ABSTRACT
Learning is the act of acquiring new or modifying and re-inforcing existing knowledge, while Memory is relatively the permanent storage of the learned information. Exposure to lead affect brain regions such as hippocampus that are involved in learning and memory. Succimer drug or meso 2,3 β Dimercaptosuccinic acid (DMSA) is a metal chelator which is used as an antidote to lead toxicity. This study aimed at assessing the effect of cowpea (Vigna uinguiculata (L) walp) on learning and memory in acute lead-induced neuro toxicity in mice using Morris water and Barnes mazes. In this study 50 mice (18-22g, aged 6-8 weeks) were used. The animals were divided into two main groups of 25 mice each of the two memory assessment paradigms. Each paradigm has 5 mice allotted to 5 sub-Groups. Distilled water 10 ml/kg, succimmer 20 mg/kg, 250, 500 and 1000 mg/kg Vigna unguiculata aqueous extract were administered orally. Lead acetate solution at 120 mg/kg was also administered orally using canular to induce acute lead toxicity on the first day. The result was not statistically significant in the acquisition sessions and the probe trials for both the Morris water and Barnes mazes when compared to control. At the end of the study, it was concluded that Vigna unguiculata at the doses administered has no effect on learning and memory in acute lead induced neurotoxicity in mice, but that does not mean it lacks total therapeutic benefit. It was recommended that Co-administration of cowpea and succimmer might be of a better therapeutic benefit.
CHAPTER ONE
1.0 Introduction
Lead is a poisonous metal, which exist in both organic (Tetraethyl lead) and inorganic (lead acetate and lead chloride) forms in the environment (ShalanΒ et al., 2005). The main sources are medicines, paintings, pipes, ammunition. And more recently, it is found in alloys for welding storage materials for chemical reagents (Garazaet al., 2006). Exposure to lead mostly occurs through the respiratory and gastrointestinal systems. Lead is conjugated by the liver and passed to the kidney, where it is excreted out in urine and the rest accumulates in various body organs. This affects many biological activities at the molecular, cellular and intercellular levels, which may result in morphological alterations that can remain even after lead level has fallen (FloraΒ et al., 2006; Ibrahimet al., 2012).
Lead poisoning or lead intoxication is defined as exposure to high levels of lead typically associated with severe health effects. Poisoning is a pattern of symptoms that occur with toxic effects from mild to high levels of exposure; toxicity is a wider spectrum of effects, including subclinical ones (those that do not cause symptoms) (Guidotfi and Ragain, 2007). The amount of lead in the blood and tissues, as well as the time course of exposure, determines toxicity. Lead poisoning may be acute (from intense exposure of short duration) or chronic (from repeat low-level exposure over a prolonged period), but the chronic is much more common (Rossi, 2008).
Diagnosis and treatment of lead exposure are based on blood lead level measured in micrograms of leadΒ perdeciliter of bloodΒ (ΞΌg/dL). A blood lead level of 10 ΞΌg/dL or above is a cause for concern; however, lead may impair development and have harmful health effects even at lower levels, and there is no known safe exposure level (Barbosa,Β etΒ al., 2005).Β
