Oxidative stress is a key modulator, which modifies the ligand-receptor interactions extracellularly and intracellularly, and influences gene expression. Free radicals can act as secondary messengers in several transduction pathways, and take part in the activation of chemotactic cytokines and surface adhesion molecules etc. Oxidative stress can induce stress response genes, and moderate oxidative stress by down regulating the gene expression of several genes. DNA synthesis, selective gene expression, enzyme activation and modification of cell proliferation are involved in redoxy signal mechanisms. Moderate free radical production can modify the function of kinases or directly activate the transcription factors, thereby also influencing the gene regulation in the nucleus. The “antioxidant” concept has meaning only in defense against free radicals for a long period. Its importance is not doubtful in the therapy of diseases in which free radicals are also involved. “Janus face” antioxidants can stop protein phophorilation and the inhibition of activation of transcription factors. They can also therefore stop cell proliferation and injure the adaptation mechanisms against oxidative stress. The direct roles of these antioxidants in original forms are doubtful in transduction therapy.