Memory Deficit Recovery after Chronic Vanadium Exposure in Mice

Abstract

Vanadium is a transitional metal with an ability to generate reactive oxygen species in the biological system. This work was designed to assess memory deficits in mice chronically exposed to vanadium. A total of 132 male BALB/c mice (4 weeks old) were used for the experiment and were divided into three major groups of vanadium treated, matched controls, and animals exposed to vanadium for three months and thereafter vanadium was withdrawn. Animals were tested using Morris water maze and forelimb grip test at 3, 6, 9, and 12 months of age. The results showed that animals across the groups showed no difference in learning but had significant loss in memory abilities after 3 months of vanadium exposure and this trend continued in all vanadium-exposed groups relative to the controls. Animals exposed to vanadium for three months recovered significantly only 9 months after vanadium withdrawal. There was no significant difference in latency to fall in the forelimb grip test between vanadium-exposed groups and the controls in all age groups. In conclusion, we have shown that chronic administration of vanadium in mice leads to memory deficit which is reversible but only after a long period of vanadium withdrawal.

Sodium metavanadate induced cognitive decline, behavioral impairments, oxidative stress and down regulation of myelin basic protein in mice hippocampus: Ameliorative roles of β‐spinasterol, and stigmasterol

“…In the probe trail of the present study, we found that, administration of sodium metavanadate alone showed significant memory impairments. This is in consonance with reports by Folarin, Olopade, Onwuka, and Olopade () that vanadium exposure led to loss of memory acumen but in contrast to their finding of no variation in learning abilities, the variance in these results may be ascribed to the difference in duration of exposure. Stigmasterol significantly shortened the escape latency prolonged by sodium metavanadate injection after 2 days of training.…”

Brain Metal Distribution and Neuro-Inflammatory Profiles after Chronic Vanadium Administration and Withdrawal in Mice

“…Earlier studies have shown that vanadium crosses the blood brain barrier (García et al, 2004) to induce neuropathology including neurobehavioral (Li et al, 2013; Saxena et al, 2013; Mustapha et al, 2014; Folarin et al, 2016), neurochemical (Sasi et al, 1994; García et al, 2004) and neurocellular (Domingo, 1996; Garcia et al, 2005; Avila-Costa et al, 2006) changes. In humans, features of acute neurotoxicity include central nervous system (CNS) perturbations, (CNS) depression, tremor, impaired conditioned reflexes, as well as congestion of brain and spinal cord (Haider et al, 1998; Soazo and Garcia, 2007).…”

“…Azeez et al (2016) showed functional deficit, glial cell activation and region-dependent myelin damage in the brain of mice after 90 days of postnatal vanadium exposure. Our previous work has shown that a life time administration of vanadium in mice leads to memory deficits and progressive recovery after long period of treatment withdrawal (Folarin et al, 2016). The present study is designed to assess brain vanadium distribution patterns, and cellular (glial and neuronal) injury after a long term exposure, as well as the related progressive changes in the brain after withdrawal from treatment.…”

Oxidative Stress and Vanadium

“…Vanadium exposed workers exhibited poor performance in the simple reaction time, digit span memory, and Benton visual retention tests [74]. Memory loss in mice exposed to vanadium for 3 months was observed; nevertheless, in these animals, memory was recovered 9 months after vanadium was removal [75]. Increased incidence of Parkinson's disease is related to environmental metal exposure.…”