Author(s): Suhasini Dehury1, Kali Prasad Pattnaik2, Asaranti Kar3, Rajashree Samal4, Kaumudi Pattnaik5
Tuberculosis is one of the oldest disease known to affect humans. Over one third of world’s population is infected with mycobacterium tuberculosis and more than 2 million people per year are dying of the disease.1 A meta-analysis of studies involving several antitubercular drug regimens showed the incidence of hepatitis to be 2-6%, out of which hepatitis due to isoniazid alone attributes to 1.6%.2 Isoniazid causes mild-to-moderate elevation of serum transaminase in approximately 0.5%-2% of patients.3 The metabolite of isoniazid, i.e. hydrazine reacts with sulfhydryl group results in glutathione depletion within hepatocytes ultimately leading to cell death.2 S-Adenosyl-L-Methionine (SAM) a metabolite of methionine is an important molecule required for many vital functions of cell as well as cellular survival. It is the principal biological methyl donor required for methylation of DNA, RNA, biological amines, phospholipids and other proteins.4 In liver, SAM is a precursor of glutathione, a major endogenous antioxidant that protects cell against injury by scavenging free radicals involved in liver damage. Thus, SAM supplementation may protect the hepatocytes from any type of oxidative stress injury. Literature scan suggests SAM supplementation can afford protection to liver cells in liver disease, viral hepatitis and paracetamol-induced hepatic damage in both preclinical and clinical studies.4 There are scanty data regarding hepatoprotective effect of SAM in isoniazid-induced liver damage.
Aims and Objectives
With the above background, the present study has been undertaken to assess the possible hepatoprotective activity of SAM in isoniazid-induced liver damage in animal model by evaluating the biochemical and histopathology parameters.