Nickel oxide nanoparticles induce cell wall modifications, root anatomical changes, and nitrosative signaling in ecotypes of Ni hyperaccumulator Odontarrhena lesbiaca.

The industrial application and environmental release of nickel oxide NPs (NiO NPs) is increasing, but the details of their relationship with plants are largely unknown. In this work, the cellular, tissue, organ, and molecular level responses of three ecotypes of Ni hyperaccumulator Odontarrhena lesbiaca grown in the presence of high doses of NiO NP (250 mg/L and 500 mg/L) were studied. All three ecotypes showed a similar accumulation of Ni in the presence of nano Ni, and in the case of NiO NPs, the root-to-shoot Ni translocation was slighter compared to the bulk Ni. In all three ecotypes, the walls of the root cells effectively prevented internalization of NiO NPs, providing cellular defense against Ni overload. Exposure to NiO NP led to an increase in cortex thickness and the deposition of lignin-suberin and pectin in roots, serving as a tissue-level defense mechanism against excessive Ni. Exposure to NiO NP did not modify or cause a reduction in some biomass parameters of the Ampeliko and Loutra ecotypes, while it increased all parameters in Olympos. The free salt form of Ni exerted more negative effects on biomass production than the nanoform, and the observed effects of NiO NPs can be attributed to the release of Ni ions. Nitric oxide and peroxynitrite levels were modified by NiO NPs in an ecotype-dependent manner. The changes in the abundance and activity of S-nitrosoglutathione reductase protein triggered by NiO NPs suggest that the enzyme is regulated by NiO NPs at the post-translational level. The NiO NPs slightly intensified protein tyrosine nitration, and the slight differences between the ecotypes were correlated with their biomass production in the presence of NiO NPs. Overall, the Odontarrhena lesbiaca ecotypes exhibited tolerance to NiO NPs at the cellular, tissue, organ/organism and molecular levels, demonstrating various defense mechanisms and changes in the metabolism of reactive nitrogen species metabolism and nitrosative protein modification.

ESE audit on management of Adult Growth Hormone Deficiency in clinical practice.

Guidelines recommend adults with pituitary disease in whom GH therapy is contemplated, to be tested for GH deficiency (AGHD); however, clinical practice is not uniform. AIMS: 1) To record current practice of AGHD management throughout Europe and benchmark it against guidelines; 2) To evaluate educational status of healthcare professionals about AGHD. DESIGN: On-line survey in endocrine centres throughout Europe. PATIENTS AND METHODS: Endocrinologists voluntarily completed an electronic questionnaire regarding AGHD patients diagnosed or treated in 2017-2018. RESULTS: Twenty-eight centres from 17 European countries participated, including 2139 AGHD patients, 28% of childhood-onset GHD. Aetiology was most frequently non-functioning pituitary adenoma (26%), craniopharyngioma (13%) and genetic/congenital mid-line malformations (13%). Diagnosis of GHD was confirmed by a stimulation test in 52% (GHRH+arginine, 45%; insulin-tolerance, 42%, glucagon, 6%; GHRH alone and clonidine tests, 7%); in the remaining, ≥3 pituitary deficiencies and low serum IGF-I were diagnostic. Initial GH dose was lower in older patients, but only women <26 years were prescribed a higher dose than men; dose titration was based on normal serum IGF-I, tolerance and side-effects. In one country, AGHD treatment was not approved. Full public reimbursement was not available in four countries and only in childhood-onset GHD in another. AGHD awareness was low among non-endocrine professionals and healthcare administrators. Postgraduate AGHD curriculum training deserves being improved. CONCLUSION: Despite guideline recommendations, GH replacement in AGHD is still not available or reimbursed in all European countries. Knowledge among professionals and health administrators needs improvement to optimize care of adults with GHD.

Nitro-oxidative signalling induced by chemically synthetized zinc oxide nanoparticles (ZnO NPs) in Brassica species.

Due to their release into the environment, zinc oxide nanoparticles (ZnO NPs) may come in contact with plants. In elevated concentrations, ZnO NPs induce reactive oxygen species (ROS) production, but the metabolism of reactive nitrogen species (RNS) and the consequent nitro-oxidative signalling has not been examined so far. In this work, Brassica napus and Brassica juncea seedlings were treated with chemically synthetized ZnO NPs (∼8 nm, 0, 25 or 100 mg/L). At low dose (25 mg/L) ZnO NP exerted a positive effect, while at elevated concentration (100 mg/L) it was toxic to both species. Additionally, B. juncea was more tolerant to ZnO NPs than B. napus. The ZnO NPs could enter the root cells due to their small (∼8 nm) size which resulted in the release of Zn2+ and subsequently increased Zn2+ content in the plant organs. ZnO NPs disturbed superoxide radical and hydrogen peroxide homeostasis and modulated ROS metabolic enzymes (NADPH oxidase, superoxide dismutase, ascorbate peroxidase) and non-enzymatic antioxidants (ascorbate and glutathione) inducing similar changes in oxidative signalling in both Brassica species. The homeostasis of RNS (nitric oxide, peroxynitrite and S-nitrosoglutathione) was also altered by ZnO NPs; however, changes in nitrosative signalling proved to be different in the examined species. Moreover, ZnO NPs triggered changes in protein carbonylation and nitration. These results suggest that ZnO NPs induce changes in nitro-oxidative signalling which may contribute to ZnO NP toxicity. Furthermore, difference in ZnO NP tolerance of Brassica species is more likely related to nitrosative than to oxidative signalling.

Distinct redox signalling and nickel tolerance in Brassica juncea and Arabidopsis thaliana.

Despite of its essentiality, nickel (Ni) in excess is toxic for plants partly due to the overproduction of reactive oxygen species (ROS) and the consequent increase in oxidative stress signalling. However, in Ni-stressed plants little is known about the signal transduction of reactive nitrogen species (RNS) and protein tyrosine nitration as the protein-level consequence of increased RNS formation. Our experiments compared the nickel accumulation and tolerance, the redox signalling and the protein nitration in the agar-grown Arabidopsis thaliana and Brassica juncea exposed to Ni (50 µM nickel chloride). Studying GUS-tagged Arabidopsis lines (ARR5::GUS, ACS8::GUS and DR5::GUS) revealed that Ni-increased lateral root (LR) emergence, and concomitantly reduced LR initiation were accompanied by elevated levels of auxin, cytokinin, and ethylene in the LRs or in upper root parts, whereas Ni-induced primary root shortening is related to decreased auxin, and increased cytokinin and ethylene levels. These suggest the Ni-induced disturbance of hormonal balance in the root system. Results of the comparative study showed that weaker Ni tolerance of A. thaliana was coupled with a Ni-induced increase in RNS, ROS, and hydrogen sulfide levels, as well as with an increase in redox signalling and consequent increment of protein nitration. However, in relative Ni tolerant B. juncea, redox signalling (except for peroxynitrite) was not modified, and Ni-induced intensification of protein tyrosine nitration was less pronounced. Data collectively show that the better Ni tolerance of Brassica juncea may be related to the capability of preventing the induction of redox signalling and consequently to the slighter increase in protein nitration.