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Wyświetlanie 1-15 z 134
Tytuł:
Main Pro-Apoptotic Member of Bcl-2 Family Proteins – Bax
Autorzy:
Żołnierczyk, Jolanta Dominika
Kiliańska, Zofia Maria
Powiązania:
https://bibliotekanauki.pl/articles/764983.pdf
Data publikacji:
2010
Wydawca:
Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
Tematy:
apoptosis
Bcl-2 family
Bax
apoptosis mitochondrial pathway
Opis:
Programmed cell death (apoptosis) plays a vital role in the regulation of cellular homeostasis. Because of apoptosis fundamental importance, this process is highly regulated. One important set of factors involved in apoptosis regulation is the Bcl-2 family proteins. Bcl-2 family members form a complex regulatory network that controls cell survival and death in response to different physiological and pathological signals. This family includes both pro- and anti-apoptotic members, and Bax protein (Mol wt 21 kDa) is a major pro-apoptotic factor with multifunctional activity. This review summarizes new data about the main representative of Bcl-2 family – Bax, its structure and mechanism(s) by which this protein modulates apoptosis.
Źródło:
Acta Universitatis Lodziensis. Folia Biologica et Oecologica; 2010, 6; 5-32
1730-2366
2083-8484
Pojawia się w:
Acta Universitatis Lodziensis. Folia Biologica et Oecologica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Higher Apoptosis Index and Proliferation Index in Colonocytes of Patients with Ulcerative Colitis in Remission
Autorzy:
Buczyński, Jarosław
Spychalski, Michał
Ławska-Wierzchniewska, Agnieszka
Dziki, Adam
Powiązania:
https://bibliotekanauki.pl/articles/1396694.pdf
Data publikacji:
2012-06-01
Wydawca:
Index Copernicus International
Tematy:
apoptosis
proliferation
ulcerative colitis
Opis:
Ulcerative colitis (UC) is a inflammatory disease of large bowel. The amount of people suffering from UC increases from year to year. Pathogenesis of this affection is still not entirely clear. Mechanisms of proliferation and apoptosis in colonocytes in the course of the disease are defectedThe aim of the study was to assess the rate of proliferation and intensity of apoptosis in colonocytes in patients with diagnose UC.Material and methods. Colon pathological samples taken from patients with diagnosed ulceraive colitis were examined. Patients were in both clinical and endoscopic remission and were treated with mesalazin. They were patient of Department of General and Colorectal Surgery. To estimate proliferation index dye with monoclonal antibody against Ki67. To determine apoptosis level immunohistochemistry with antybody against Bax was used.Results. Average Ki-67 in the test group was 42,13%, the largest value amounted to 57% and the lowest of 33%. Average value of Bax was 1.47 and ranged between 0-3. High index of bax appear not only in the bottom of the crypt, but also at their outlet.Conclusions. In ulecerative colitis genetic and immunological disturbances occur despite treatment. Mesalazine acting only on certain routes associated with the UC holds the remission, without, however "the molecular remission". Thus, it appears that the results of our research are another proof of the necessary caution in weaning support treatment.
Źródło:
Polish Journal of Surgery; 2012, 84, 6; 271-275
0032-373X
2299-2847
Pojawia się w:
Polish Journal of Surgery
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Conventional calpains and programmed cell death
Autorzy:
Łopatniuk, Paulina
Witkowski, Jacek
Powiązania:
https://bibliotekanauki.pl/articles/1039875.pdf
Data publikacji:
2011
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
neurodegeneration
calpain
cancer
apoptosis
Opis:
The evidence on the crucial role of a family of calcium-dependent cysteine proteases called calpains in programmed cell death is rich and still growing. However, understanding of the mechanisms of their functions in apoptosis is not full yet. Calpains have been implicated in both physiological and pathological cell death control, especially in various malignancies, but also in the immune system development and function. There is also growing evidence on calpain involvement in apoptosis execution in certain pathological conditions of the central nervous system, in cardiovascular diseases, etc. Understanding of the clinical significance of calpain activation pathways, after intense studies of the influence of calpain activity on drug-induced apoptosis, seems especially important lately, as calpains have become noticed as potential therapeutic targets. To allow pharmacological targeting of these enzymes, thorough knowledge of their patterns of activation and further interactions with already known apoptotic pathways is necessary. A comprehensive summary of both well established and recently obtained information in the field is an important step that may lead to future advances in the use of calpain-targeted agents in the clinic.
