (SOD, CAT and GSH) and anti-inflammatory cytokine (IL-10). Also, LDHMM caused some histopathological changes such as reactive gliosis and glia cell proliferation. LDHMM elevated the lead, cadmium and mercury concentrations in the brain. Severity of the distorted cortical parameters were ameliorated by CALE administration. The CALE induced significant protective effect on LDHMM-mediated neurotoxicity in a dose-dependent manner which may be a result of its antioxidant anti-inflammatory and metal chelation mechanisms.

Keywords

• Neurotoxicity
• Heavy metal exposure
• Metal chelation
• Oxidative stress
• Costus afer