The plant hormone ethylene or the gaseous signalling molecule nitric oxide (NO) may enhance salt stress tolerance by maintaining ion homeostasis, first of all K+/Na+ ratio of tissues. Ethylene and NO accumulation increased in the root apices and suspension culture cells of tomato at sublethal salt stress caused by 100 mM NaCl, however, the induction phase of programmed cell death (PCD) was different at lethal salt concentration. The production of ethylene by root apices and the accumulation of NO in the cells of suspension culture did not increase during the initiation of PCD after 250 mM NaCl treatment. Moreover, cells in suspension culture accumulated higher amount of reactive oxygen species which, along with NO deficiency contributed to cell death induction. The absence of ethylene in the apical root segments and the absence of NO accumulation in the cell suspension resulted in similar ion disequilibrium, namely K+/Na+ ratio of 1.41 ± 0.1 and 1.68 ± 0.3 in intact plant tissues and suspension culture cells, respectively that was not tolerated by tomato.
The hypersensitive response (HR), a type of programmed cell death (PCD) during biotic stress is mediated by salicylic acid (SA). The aim of this work was to reveal the role of proteolysis and cysteine proteases in the execution of PCD in response of SA. Tomato plants were treated with sublethal (0.1 mM) and lethal (1 mM) SA concentrations through the root system. Treatment with 1 mM SA increased the electrolyte leakage and proteolytic activity and reduced the total protein content of roots after 6 h, while the proteolytic activity did not change in the leaves and in plants exposed to 0.1 mM SA. The expression of the papain-type cysteine protease SlCYP1, the vacuolar processing enzyme SlVPE1 and the tomato metacaspase SlMCA1 was induced within the first three hours in the leaves and after 0.5 h in the roots in the presence of 1 mM SA but the transcript levels did not increase significantly at sublethal SA. The Bax inhibitor-1 (SlBI-1), an antiapoptotic gene was over-expressed in the roots after SA treatments and it proved to be transient in the presence of sublethal SA. Protease inhibitors, SlPI2 and SlLTC were upregulated in the roots by sublethal SA but their expression remained low at 1 mM SA concentration. It is concluded that in contrast to leaves the SA-induced PCD is associated with increased proteolytic activity in the root tissues resulting from a fast up-regulation of specific cysteine proteases and down-regulation of protease inhibitors.
In this study PTEs, [potentially toxic elements (Cr, Cu, Mn, Ni, Pb, and Zn)] were investigated in the upper layer of floodplain soils that occurred as a result of accident in the area of two mine tailings in Northwestern Romania. A large amount of sediment was deposited on the soil of floodplains along the Hungarian section of River Tisza, which could represent a threat to the environment. Floodplain soil samples were collected from four locations in Hungary from an area of the river stretching to about 250 km. BCR (Bureau Communautaire de Référence) sequential extraction method was used to analyze both post-flood and present samples. Most of the analyzed elements (Cd, Cr, Cu, Ni, Pb, Zn) were found in the residual fraction, but there is a notable soluble amount in hydroxylammonium chloride extractable fraction. The results allow a comparison of the changes that have taken place over time, in addition to serving as a basis for further studies.
It is known that rarely the chronic myeloid leukaemia can occur after or with other malignancies, but its association with myelodysplastic syndrome has not been published yet. 71-year-old man with ischemic heart disease and ulcus ventriculi in his medical history was admitted to our ward due to serious pancytopenia. Evaluation of the bone marrow reviled myelodisplastic syndrome with 5q deletion and lenalidomide treatment was initiated, which led to a satisfactory improvement of his blood counts. However after eight cycles of lenalidomide treatment a significant leukocytosis raised the possibility of acute leukemic transformation, but the laboratory examinations verified the diagnosis of a chronic myeloid leukaemia with characteristic t(9;22) translocation, while the 5q-clone was not detectable with FISH. Nilotinib (300 mg BID) was started, and we stopped lenalidomide. After nine months on nilotinib deep pancytopenia occurred and the repeated bone marrow evaluation confirmed the recurrence of the 5q- MDS clone, while the CML was in major molecular response. Due to the cytopenias we reduced the nilotinib dose (150 mg BID) and restarted the previously effective lenalidomide, but in two month the 5q-clone transformed into an acute myeloid leukaemia. Lenalidomide was terminated and azacitidine+venetoclax protocol was initiated and we continued the reduced dose nilotinib also. The bone marrow evaluation after the first cycle reviled a good therapeutic response, but unfortunately the patient died in febrile neutropenia during the second cycle of the treatment. We present this case for publication due to the rare coexistence of these two diseases and their diagnostic challenges.