الفهرس 
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Abstract
Homocysteine -lyase (Hcy--lyase; Desulfhydrase) (E.C 4.4.1.2) is pyridoxal dependent enzyme, catalyze -elimination of homocysteine to hydrogen sulphide, ammonia and -ketobutyrate (Han et al., 1998). For the higher affinity of homocysteine -lyase for methionine and cysteine, it was designated as L-methioninase on various publications (Ito et al., 1975; Tanaka et al., 1977 and Lockwood and Coombs, 1991).Hcy -lyase was received much attention during the last decade for its potency as anticancer, anti-cardiovascular agent, anti-diabetes and against other sulfur-metabolic disorders (Refsum, 1998 and Carmel and Jacobsen, 2001). Biochemically, the balance between the level of cystathionine and homocysteine is controlled by transsulfuration and reverse-transsulfuration system. Inactivation of cystathionine β-synthase causing hyperaccumulation of homocysteine (Homocysteinuria) (more than 15 M), that is the major risk of cardiovascular diseases, skeletal abnormalities (De Bree et al., 2002), Alzheimer’s (Morris, 2003), and megaloblastic anemia (Mudd et al., 1985). Also, homocysteinuria causes mental retardation, dislocation of optic lenses and osteoporosis (Schuh et al., 1984). It thought to be the cause of about 10% of total risk factor for cardiovascular (Graham et al., 1997). Each 1 M increment in blood homocysteine induces the risks of cardiovascular disease by about 6-7 fold (Stanger, 2004). Practically, plasma homocysteine more than 100 M was designated as severe homocysteinuria (Kang et al., 1992 and Jacobsen, 1998). Thus, from coenzymes view, supplementation of vitamins B6, 12 and folic acid may greatly enhance the reduction in level of homocysteine via activation of cystathionine β-synthase and methionine synthase (Mudd et al., 1985 and Stanger, 2004). However, miss-expressed or