Tomato plants use non-enzymatic antioxidant pathways to cope with moderate UV-A/B irradiation: A contribution to the use of UV-A/B in horticulture.

Plants developed receptors for solar UV-A/B radiation, which regulate a complex network of functions through the plant's life cycle. However, greenhouse grown crops, like tomato, are exposed to strongly reduced UV radiation, contrarily to their open-field counterparts. A new paradigm of modern horticulture is to supplement adequate levels of UV to greenhouse cultures, inducing a positive mild stress necessary to stimulate oxidative stress pathways and antioxidant mechanisms. Protected cultures of Solanum (cv MicroTom) were supplemented with moderate UV-A (1h and 4h) and UV-B (1min and 5min) doses during the flowering/fruiting period. After 30days, flowering/fruit ripening synchronization were enhanced, paralleled by the upregulation of blue/UV-A and UV-B receptors' genes cry1a and uvr8. UV-B caused moreover an increase in the expression of hy5, of HY5 repressor cop1 and of a repressor of COP1, uvr8. While all UV-A/B conditions increased SOD activity, increases of the generated H2O2, as well as lipid peroxidation and cell mebrane disruption, were minimal. However, the activity of antioxidant enzymes downstream from SOD (CAT, APX, GPX) was not significant. These results suggest that the major antioxidant pathways involve phenylpropanoid compounds, which also have an important role in UV screening. This hypothesis was confirmed by the increase of phenolic compounds and by the upregulation of chs and fls, coding for CHS and FLS enzymes involved in the phenylpropanoid synthesis. Overall, all doses of UV-A or UV-B were beneficial to flowering/fruiting but lower UV-A/B doses induced lower redox disorders and were more effective in the fruiting process/synchronization. Considering the benefits observed on flowering/fruiting, with minimal impacts in the vegetative part, we demonstrate that both UV-A/B could be used in protected tomato horticulture systems.

The influence of Citrate or PEG coating on silver nanoparticle toxicity to a human keratinocyte cell line.

Surface coating of silver nanoparticles may influence their toxicity, in a way yet to decipher. In this study, human keratinocytes (HaCaT cells) were exposed for 24 and 48h to well-characterized 30nm AgNPs coated either with citrate (Cit30 AgNPs) or with poly(ethylene glycol) (PEG30 AgNPs), and assessed for cell viability, reactive oxygen species (ROS), cytokine release, apoptosis and cell cycle dynamics. The results showed that Cit30 AgNPs and PEG30 AgNPs decreased cell proliferation and viability, the former being more cytotoxic. The coating molecules per se were not cytotoxic. Moreover, Ag(+) release and ROS production were similar for both AgNP types. Cit30 AgNPs clearly induced apoptotic death, while cells exposed to PEG30 AgNPs appeared to be at an earlier phase of apoptosis, supported by changes in BAX, BCL2 and CASP-3 expressions. Concerning the impact on cell cycle dynamics, both Cit30 and PEG30 AgNPs affected cell cycle regulation of HaCaT cells, but, again, citrate-coating induced more drastic effects, showing earlier downregulation of cyclin B1 gene and cellular arrest at the G2 phase. Overall, this study has shown that the surface coating of AgNPs influences their toxicity by differently regulating cell-cycle and cell death mechanisms.