EFFECTS OF VITAMIN C ON SOME HAEMATOLOGICAL PARAMETERS AND BIOMARKERS OF OXIDATIVE STRESS IN ALBINO WISTAR RATS EXPOSED TO SHORT-TERM LEAD ACETATE
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EFFECTS OF
VITAMIN C ON SOME HAEMATOLOGICAL PARAMETERS AND BIOMARKERS OF OXIDATIVE STRESS
IN ALBINO WISTAR RATS EXPOSED TO SHORT-TERM LEAD ACETATE
Abstract
The effects
of vitamin C on some heamatological parameters and biomarkers of oxidative
stress in albino wistar rats exposed to lead acetate over a short term (3
weeks) was investigated. Studies have revealed that lead has a wide range of
health effects that can result from exposure, and that lead can cause health
effects at blood lead levels previously thought to be safe. An increasing body
of evidence suggests that lead is associated with a number of health
conditions. Twenty albino wistar rats were randomly divided into four
experimental groups of five rats each, Control group were fed normal rat feed with
distilled water, Group 2,3 and 4 were fed normal rat feed, water and received
daily oral administration of lead acetate 250mg/kg daily. In addition groups 3
and 4 received 100mg/kg and 150mg/kg oral administration of vitamin C
respectively, for three weeks. Mild effect of lead acetate was observed in
haematological parameters as indicated by slightly increase ,which was not
statistically signifiant, in RBC and MPV. In contrast, a slight decrease was
seen in haemoglobin, PCV, MCV, MCH, MCHC and platelet count. Descrease in
MCV,MCH and MCHC indicated shrink in size of RBCs and onset of microcytic
anemia due to onset of iron deficiency. However, derease observed was not
stgatistically signifiant. Also the effect of lead acetate was mild on
biochemical enzyme activities, indicated byincreased level of MDA activity;
whih indicate oxidative stress,however the increase was not statistically
significant. SOD and GPx level were slightly decreased, which was not
statistially signifiant. The doses of vitamin C supplement did not reverse the
effect of lead acetate on some haematological parameters and some biochemical
enzyme activities, it however reverse the effect of lead acetate on MDA level.
In conclusion, exposure to lead acetate over a short term has little effect on
haematological parameters and biochemical enzyme activities. The doses of
vitamin C use in this study has ameliorative effect on MDA activity but has no
effect on some alteration on haematological parameters and some biochemical
enzyme activities.
CHAPTER ONE
1.0 INTRODUCTION
1.1 GENERAL
INTRODUCTION
Lead is a
naturally occurring bluish-gray heavy metal found in small amounts in the
earth‟s crust.
However, it
is rarely found naturally as a metal. It is usually found combined with two or
more other elements to form lead compounds (ATSDR, 2007). Metallic lead is
resistant to corrosion (i.e., not easily attacked by air or water). When
exposed to air or water, thin films of lead compounds are formed that protect
the metal from further attack (ATSDR, 2007). Lead is poisonous when inhaled or
eaten. Lead content in air, food and tap water has increased several folds
during recent years due to extensive use of this metal in petrol, paints,
battery and other industries (Tuarmaa, 1995). According to WHO (2000) lead is a
metal with no known biological benefit to humans. Too much lead can damage
various systems of the body including the nervous and reproductive systems and
the kidney.
Generally,
heavy metals produce their toxicity by forming complexes or ligands with
organic compounds thereby affecting the function of biological molecules,
inactivate some biochemical enzymes and affect protein structure (Pirkle, 1998)
Because of its potential health problems, the amount of lead used in these
products today has lessened or has been removed. Lead and other heavy metals create
reactive radicals which damage cell structure including DNA and cell membrane
(Flora, 2008). Lead poisoning can cause a variety of symptoms and signs which
vary depending on the individual and the duration of lead exposure (Kosnett,
2005, Karri, 2008 ).
The amount
of lead in blood and tissues, as well as the time course of exposure,
determines the level of toxicity (Pearson and Schonfeld, 2003).
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