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 – 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 (Shalan 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 (Flora 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 lead per
deciliter of
blood (μg/dL). A blood lead level of 10 μg/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,
et al., 2005).