**4. The dual effect of ROS: from toxicity to signaling**

#### **4.1. Toxicity of ROS**

The oxidative stress may cause damage to DNA resulting in cancer and aging [62], and the presence of reactive oxygen also may initiate a chain reaction at the cellular level resulting in damage to critical cell bio-molecules [63–65]. The uncontrolled accumulation of ROS, particularly of OH• is highly toxic for the cell. These radicals are highly toxic and thus generate oxidative stress in plants. ROS can react with the majority of biomolecules, thus resulting in oxidative stress that can become irreversible and cause cellular damage [1–5]. Many harmful effects of ROS on cellular macromolecules have been identified [1–5]. All are capable of reacting with membrane lipids, nucleic acids, proteins and enzymes, and other small molecules, resulting in cellular damage [1–5]. Lipid peroxidation, which is a free-radical chain process leading to the deterioration of polyunsaturated fatty acids (PUFAs), is the best known cellular hazard among these, and has been studied intensively in food science [66]. Lipid peroxidation is initiated by free-radical attack upon a lipid, that gives starting to a chain reaction, removing a hydrogen atom from another fatty acid chain to form a lipid hydroperoxide (LOOH) in a propagation step [67]. This process is likely to degrade PUFAs present in membranes or in reserve lipids of oily seeds. Beside membranes, nucleic acids and proteins are also potential targets of ROS [67]. The hydroxyl radical, OH•, can damage both nuclear and organelle DNA directly, by having ability to attack deoxyribose, purines and pyrimidines [67, 68]. Enzymes can also be inactivated easily by ROS, by degrading amino acids [69, 70]. ROS can damage transport proteins, receptors and ion channels and then lead to extensive cellular dysfunction [1–5, 69, 70].
