Selenium abates manganese-induced striatal and hippocampal toxicity via abrogation of neurobehavioral deficits, biometal accumulation, oxidative stress, inflammation, and caspase-3 activation in rats.

Excessive exposure to manganese (Mn) is associated with neurotoxicity characterized by oxidative stress, inflammation, and apoptosis induction. Selenium (Se) has been shown to possess antioxidant, anti-inflammatory, and anti-apoptotic properties in humans and animals. The present study investigated the neuroprotective mechanism of Se in rats sub-chronically treated with Mn at 30 mg/kg body weight or orally co-treated with Se at 0.2 and 0.4 mg/kg body weight for 35 consecutive days. Locomotive and exploratory profiles were recorded and computed with the aid of ANY-Maze (a video-tracking software) for 5-min trial, in a novel apparatus. The ANY-Maze analysis showed that Se significantly (p < 0.05) abated Mn-induced locomotive impairment evidenced by increased in maximum speed, total time traveled, absolute turn angle, number of line crossing, rotation and forelimb grip and decreased total time immobile, grooming, and negative geotaxis as verified by the enhanced track plot density. Furthermore, the striatum and hippocampus of the rats were excised and the levels of Mn and Se, oxidative stress markers, proinflammatory cytokines including acetylcholinesterase and caspase-3 activities were assayed. The result shows that Se abates Mn-mediated accumulation of Mn. Also, Se ameliorated Mn-induced decrease in antioxidant enzymes as well as glutathione level and increase in acetylcholinesterase activity, lipid peroxidation, proinflammatory cytokines (i.e., interleukin (IL)-6, IL-1ß, tumor necrosis factor alpha), and caspase-3 activation in the striatum and hippocampus of the rats. Collectively, Se abated Mn-induced striatal and hippocampal toxicity via abrogation of neurobehavioral deficits, biometal accumulation, oxidative stress, inflammation, and caspase-3 activation in rats. Se may serve as a neuroprotective agent against Mn-mediated neurotoxicity.

Levels of Some Heavy Metals and Health Risks Assessment of Three Different Species of Catfishes in Ikoli Creek, Bayelsa State, Nigeria.

Heavy metals are the most common form of aquatic pollutants and are of great health risk to consumers of contaminated sea food. This study investigated the level of heavy metals in three species of catfishes Chrysichthys nigrodigitatus (marine catfish), Clarias gariepinus (African catfish), and Schilbe mystus (silver catfish) in Ikoli Creek, Bayelsa State. The potential human health risks to consumers in the study area were investigated. The heavy metal concentration in the three species of catfishes was found in the following order: Fe > Zn > Cr > Pb > Cd. The levels were below WHO/FAO guideline, except for Fe having the highest value of 88.23 ± 0.09 mg/kg in C. gariepinus, 85.54 ± 0.26 mg/kg in S. mystus, and 66.36 ± 0.10 mg/kg in C. nigrodigitatus, which were above the acceptable regulatory limits in the fishes. The Chronic Daily Intake (CDI) values of all the metals were lower than the USEPA-recommended limits except for Cd in C. nigrodigitatus, C. gariepinus, and S. mystus. The Target Hazard Quotient for C. nigrodigitatus, C. gariepinus, and S. mystus was > 1. Life Cancer Risk from the consumption of Cr in C. nigrodigitatus and S. mystus was 1.65E-03 and 8.11E-04, indicating a probable risk of one chance of cancer for the populace that consumed fishes obtained from Ikoli creek. Heavy metal contamination of fishes caught in Ikoli creek may pose a health risk to the local populace via consumption of fishes.