Stress-protective osmolytes stabilize biomolecules and mediate plant defense responses, which help to remove the negative effects of stress in plants. However, the responses of ectoine (ECT, 1,4,5,6-tetrahydro-2-methyl-4-pyrimidinecarboxylic acid), as an osmolyte, need to be investigated for a better understanding of the defense pathways on water status, antioxidant system, and photosynthetic machinery against heavy metal stress. The different ECT concentrations (0.25–0.5 mM) were applied to Zea mays L. cv Karadeniz Yildizi with/without cadmium stress (100–200 μM Cd). Stress caused an inhibition in growth (RGR), water content (RWC), and osmotic potential (ΨΠ). After stress exposure, ECTs provided effective water management by elevating RGR, RWC and ΨΠ. The maize exposed to stress exhibited notable repression in the photosynthetic system depending on decreasing Fv/Fm, qP and, ΦPSII and increasing NPQ. The consumption of excess energy on photosynthetic machinery was controlled by ECTs via reversing these parameters. Cd toxicity resulted in downregulated-transcript levels of psbA, psbD, and psaB, which impaired the stability of PSI and PSII. After both Cd treatments, ECTs markedly induced the expression levels of psaA and psaB, which showed effective protection of photochemical activity. Cd-applied plants exhibited a decrease in superoxide dismutase (SOD), catalase (CAT), peroxidase (POX), ascorbate peroxidase (APX), glutathione peroxidase (GPX), and glutathione reductase (GR), causing the accumulation of TBARS in lipid peroxidation. Under Cd+ECTs, SOD, glutathione S-transferase (GST) and POX had effective radical scavenging, thereby maintaining low contents of H2O2 and TBARS. ECTs alleviated the low Cd treatment-impaired redox state and participated in the ascorbate (AsA) and glutathione (GSH) regeneration. Consequently, ECT-mediated tolerance of maize was proved by increased growth, water potential, antioxidant capacity (especially SOD, POX), up-regulation of genes encoding proteins related to PSI, and PSII and AsA-GSH redox systems under Cd toxicity.