Apoptosis Of Red Blood Cells Research Articles

Cerium oxide nanoparticles protect red blood cells from hyperthermia-induced damages.

Heat stroke and severe fever cause anemia, although the underlying mechanism remains unclear. Here, we report the use of Cerium oxide nanoparticles in protection of red blood cells against damage caused by exposure to short-term hyperthermia (42°C, 10 min). Red blood cells exposed to hyperthermia exhibited extradition senescence with higher density, smaller size and lower zeta potential relative to those under normal physiological environment (37°C, 10 min). Furthermore, hyperthermia-exposed cells exhibited significantly higher reactive oxygen species (ROS) production compared to the normal conditions. Importantly, the preconditional treatment, using Ceria nanoparticles (CNPs), ameliorated senescence and apoptosis in red blood cells damaged by hyperthermia by reducing ROS levels. Summarily, short-term hyperthermia caused a significant increase in ROS in red blood cells, and resulted in senescence and apoptosis. These may be possible mechanisms of pathological changes in red blood cells exposed to heat stroke or severe fever. Overall, these findings indicate that CNPs strongly inhibit ROS production, and effectively ameliorates hyperthermia-induced damages in red blood cells.

Aeromonas hydrophila infection activates death receptor apoptosis pathway in the red blood cells of grass carp (Ctenopharyngodon idellus)

Fish blood contains RBCs (Red blood cells) as the major cells. Unlike the absence of nucleus in mammalian RBC, fish RBC contains a nucleus. Previous researches have indicated that fish RBCs have a significant function in immune responses. However, the mechanism underlying the immune responses against bacterial infection of teleost RBCs remains enigmatic. To decipher the mechanisms, after the infection of Aeromonas hydrophila, transcriptomic profiling of grass carp RBCs was analyzed. Outcomes demonstrated that there were 2144 altogether DEGs (Differently Expressed Genes) between the A. hydrophila-infected and non-infected groups, which includes 817 up-regulated and 1327 down-regulated DEGs. Differently Expressed Genes were allocated to 45 GO terms, including 20 natural procedure terms, 14 cell related element, and 11 terms related to molecular functions. In addition, to validate our transcriptomic data, the expression levels of cytokines by Quantitative Reverse Transcription Polymerase Chain Reaction showed that they (e.g. CCL4, CCL11, CCL20, IL-4, IL-12, and IFNα) were significantly increased after A. hydrophila infection, which was identical to the expression patterns of transcriptomic data. The infection could cause the apoptosis of RBCs which was confirmed by annexin V/PI assay. To further elucidate the apoptosis pathway, the expression levels of genes by mRNA included in cellular apoptosis were monitored. The outcomes indicated that the expressions of mRNA of p53, Fas, Leucine-rich repeats, death domain-containing (LRDD) and caspase 8 were all significantly increased, respectively. Our results support the notion that A. hydrophila infection could activate Fas-related death receptor apoptosis pathway in grass carp RBCs, which will reveal another insight on the mechanisms underlying the antibacterial immunity of teleost fish RBCs.

UVA-Induced DNA Damage and Apoptosis in Red Blood Cells of the African Catfish Clarias gariepinus.

Ultraviolet-A light (UVA)-induced DNA damage and repair in red blood cells to investigate the sensitivity of African catfish to UVA exposure is reported. Fishes were irradiated with various doses of UVA light (15, 30, and 60 min day-1 for 3 days). Morphological and nuclear abnormalities in red blood cells were observed in the fish exposed to UVA compared with controls. Morphological alterations such as acanthocytes, crenated cells, swollen cells, teardrop-like cells, hemolyzed cells, and sickle cells were observed. Those alterations were increased after 24 h exposure to UVA light and decreased at 14 days after exposure. The percentage of apoptosis was higher in red blood cells exposed to higher doses of UVA light. No micronuclei were detected, but small nuclear abnormalities such as deformed and eccentric nuclei were observed in some groups. We concluded that exposure to UVA light induced DNA damage, apoptosis, and morphological alterations in red blood cells in catfish; however, catfish were found to be less sensitive to UVA light than wild-type medaka.

Apoptosis and morphological alterations after UVA irradiation in red blood cells of p53 deficient Japanese medaka (Oryzias latipes)

Morphological alterations in red blood cells were described as hematological bioindicators of UVA exposure to investigate the sensitivity to UVA in wild type Japanese medaka (Oryzias latipes) and a p53 deficient mutant. The fewer abnormal red blood cells were observed in the p53 mutant fish under the control conditions. After exposure to different doses of UVA radiation (15min, 30min and 60min/day for 3days), cellular and nuclear alterations in red blood cells were analyzed in the UVA exposed fish compared with non-exposed controls and those alterations included acanthocytes, cell membrane lysis, swollen cells, teardrop-like cell, hemolyzed cells and sickle cells. Those alterations were increased after the UVA exposure both in wild type and the p53 deficient fish. Moreover, apoptosis analyzed by acridine orange assay showed increased number of apoptosis in red blood cells at the higher UVA exposure dose. No micronuclei but nuclear abnormalities as eccentric nucleus, nuclear budding, deformed nucleus, and bilobed nucleus were observed in each group. These results suggested that UVA exposure induced both p53 dependent and independent apoptosis and morphological alterations in red blood cells but less sensitive to UVA than Wild type in medaka fish.

Peroxynitrite induces senescence and apoptosis of red blood cells through the activation of aspartyl and cysteinyl proteases

Changes in the oxidative status of erythrocytes can reduce cell lifetime, oxygen transport, and delivery capacity to peripheral tissues and have been associated with a plethora of human diseases. Among reactive oxygen and nitrogen species of importance in red blood cell (RBC) homeostasis, superoxide and nitric oxide radicals play a key role. In the present work, we evaluated subcellular effects induced by peroxynitrite, the product of the fast reaction between superoxide and nitric oxide. Peroxynitrite induced 1) oxidation of oxyhemoglobin to methemoglobin, 2) cytoskeleton rearrangement, 3) ultrastructural alterations, and 4) altered expression of band-3 and decreased expression of glycophorin A. With respect to control cells, this occurred in a significantly higher percentage of human RBC (approximately 40%). The presence of antioxidants inhibited these modifications. Furthermore, besides these senescence-associated changes, other important modifications, absent in control RBC and usually associated with apoptotic cell death, were detected in a small but significant subset of peroxynitrite-exposed RBC (approximately 7%). Active protease cathepsin E and mu-calpain increased; activation of caspase 2 and caspase 3 was detected; and phosphatidylserine externalization, an early marker of apoptosis, was observed. Conversely, inhibition of cathepsin E, mu-calpain, as well as caspase 2 and 3 by specific inhibitors resulted in a significant impairment of erythrocyte "apoptosis" Altogether, these results indicate that peroxynitrite, a milestone of redox-mediated damage in human pathology, can hijack human RBC toward senescence and apoptosis by a mechanism involving both cysteinyl and aspartyl proteases.