The generation and scavenging of varied reactive species, including reactive oxygen species (ROS), during metabolic reactions in varied cellular compartments are typical. At ROS-generation-scavenging equilibrium, ROS and its reaction products contribute to plant signaling. Notably, the impact of adverse growth conditions on plants is inevitable. These adverse growth conditions cause an imbalance between the generation and scavenging of ROS through either elevating ROS generation or diminishing their scavenging. In either case, ROS significantly violate cellular redox homeostasis and thereby impact overall plant health. Key soluble redox compounds ascorbate (AsA) and glutathione (GSH); enzymatic antioxidants such as ascorbate peroxidases (APX); monodehydroascorbate reductase; (MDHAR) and dehydroascorbate reductase (DHAR); catalase (CAT); glutathione reductase (GR); superoxide dismutase (SOD); and some proteinaceous thiol members including thioredoxin (Trx), glutaredoxin (Grx) and peroxiredoxin (Prx) proteins significantly maintain cellular redox homeostasis at its optimum, and protect the cells against potential damages caused by cellular redox violators. Notably, the outcome of the interaction between cellular redox homeostasis violators and protectors can be modulated by many exogenously supplied stimulants. This presentation aims to (i) briefly analyze the chemical behavior and production sites of ROS; (ii) highlight the dual behavior of ROS through overviewing ROS communication with other signaling molecules; ROS roles in stress signaling; and elevated ROS-accrued oxidative damage to biomolecules; (iii) discuss selected cellular redox homeostasis protectors; alternative oxidase; respiratory burst oxidase homologs; NADP-dependent malate dehydrogenase and the malate valve; plastid terminal oxidase; and proteinaceous thiol members; (iv) discuss selected exogenously supplied stimulant-induced modulation of cellular redox homeostasisprotectors; and also to (iv) highlight major aspects so far seldom explored about the subject.