Źródło:
Acta Biochimica Polonica; 2011, 58, 3; 287-296
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Blood platelets apoptosis in hemodialyzed patients
Autorzy:
Sobol, A.
Kamińska, M.
Walczyńska, M.
Stasiak, M.
Szymański, J.
Walkowiak, M.
Walkowiak, B.
Powiązania:
https://bibliotekanauki.pl/articles/284932.pdf
Data publikacji:
2009
Wydawca:
Akademia Górniczo-Hutnicza im. Stanisława Staszica w Krakowie. Polskie Towarzystwo Biominerałów
Tematy:
blood platelets
hemodialysis
apoptosis
Opis:
Blood platelet proteome of hemodialyzed uremic patients exhibits significant difference in comparison to the blood platelet proteome of healthy subjects. This alteration is manifested by the presence of high concentrations of low molecular peptides within the whole range of pI. Increased platelet apoptosis has been put forward as a possible cause of this phenomenon (1). The aim of the present research was to assess whether blood platelet populations from hemodialyzed uremic patients exhibit more binding sites for Annexin V (a marker of apoptosis) than control samples from healthy donors. Blood was obtained from uremic patients immediately before and after hemodialysis. At the same time samples from control healthy donors were also collected. Blood was anticoagulated with sodium citrate and was immediately exposed to propidium iodide, fluorescent labeled Annexin V and CD61 antibodies. The samples were incubated for 10 minutes in the dark and next the labeled samples were processed in a BectonDickinson FACScan flow cytofluorymeter. Our preliminary study was performed for 12 hemodialyzed patients, 13nondialyzed uremic patientsand 12 controls. It was found that the blood platelet population of hemodialyzed patients exhibited significantly higher level of fluorescence intensity attributed to Annexin V. Furthermore, this intensity was comparable before and after hemodialysis and was independent on patient age. The results support the hypothesis that blood platelet contact with artificial surfaces during the process of hemodialysys may be partially responsible for triggering blood platelet apoptosis.
Źródło:
Engineering of Biomaterials; 2009, 12, no. 89-91; 29-30
1429-7248
Pojawia się w:
Engineering of Biomaterials
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Overexpression of BimSs3, the novel isoform of Bim, can trigger cell apoptosis by inducing cytochrome c release from mitochondria
Autorzy:
Liu, Lingfeng
Chen, Jinzhong
Zhang, Jiayi
Ji, Chaoneng
Zhang, Xiaomeng
Gu, Shaohua
Xie, Yi
Mao, Yumin
Powiązania:
https://bibliotekanauki.pl/articles/1041049.pdf
Data publikacji:
2007
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
cytochrome c
apoptosis
BimSs3
Opis:
Bim is defined as the pro-apoptotic BH3-only protein of the Bcl-2 family, which is a critical sensor and mediator in the mitochondrial-dependent apoptosis. In a previous work, we have cloned a novel transcript of Bim (GenBank accession number: AY305716) from the fetal brain cDNA, which is widely expressed in some carcinoma tissues and normal human tissues. According to the sequence analysis and the newly-defined nomenclature system of Bim isoforms (Adachi et al., 2005, Cell Death Differ 2: 192), we term it BimSs3 according to its characteristic structure. The subcellular location analysis indicated that the fused protein GFP-BimSs3 is distributed in the whole cell, mainly to the nucleus. Overexpression of BimSs3 in HEK293 cells causes apoptosis (28.16 ± 1.55%) compared to the negative control (5.44 ± 2.63%). It also causes cytochrome c release from the mitochondrial fraction to the cytosolic fraction during apoptosis. Western blotting assay indicates the molecular mass of GFP-BimSs3 is approximately 31.0 kDa (GFP: 27 kDa). Hence the open reading frame of BimSs3 may initiate at the second ATG and encodes a 36 amino-acid peptide with BH3 domain.
