Physiological responses of maca (Lepidium meyenii Walp.) plants to UV radiation in its high-altitude mountain ecosystem

Ultraviolet (UV) radiation is a small fraction of the solar spectrum, which acts as a key environmental modulator of plant function affecting metabolic regulation and growth. Plant species endemic to the Andes are well adapted to the harsh features of high-altitude climate, including high UV radiation. Maca (Lepidium meyenii Walpers) is a member of Brassicaceae family native to the central Andes of Peru, which grows between 3500 and 4500 m of altitude, where only highland grasses and few hardy bushes can survive. Even though maca has been the focus of recent researches, mainly due to its nutraceutical properties, knowledge regarding its adaptation mechanisms to these particular natural environmental conditions is scarce. In this study, we manipulated solar UV radiation by using UV-transmitting (Control) or blocking (UV-block) filters under field conditions (4138 m above the sea level) in order to understand the impact of UV on morphological and physiological parameters of maca crops over a complete growing season. Compared to the UV-blocking filter, under control condition a significant increase of hypocotyl weight was observed during the vegetative phase together with a marked leaf turnover. Although parameters conferring photosynthetic performance were not altered by UV, carbohydrate allocation between above and underground organs was affected. Control condition did not influence the content of secondary metabolites such as glucosinolates and phenolic compounds in hypocotyls, while some differences were observed in the rosettes. These differences were mainly related to leaf turnover and the protection of new young leaves in control plants. Altogether, the data suggest that maca plants respond to strong UV radiation at high altitudes by a coordinated remobilization and relocation of metabolites between source and sink organs via a possible UV signaling pathway

Evaluate the effect of UVB radiation on the growth and physiology of Lepidium meyenii crops by biochemical, biophysical and physiological approaches

Le radiazioni UV-B possono essere estremamente dannosi sulla morfologia e fisiologia delle piante, compromettendo seriamente il loro sviluppo. In questa tesi, sono stati analizzati gli effetti delle radiazioni UV-B su una pianta peruviana, Lepidium meyenii Walp, che cresce nel distretto di Junin (Peru) a 4500 m. Questa pianta è esposta ad un'intensa radiazione UV-B, che causa delle modificazioni nella crescita e nella traslocazione e sintesi dei metaboliti secondari tra organi source e sink

UV-B Radiation as a Novel Tool to Modulate the Architecture of In Vitro Grown <i>Mentha spicata</i> (L.)

In vitro culturing can generate plants with a distorted morphology. Some distortions affect the plant’s survival after transfer to an ex vitro environment, while others can affect the aesthetic value. Therefore, exogenous hormones are often applied in in vitro cultures to modulate plant architecture. In this study, it was hypothesised that regulatory effects of UV-B radiation on plant morphology can be exploited under in vitro conditions, and that UV exposure will result in sturdier, less elongated plants with more branches and smaller leaves, mediated by changes in plant hormones. Plants were grown in tissue-culture containers and exposed to ~0.22 W m−2 UV-B for 8 days. Subsequently, plants were transferred to soil and monitored for a further 7 days. Results show that UV induced a marked change in architecture with a significant increase in axillary branches, and reductions in leaf area, plant height and root weight. These changes were associated with significant alterations in concentrations of hormones, including IAA, GA7, GA3 and iP–9–G. Changes in hormone concentrations suggest a regulatory, rather than a stress response to UV-B. Therefore, it is proposed that the application of UV in in vitro culture can be an innovative approach to manipulate plant architecture

UV Radiation Induces Specific Changes in the Carotenoid Profile of Arabidopsis thaliana

