# Antioxidant Production in _Dunaliella_
## 2 Antioxidants
### Generation and Detoxification of ROS
O\({}_{2}\)\({}^{\bullet-}\) is generated during oxidisation of unsaturated fatty acids [91], from the activity of cytochrome P450 [92] and the cytochrome \(b5\) family members [93,94]. Also, O\({}_{2}\)\({}^{\bullet-}\) is produced in the peroxisome where xanthine oxidases catalyse the oxidation of xanthine and hypoxanthine to uric acid [45], and in the plasma membrane due to the reduction of O\({}_{2}\) by NADPH oxidases [49]. \begin{table}
\begin{tabular}{c c c c c} \hline
**ROS** & **Reaction** & **Life Span** & **Function** & **Sources of ROS** & **Scavenging Antioxidants** \\ \hline HO\({}_{2}\)\({}^{\bullet}\) & \begin{tabular}{c} Protonation of \\ superoxide ions \\ \(\text{O}_{2}\)\({}^{\bullet-}+\text{H}^{+}\rightarrow\) \\ \(\text{HO}_{2}\)\({}^{\bullet}\)\({}^{\bullet}\) \\ \end{tabular} & \begin{tabular}{c} Attacks PUFA in \\ the negatively \\ charged membrane \\ surface \\ \end{tabular} & \begin{tabular}{c} Mitochondria, \\ microsomes and \\ peroxisomes \\ \end{tabular} & \\ \hline HO\({}_{\bullet}\)(Three & \begin{tabular}{c} Fenton reaction: \\ H\({}_{2}\)O + Fe\({}^{2+}\rightarrow\) \\ HO\({}^{\bullet}\) + HO\({}^{\circ}\) + Fe\({}^{3+}\) \\ \end{tabular} & 1 ps & \begin{tabular}{c} Attack unsaturated \\ fatty acids in \\ membranes \\ \end{tabular} & Mitochondria & \begin{tabular}{c} ASc, GSH, \\ flavonoids, lipoic \\ acid, proline \\ \end{tabular} \\ of \({}^{3}\)O\({}_{2}\))\({}^{\bullet-}\) & \begin{tabular}{c} \(\text{O}_{2}\)\({}^{\bullet-}+\text{H}_{2}\text{O}_{2}\rightarrow\) \\ HO\({}^{\bullet}\) + HO\({}^{\circ}\) + O\({}_{2}\) \\ \end{tabular} & & \\ \hline Nitric oxide (NO\({}_{\bullet}\)) & \begin{tabular}{c} L-arginine + O\({}_{2}\) \\ Nitric oxide synthase \\ \(\rightarrow\) NO\({}^{\bullet}\) + \\ Citrulline \\ \end{tabular} & \begin{tabular}{c} Intercellular \\ messenger, the \\ quencher of O\({}_{2}\)\({}^{\bullet-}\), \\ defense against \\ various protozoa, \\ fungi, and \\ mycobacteria \\ \end{tabular} & \begin{tabular}{c} Peroxisome, \\ cytosol \\ \end{tabular} & GSH \\ \hline Peroxynnitrite & \begin{tabular}{c} NO\({}^{\bullet}\) + O\({}_{2}\)\({}^{\bullet-}\rightarrow\) \\ ONOO\({}^{-}\) \\ \end{tabular} & \begin{tabular}{c} React with amino \\ acids residues in \\ enzymes causing \\ inactivation \\ \end{tabular} & \begin{tabular}{c} Peroxiredoxin, \\ Uric acid \\ \end{tabular} \\ \hline Lipid hydroperoxide & Oxidation of PUFA & \
\begin{tabular}{c} Tissue injuries and \\ diseases \\ \end{tabular} &
\begin{tabular}{c} Mitochondrial \\ membrane PUFA \\ \end{tabular} \\ \hline \end{tabular}
\end{table} 
Table 2: _Cont._Superoxide ions (O2\({}^{\bullet-}\)) are converted into hydrogen peroxide (H2O2) by the catalytic activity of SOD. H2O2 is also produced in peroxisomes when glycolate from the photorespiration is recycled. In addition, H2O2 can be formed by D-amino acid oxidase, urate oxidase, flavin oxidase, L-\(\alpha\)-hydroxy acid oxidase, and fatty acyl-CoA oxidase, and by cell wall peroxidases. Reactive OH\({}^{\bullet}\) is produced from the reaction of O2\({}^{\bullet-}\) and H2O2 at neutral pH and ambient temperature (Haber-Weiss reaction) or from H2O2 during the Fenton reaction [96]. In contrast, the addition of a proton (H\({}^{+}\)) to O2\({}^{\bullet-}\) generates perhydroxyl radicals (HO2\({}^{\bullet}\)). In some cases, intracellular ROS could also form during auto-oxidation of small molecules (epinephrine, flavins, and hydroquinones) [97; 98]. The singlet oxygen (\({}^{1}\)O2) is generated from the reaction of oxygen (\({}^{3}\)O2) with the triplet state of chlorophyll produced by the dissipation of insufficient energy during photosynthesis [45]. Under normal physiological conditions, ROS is neutralised by the cells' antioxidant systems where antioxidant enzymes and antioxidant molecules maintain the delicate intracellular redox balance and mitigate undesirable cellular damage caused by ROS, Table 2[48; 50].