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The criteria of life and aging from a molecular viewpoint. The role of protein aggregation in the process of aging

100%

Spólnik P. , Konieczny L. , Piekarska B. , Rybarska J. , Stopa B. , Zemanek G.

2011

tom Vol. 7, no. 1

23--30

Biological knowledge is expanding rapidly, delving deep into nature’s mechanisms. However, the essence of life as a molecular process still remains unclear. Organized and independently operating biological systems are commonly thought to be living. Unfortunately, these characteristics are too general and altogether insufficient to accurately delimit the boundaries of life. The problem of the relation of many primitive biological entities to the living world is still open. The properties of self-dependent biological systems clearly derive from their highly organized automatic nature. The comparative analysis of genomes of primitive biological organisms seems to be the most promising approach, which may eventually lead to the understanding of life at the molecular level and its definition. The erythrocyte appears to be of particular interest as a model of a living system that is at a boundary. Its biological origin, automatically controlled metabolism, and programmed death sharply defined in time qualify it as the living structure, even though it is completely deprived of a genetic apparatus. However, its membership among living systems seems to be well-founded. Protein aggregation is one of the common characteristics of aging. It is a consequence of abnormalities of protein structure induced by destructive actions but also by abnormalities of synthesis. Aggregation of membrane proteins probably affects the activity of certain enzymes or transport proteins, which are important as energy providers for aging erythrocytes. After the erythrocyte has passed through the vascular system a given number of times, it is not able to undergo a certain set of indispensable metabolic rearrangements. A living thing is then a form of animated nature which has the features of independence as a result of automation and possesses its own compatible with nature program of action which is time-limited beforehand.

Induction of hemolysis and eryptosis by occupational pollutant nickel chloride is mediated through calcium influx and p38 MAP kinase signaling

75%

Alfhili M. A. , Alamri H. S. , Alsughayyir J. , Basudan A. M.

International Journal of Occupational Medicine and Environmental Health

2021

tom 35

nr 1

1-11

ObjectivesNickel (Ni) is an abundant environmental hazard and an occupational pollutant. Exposure to Ni compounds is prevalent in electroplating workers and in the printing industry, among others. The toxicity of Ni manifests as dermatological, gastrointestinal, respiratory, allergic, and cardiovascular symptoms. In particular, hyperbilirubinemia and reticulocytosis have been detected in intoxicated subjects; an observation possibly implicating selective red blood cell (RBC) toxicity. Herein, the interaction of nickel chloride (NiCl2) with human RBCs and associated molecular mechanisms are described.Material and MethodsCells from healthy donors were incubated for 24 h at 37°C in the presence or absence of 0.5‒10 mM of NiCl2, and cytotoxicity was determined through hemoglobin leakage by colorimetry under different experimental conditions. Eryptotic markers were also identified by flow cytofluorometry using Annexin-V-FITC tagging for phosphatidylserine (PS) exposure, light scatter properties for cellular dimensions, Fluo4/AM labeling for intracellular calcium, and H2DCFDA staining for reactive oxygen species (ROS). Additionally, small molecule inhibitors were used to probe the signaling pathways involved.ResultsIt was found that NiCl2 at 10 mM caused profound intracellular calcium overload and significant calcium-dependent hemolysis. Also, NiCl2 reduced forward scatter and increased side scatter, Annexin-positive cells, and ROS levels. Importantly, NiCl2-induced hemolysis was significantly attenuated by the exclusion of extracellular calcium, and in the presence of p38 MAP kinase (MAPK) inhibitor SB203580.ConclusionsIt is concluded that NiCl2 induces p38 MAPK-dependent hemolysis, and stimulates the canonical features of premature eryptosis. This report presents the first description of the molecular mechanisms underlying the hemolytic and eryptotic potential of NiCl2 and, thus, may explain changes in hematological parameters observed in poisoning victims.

Participation of leukotriene C4 in the regulation of suicidal erythrocyte death

63%

Foller M. , Mahmud H. , Gu S. , Wang K. , Floride E. , Kucherenko Y. , Luik S. , Laufer S. , Lang F.

Journal of Physiology and Pharmacology

2009

tom 60

nr 3

135-143

Eryptosis, the suicidal death of erythrocytes, is characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine exposure at the erythrocyte surface. Eryptosis is triggered by increase in cytosolic Ca2+ concentration upon energy depletion. The present study explored the involvement of leukotrienes. Western blotting was employed to detect the cysteinyl-leukotriene receptor cysLT1, competitive immune assay to determine leukotriene release from erythrocytes, Fluo3 fluorescence to estimate cytosolic Ca2+ concentration, forward scatter to analyse cell volume and annexin V-binding to disclose phosphatidylserine exposure. As a result, erythrocytes expressed the leukotriene receptor CysLT1. Glucose depletion (24 hours) significantly increased the formation of the cysteinyl-leukotrienes C4/D4/E4. Leukotriene C4 (10 nM) increased Ca2+ entry, decreased forward scatter, activated caspases 3 and 8, and stimulated annexin V-binding. Glucose depletion similarly increased annexin V-binding, an effect significantly blunted in the presence of the leukotriene receptor antagonist cinalukast (1 µM) or the 5-lipoxygenase inhibitor BW B70C (1 µM). In conclusion, upon energy depletion erythrocytes form leukotrienes, which in turn activate cation channels, leading to Ca2+ entry, cell shrinkage and cell membrane scrambling. Cysteinyl-leukotrienes thus participate in the signaling of eryptosis during energy depletion.