Abstract
This  experiment  pertains  to  the  protective  role  of Vernonia  amygdalina  pre-treatment  on  some  biochemical  indices  in
dimethylnitrosamine (DMN)-induced liver damage in male albino rats. Four (4) groups of six (6) rats each were used for the
study. Group 1served as control, group 2 and 3 were pre-treated with 400mg/kg Vernonia amygdalina for one week while
group 3 and 4 each received single dose of 20mg/kg DMN (orally) after one week. The rats were sacrificed 48hrs after DMN
administration. In rats administered 20mg/kg DMN, liver damage was clearly shown by increased activities of serum hepatic
marker enzymes namely aspartate aminotransaminase (AST), alanine aminotransaminase (ALT), alkaline phosphatase (ALP),
and gamma glutamyltransferase (GGT), increased lipid profile parameters such as total cholesterol and triglycerides as well as
increased level of lipid  peroxidation indices, malondialdehyde (MDA) in liver. The toxic effect of DMN was also indicated by
significantly decreased levels of antioxidants such as superoxide dismutase (SOD), catalase (CAT) and reduced glutathione
(GSH).  However,  in  rats  pre-treated  with  400mg/kg Vernonia  amygdalina  and  dosed  thereafter  with  DMN,  there  were
significant  reversal  in  the  activities  of  serum  hepatic  marker  enzymes,  lipid  profiles,  lipid  peroxidation  and  significant
restoration of antioxidant levels in the liver when compared to DMN-alone treated rats. Histopathological studies in the liver of
rats also showed that Vernonia amygdalina pre-treatment markedly reduced the toxicity of DMN and significantly preserved
the  normal  histological  architecture  of  the  tissue.  The  findings  of  this  study  suggest  that  pre-treatment  with Vernonia
amygdalina  leaves  has  a  protective  and  beneficial  effect  on  liver  subjected  to  DMN-induced  oxidative  stress,  possibly  by
decreasing lipid peroxidation and enhancing endogenous antioxidant production.