UV-B and UV-A radiation are natural components of solar radiation that can cause plant stress, as well as induce a range of acclimatory responses mediated by photoreceptors. UV-mediated accumulation of flavonoids and glucosinolates is well documented, but much less is known about UV effects on carotenoid content. Carotenoids are involved in a range of plant physiological processes, including photoprotection of the photosynthetic machinery. UV-induced changes in carotenoid profile were quantified in plants (Arabidopsis thaliana) exposed for up to ten days to supplemental UV radiation under growth chamber conditions. UV induces specific changes in carotenoid profile, including increases in antheraxanthin, neoxanthin, violaxanthin and lutein contents in leaves. The extent of induction was dependent on exposure duration. No individual UV-B (UVR8) or UV-A (Cryptochrome or Phototropin) photoreceptor was found to mediate this induction. Remarkably, UV-induced accumulation of violaxanthin could not be linked to protection of the photosynthetic machinery from UV damage, questioning the functional relevance of this UV response. Here, it is argued that plants exploit UV radiation as a proxy for other stressors. Thus, it is speculated that the function of UV-induced alterations in carotenoid profile is not UV protection, but rather protection against other environmental stressors such as high intensity visible light that will normally accompany UV radiation

Neuroactive steroid treatment modulates myelin lipid profile indiabetic peripheral neuropathy

Diabetic peripheral neuropathy causes a decrease in the levels of dihydroprogesterone and 5- androstane-3,17-diol (3-diol) in the peripheral nerves. These two neuroactive steroids exert protective effects, by mechanisms that still remain elusive. We have previously shown that the activation of Liver X Receptors improves the peripheral neuropathic phenotype in diabetic rats. This protective effect is accompanied by the restoration to control values of the levels of dihydroprogesterone and 3-diol in peripheral nerves. In addition, activation of these receptors decreases peripheral myelin abnormalities by improving the lipid desaturation capacity, which is strongly blunted by diabetes, and ultimately restores the myelin lipid profile to non-diabetic values. On this basis, we here investigate whether dihydroprogesterone or 3-diol may exert their protective effects by modulating the myelin lipid profile. We report that both neuroactive steroids act on the lipogenic gene expression profile in the sciatic nerve of diabetic rats, reducing the accumulation of myelin saturated fatty acids and promoting desaturation. These changes were associated with a reduction in myelin structural alterations. These findings provide evidence that dihydroprogesterone and 3-diol are protective agents against diabetic peripheral neuropathy by regulating the de novo lipogenesis pathway, which positively influences myelin lipid profile

LT175 is a novel PPARα/β ligand with potent insulin-sensitizing effects and reduced adipogenic properties

Background: PPARs are attractive targets of antidiabetic agents. However, PPAR ligands show side effects that hinder their clinical use. Results: LT175 improves insulin sensitivity and reduces body weight via selective gene activation in adipose tissue. Conclusion: LT175 shows an improved pharmacological profile linked to characteristic binding and differential coregulator recruitment. Significance: LT175 may be a scaffold molecule to design a safer generation of PPAR ligands

Lack of Sterol Regulatory Element Binding Factor-1cImposes Glial Fatty Acid Utilization Leading to Peripheral Neuropathy

Myelin is a membrane characterized by high lipid content to facilitate impulse propagation. Changes in myelin fatty acid (FA) composition have been associated with peripheral neuropathy, but the specific role of peripheral nerve FA synthesis in myelin formation and function is poorly understood. We have found that mice lacking sterol regulatory element-binding factor-1c (Srebf1c) have blunted peripheral nerve FA synthesis that results in development of peripheral neuropathy. Srebf1c-null mice develop Remak bundle alterations and hypermyelination of small-caliber fibers that impair nerve function. Peripheral nerves lacking Srebf1c show decreased FA synthesis and glycolytic flux, but increased FA catabolism and mitochondrial function. These metabolic alterations are the result of local accumulation of two endogenous peroxisome proliferator-activated receptor-α (Pparα) ligands, 1-palmitoyl-2-oleyl-sn-glycerol-3-phosphatidylcholine and 1-stearoyl-2-oleyl-sn-glycerol-3-phosphatidylcholine. Treatment with a Pparα antagonist rescues the neuropathy of Srebf1c-null mice. These findings reveal the importance of peripheral nerve FA synthesis to sustain myelin structure and function