Presence of proline in salinized nutrient solution re-enforces the role of this amino acid in osmoregulation and protects lipid membrane peroxidation in Arabidopsis thaliana

Abstract Very little is known about the effect of proline addition on the accumulation of inorganic solutes (Na ) and soluble sugars in the model plant Arabidopsis thaliana. Therefore, the aim of the present study was to assess the effect of 10 mM proline (P) supply in the culture medium on water status and solute accumulation of Arabidopsis thaliana seedlings exposed to 50 mM NaCl (S). The decrease of leaf osmotic potential was more pronounced in P+S as compared to S plants, indicating that former plants were able to accumulate more compounds involved in the osmotic adjustment process. Leaf potassium concentration was reduced by 15, 21 and 25% in P, S and P+S plants respectively, as compared to the control. When compared to S or P treatments, leaf proline and soluble sugar were more accumulated under P+S treatment. Under saline conditions, exogenous proline increased leaf Na + , Ca 2+ and Mg 2+ concentrations by 27, 281 and 252%, respectively, as compared to the control. Interestingly, proline addition mitigated significantly the deleterious effects of salt on lipid membrane peroxidation. Regarding the contribution of soluble sugars to osmotic adjustment (OA), it amounted to 6% in S or P+S, plants. For proline, its contribution to OA did not exceed 3.4% under salinity (S), whereas in (P+S) treatment, it increased to 14.7%. As a whole, the positive effect of proline exogenous application under saline conditions could be partly explained by the enhanced role of this organic compound in osmoregulation and its likely protective effect against membrane lipid peroxidation

Polimorfizmy L55M i Q192R genu paraoksonazy jako markery genetyczne nefropatii cukrzycowej u młodzieży z cukrzycą typu 1

Introduction: Paraoxonase 1 (PON1) polymorphisms have been largely involved in diabetes complications. The aim of the study is to evaluate the effects of PON1 polymorphisms (L55M and Q192R) on diabetic nephropathy (DN). Material and methods: The study involved 116 children and adolescents with type 1 diabetes (T1D) and 91 healthy subjects. Albumin excretion rate (AER) was determined by immunoturbidimetry. PON1 activity was measured by a spectrophotometric method, and genotyping of PON1 gene was assessed by multiplex PCR followed by RFLP. Results: PON1 activity was inversely correlated to AER (r = –0.245, p = 0.008). A significant decrease (p = 0.037) in PON1 activity was shown between patients with nephropathy and those without (162 [57–618] vs. 316 [37–788] IU/L, respectively). The distribution of AER was, for L55M polymorphism MM > LM > LL (p = 0.002), and for Q192R polymorphism QQ > QR > RR (p < 0.001). The opposite distribution was noted for PON 1 activity (p < 0.001). LMQQ and MMQQ haplotypes seem to increase AER (p = 0.004, p = 0.003, respectively) and to reduce PON1 activity (p = 0.011, p = 0.052, respectively) in youths with T1D. However, LLRR haplotype seems to have the opposite effect. Conclusions: This study demonstrated that PON1 polymorphisms L55M and Q192R seem to be genetic markers involved in the development of DN in T1D. (Endokrynol Pol 2017; 68 (1): 35–41)Wstęp: Polimorfizm genu paraoksonazy 1 (PON1) przyczynia się w dużym stopniu do występowania powikłań cukrzycy. Badanie przeprowadzono w celu oceny wpływu polimorfizmów genu PON1 (L55M i Q192R) na rozwój nefropatii cukrzycowej (diabetic nephropathy, DN). Materiał i metody: W badaniu uczestniczyło 116 dzieci i młodzieży z cukrzycą typu 1 (type 1 diabetes, T1D) i 91 zdrowych osób. Zmierzono wydzielanie albumin z moczem (albumin excretion rate, AER), stosując metodę immunoturbidymetryczną. Aktywność PON1 określono metodą spektrofotometrii, a do genotypowania genu PON1 zastosowano metodę Multiplex PCR, a następnie RFLP. Wyniki: Aktywność PON1 była ujemnie skorelowana z AER (r = –0,45; p = 0,008). Wykazano istotne zmniejszenie (p = 0,037) aktywności PON1 u chorych z nefropatią w porównaniu z osobami bez nefropatii (odpowiednio 162 [57–618] vs. 316 [37–788] j.m./l). Rozkład AER był następujący: w przypadku polimorfizmu L55M — MM > LM > LL (p = 0,002), a w przypadku polimorfizmu Q192R — QQ > QR > RR (p < 0,001). Rozkład aktywności PON1 był odwrotny (p < 0,001). U młodzieży z T1D haplotypy LMQQ i MMQQ wpływały na zwiększenie AER (odpowiednio p = 0,004 i p = 0,003) i zmniejszenie aktywności PON1 (odpowiednio p = 0,011 i p = 0,052). Natomiast obecność haplotypu LLRR powodowała odwrotny efekt. Wnioski: Badanie wykazało, że polimorfizmy L55M i Q192R są genetycznymi markerami uczestniczącymi w rozwój nefropatii cukrzycowej u chorych na T1D. (Endokrynol Pol 2017; 68 (1): 35–41