A glutathione (GSH)-over producing mutant, dwf1, was isolated in grass pea (Lathyrus sativus L.). Possible cause of this overproduction and antioxidane defense response to cadmium (Cd) were investigated in nutrient solution, unsupplemented (control) or supplemented with 50 µM CdCl2 and 1 mM Lbuthionine-(S,R)-sulphoximine (BSO) in different combinations. Compared with mother variety, the mutant exhibited >2.5-fold increase in foliar GSH-content and normal or enhanced activities of antioxidant defense enzymes, enabling it to maintain quite normal growth even under Cd treatment. However, introduction of 1mM BSO in the medium alone or in combination with Cd reduced GSH level 3- 3.5-fold in the mutant, confirming that high GSH-biosynthesis was required for its overproduction. The reduction of GSH redox state led to activities of defense enzymes below normal level with an obvious negative impact on growth of the mutant plants, and the effect was more severe in its mother plant. The result indicated central role of GSH played to prevent Cd-induced oxidative stress. Inheritance studies revealed involvement of two different loci, cad L-1 and liL-1, in controlling cadmium tolerance and leaf injury, respectively. Primary trisomic analysis assigned cadL-1 locus on extra chromosome of grass pea trisomic II in tight linkage with liL-1 locus and indicated a possible pleiotropy of cadL-1 locus on glutathione content of grass pea
