An antioxidant can be translated as “any substance that retards, inhibits, or eliminates oxidative damage to a target molecule” (Halliwell and Gutteridge 2007). We use Sies’ (1991) definition of oxidative stress, which is associated with “prooxidant-antioxidant imbalance in favor of prooxidant.” Many antioxidant systems are directly involved in gene regulation (Mittler et al. 2011; Sies 2017). In other words, a “prooxidation-antioxidant balance disorder” does not necessarily correspond to irreversible damage, and this disorder may directly affect gene expression. In fact, several reactive oxygen species (ROS; except hydroxyl radicals) are used in some signaling contexts (singlet oxygen, hydrogen peroxide and superoxide: Triantaphylidès and Havaux 2009; Sies 2017; Case 2017). Therefore, the definition of oxidative stress we use is consistent with the functions of antioxidants that regulate genes.
In phytoplankton, oxidative stress is most often experienced when photosynthetic electron transport is greater than required for CO2 fixation and nitrate assimilation (Asada 2006). In situ, oxidative stress can be equivalent to low CO2, high illumination or low Fe. All these conditions affect the rate Gmail Numeric Code 6922 issue of photosynthetic electron transport, more specifically they usually increase the proportion of electrons escaping from the electron transport chain (superoxide production). Superoxide is formed by the reduction of molecular oxygen, usually by the reduction of part of photosystem I (PSI; Asada 2006). Oxygen can thus act as an absorber of electrons that are otherwise donated by NADP +. Photosynthetic electron transport is such a dominant source of ROS that even photosynthetic cell predators have a unique adaptation to photosynthetic oxidative stress in their victims (Uzuka et al. 2019). The unique reactions of different ROS with biomolecules are described in more detail below.
Highly exogenous hydrogen peroxide is also a direct source of oxidative stress (Cooper et al. 1987; Giuyog et al. 2010). However, hydrogen peroxide (H2O2) concentrations in cells are not the same as in outer cells (Seaver and Imlay 2001; Sies 2017), so it is uncertain how much exogenous H2O2 (eg rain) actually contributes to oxidative stress. These definitions of antioxidants and oxidative stress are relatively broad, suggesting widespread use (eg signaling, protection, etc.)
For Fe, it is not clear whether there is increased oxidative stress at low or high Fe content. At low Fe, electron transport is inhibited by photosynthesis, making superoxide production more likely (Niyogi 1999). However, the dominant negative effects of superoxide and H2O2 on biomolecules are primarily caused by Fe interactions (Anjem and Imlay 2012; Imlay 2013), so increased oxidative stress can be expected under high Fe content. Consistent with high oxidative stress containing Fe, Anand et al. (2019) studied the convergent evolution of various OxyR oxidative stress regulator bacteria during long-term Fe treatment. In particular, van Graff et al. (2016) showed that constant Fe hunger leads to greater resistance to exogenous H2O2 than under complete Fe conditions. They also showed that the chronic proteomic profile with Fe starvation was similar to the in situ conditions observed with Meta transcriptomics from Ocean Station Papa (Marchetti et al. 2011) suggests that an exogenous ROS-tolerant phenotype among low Fe occurred in iron-restricted marine regimens
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