most abundant antioxidant enzymes, which catalyze the reduction of hydrogen peroxide (H\({}_{2}\)O\({}_{2}\)) to water. APXs (hylakoid-bound APX and stromal APX) and Cys peroxiredoxins detoxify H\({}_{2}\)O\({}_{2}\) in chloroplasts and cytoplasmic and peroxisomal APX in cytoplasm and peroxisomes, respectively. Catalase functions in glycosylomes and peroxisomes. Representatives of non-enzymatic antioxidants in higher plants are ascorbic acid (vitamin C), glutathione, flavonoids, isoprenoids, carotenoids,tocopherol (vitamin E), ubiquinone, and plastoquinone. Similar to antioxidant enzymes, non-enzymatic antioxidants function in different cell compartments, but in both aqueous (ascorbic acid, glutathione, and flavonoids) and membrane phases (flavonoids and isoprenoids). Recently, the potential antioxidant activity of compounds that were not previously considered as such (sugars, proline, etc.) has been actively studied. However, they are not the subject of this review, as the mechanism of their antioxidant activity remains unclear and may be associated with their protective and signaling effects. Over the last few decades, scientists not only successfully increased the intensity of biosynthesis of antioxidant enzymes, but also multiplied the level of the antioxidants to improve plants sustainability. Although creating mutant plants with modified biosynthesis of non-enzymatic antioxidants is complicated, since multiple pathways and enzymes are involved in their biosynthesis, these plants may have some advantages over plants with overexpression of antioxidant enzymes. First of all, low molecular weight antioxidants can interact with different types of ROS, not just one, as in the case of antioxidant enzymes. Moreover, it is known that stress conditions often result in exhaustion of the substrates of the antioxidant enzymes, especially at the initial phase of the introduction of stress factors. For example, it has been shown that ascorbate--the substrate for APX and a low molecular weight antioxidant itself--is rapidly depleted in chloroplasts when H\({}_{2}\)O\({}_{2}\) is supplied [9]. The lack of ascorbate results in deactivation of ascorbate peroxidase and the failure of chloroplasts to neutralize H\({}_{2}\)O\({}_{2}\). Furthermore, as described above, most antioxidant enzymes are located in the aqueous phases of the cell, while they are practically absent in the membranes. Considering that membranes contain vital electron transport chains--such as the photosynthetic electron-transport chain in the thylakoid membranes of chloroplasts and respiratory electron-transport chain in the inner mitochondrial membrane--the need to protect the components of these chains becomes obvious. In this regard, important low molecular weight antioxidants are isoprenoids and tocopherols. Low molecular weight antioxidants often perform not only antioxidant functions but also other functions in plant cells. For example, flavonoids are effective in controlling insect pests [10]. Ascorbate and tocopherols can improve nutritional properties of plants and seed quality. In addition, ascorbate is able to protect \(\alpha\)-tocopherol from oxidation [11]. Thus, all the advantages described above underline the importance of altering non-enzymatic antioxidants to enhance the antioxidant capacity of plant cells, thereby reducing the oxidative status of plants under stress conditions. There are two primary approaches to increase the levels of low molecular weight antioxidants: (i) enhancing the expression of one or more genes encoding key enzymes involved in the biosynthesis of the target antioxidant; (ii) reducing the expression of genes encoding enzymes involved in the utilization or consumption of the specific antioxidant. These approaches can be achieved using both classical transgenesis and genome editing methods, either directly by altering the expression intensity of antioxidant biosynthesis genes or indirectly by regulating the activity of transcription factors for the corresponding genes.