## 4 Light Intensity- and Spectrum-Associated Adjustment of Metabolism
### Light Control of Secondary Metabolism
#### 4.6.1 Effect of Light Intensity on Secondary Metabolism
A further relationship between flavonoids and the redox system was proposed by [PERSON] et al. (2010) based on the induction of flavonoid biosynthesis by photosynthetic redox imbalance in _Lemma gibba_ exposed to various stresses [231]. Since the relationship between the flavonoid synthesis and redox system was confirmed both in a dicot and monocot species, the light intensity-dependent redox changes seem to be general regulators of flavonoid levels in plants. Anthocyanins are pigmented flavonoids, with sugars at position three or sometimes in another position [122]. Their HL-induced accumulation was demonstrated in _Arabidopsis_, and this change was redox-associated based on its fine-tuning by isoforms of TRX [232]. A further relationship of anthocyanins with the redox system is indicated by their antioxidative properties and role in the tolerance to abiotic stress-induced oxidative stress [233]. Under abiotic stress, the induction of anthocyanin biosynthesis on the upper epidermis of leaves is mediated by ROS signalling and transcription factors such as MYB/bHLH/WD40 in _Arabidopsis_[234; 235]. The alterations in ROS formation may derive from the changes in the redox state of the photosynthetic electron transport chain which have been suggested to affect both AsA and anthocyanin accumulation [229]. In _Arabidopsis_, anthocyanin biosynthesis is regulated by H\({}_{2}\)O\({}_{2}\) homeostasis, which is controlled by AsA and glutathione accumulation, and glutathione redox state under HL. Accordingly, the AsA-deficient mutant _vtc2-1_ accumulated significantly less anthocyanin under HL [229]. This change may be the result of transcriptional regulation since in _vtc1_ and _vtc2_ mutants, the induction of the key transcription factors, PAP1 (PRODUCTION OF ANTHOCYANIN PIGMENT), GL3 (GLABRA 3), and EGL3 (ENHANCER OF GLABRA), as well as transcripts of anthocyanin biosynthesis enzymes, were HL-impaired. AsA deficiency may also affect anthocyanin levels through its influence on flavonoid biosynthesis since the activity of three related 2-oxoglutate-dependent dioxygenases (2 ODDs), F3H, FLS, and leucoanthocyanidin dioxygenase (LDOX), require AsA for the reduction of over-oxidized FeIV to FeII in the active site of the enzyme to avoid inactivation. In addition, low AsA content reduced the accumulation of phenylpropanoids, which play an important role in the biosynthesis of anthocyanins. Regarding the light-dependent, redox-mediated control of anthocyanin synthesis, it has also been shown that H\({}_{2}\)O\({}_{2}\) or glutathione-mediated redox signals acted upstream of the PAP1 transcription factor [233]. Despite the enhanced anthocyanin biosynthesis capacity, the transgenic plants were, for instance, not able to induce anthocyanin synthesis under drought-induced oxidative stress. The possible mechanism of anthocyanin catabolism was suggested to be implemented via polyphenol oxidases (PPOs), anthocyanin \(\beta\)-glucosidase, or class III peroxididases (POXs) _in planta_, enzymes which link the process to the light-responsive redox system. PPOs are localised in the plastids, whereas POXs are distributed in several cell compartments, including vacuoles. Thus, POXs are more likely candidates for in vivo anthocyanin degradation [227; 236]. Accumulation of POXs, phenolics, and AsA in the vacuoles and the apoplast is light-dependent, serving as an important sink for H\({}_{2}\)O\({}_{2}\)[237]. A further link of the anthocyanin catabolism to the redox system is indicated by the observation that anthocyanin \(\beta\)-glucosidase and peroxididases could be Trx targets [204]. Alkaloids are a large, diverse group of nitrogen-containing secondary metabolites with more than 15,000 members. Most alkaloids participate in the defence against plant herbivores, especially mammals [122].