Cadmium (Cd) contamination of agricultural soil has becomea serious threatto global food security. The present study highlights the role of added sulfate(SO42-) in modulating sulfurmetabolism and antioxidant defense system conferring tolerance against Cd stress in maize. Expression patterns of antioxidant genes, transporters involved in SO42-and Cd accumulation, antioxidant enzyme activity, membrane damage, in vivo reactive oxygen species (ROS) detectionandhydrogen peroxide(H2O2)accumulation under Cd stress in presence (T2) or absence (T1) of excess SO42-were studied to get an overview of cellular manoeuveringin conquering Cd induced oxidative stress damages. Moreover, dynamic correlations between miR398a, miR395d, miR408a and their target genes under Cd exposure were validated through qRT-PCR. Supplementation of the ¼ Murashige and Skoog(MS) media with excess sulfate[600 μM (NH4)2SO4] markedly restored the shoot biomass under Cd stress (100 μM CdCl2). Presence of excess SO42-in the nutrient media significantly reduced Cd uptake as well as tissue Cd accumulation in T2plants. Foliardark blue and deep brown spots revealedafter histochemical staining with nitroblue tetrazolium(NBT) and 3’3’-diaminobenzidine(DAB) respectively indicated severe oxidative burst in T1plants under Cd treatment. Thechloromethyl derivative of 2′, 7′-Dichlorofluorescin diacetate(CM-H2DCFDA) and dihydroethidium(DHE) staining further supported enhanced ROS formation in roots of Cd challenged T1plants. Enhanced reduced glutathione(GSH) level both in root and above ground part of T2plants might be responsible for their better performance under Cd stressedcondition as evident from non-significant increase in superoxide anion(O2-), low H2O2and thiobarbituric acid reactive substances(TBARS)levels as compared to T1plants.Taken together, our findings indicate that fine adaptation of sulfate uptake and assimilation in sulfatesupplemented maize plants (T2) might satisfy two contrasting needs: (a) maintaining high GSH pool essential for sustaining balanced redox status under stress condition; (b) alleviating Cd stresseffects by means of GSH mediated detoxification pathways