Źródło:
Acta Biochimica Polonica; 2007, 54, 3; 603-610
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Inhibition of mitochondrial bioenergetics: the effects on structure of mitochondria in the cell and on apoptosis.
Autorzy:
Lyamzaev, Konstantin
Izyumov, Denis
Avetisyan, Armine
Yang, Fuyu
Pletjushkina, Olga
Chernyak, Boris
Powiązania:
https://bibliotekanauki.pl/articles/1043303.pdf
Data publikacji:
2004
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
oxidative phosphorylation
inhibitors
mitochondria
apoptosis
Opis:
The effects of specific inhibitors of respiratory chain, FoF1ATP synthase and uncouplers of oxidative phosphorylation on survival of carcinoma HeLa cells and on the structure of mitochondria in the cells were studied. The inhibitors of respiration (piericidingg, antimycin, myxothiazol), the F1-component of ATP synthase (aurovertin) and uncouplers (DNP, FCCP) did not affect viability of HeLa cells, apoptosis induced by TNF or staurosporin and the anti-apoptotic action of Bcl-2. Apoptosis was induced by combined action of respiratory inhibitors and uncouplers indicating possible pro-apoptotic action of reactive oxygen species (ROS) generated by mitochondria. Short-term incubation of HeLa cells with the mitochondrial inhibitors and 2-deoxyglucose followed by 24-48 h recovery resulted in massive apoptosis. Apoptosis correlated to transient (3-4 h) and limited (60-70%) depletion of ATP. More prolonged or more complete transient ATP depletion induced pronounced necrosis. The inhibitors of respiration and uncouplers caused fragmentation of tubular mitochondria and formation of small round bodies followed by swelling. These transitions were not accompanied with release of cytochrome c into the cytosol and were fully reversible. The combined effect of respiratory inhibitors and uncouplers developed more rapidly indicating possible involvement of ROS generated by mitochondria. More prolonged (48-72 h) incubation with this combination of inhibitors caused clustering and degradation of mitochondria.
Źródło:
Acta Biochimica Polonica; 2004, 51, 2; 553-562
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effect of aging on UVC-induced apoptosis of rat splenocytes.
Autorzy:
Radziszewska, Ewa
Piwocka, Katarzyna
Bielak-Żmijewska, Anna
Skierski, Janusz
Sikora, Ewa
Powiązania:
https://bibliotekanauki.pl/articles/1044357.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
aging
transcription factors
apoptosis
splenocytes
Opis:
UVC-induced apoptotic symptoms such as morphological changes, DNA fragmentation, Bcl-2 and Bax protein expression were examined in primary splenocyte cultures from young (3 months) and old (24 months) rats. The activities of AP-1 and CRE transcription factors in UVC-irradiated splenocytes were also assessed. At 24 h after UVC irradiation 40% of cells derived from young rats were found to be apoptotic, which was twice as much as in splenocytes from old rats. Apoptosis in cells from old rats did not give typical symptoms like a "DNA ladder" and Bcl-2 protein downregulation, in contrast to splenocytes from young rats. No AP-1 transcription factor activity was found in UVC-irradiated splenocytes from old animals and only a trace activity in splenocytes from young animals. This indicates that, UVC-induced apoptosis in rat splenocytes is practically AP-1 independent and that cells from old rats are less sensitive to UVC irradiation than splenocytes from young rats.
Źródło:
Acta Biochimica Polonica; 2000, 47, 2; 339-347
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Curcumin augments the cytostatic and anti-invasive effects of mitoxantrone on carcinosarcoma cells in vitro
Autorzy:
Luty, Marcin
Kwiecień, Edyta
Firlej, Magdalena
Łabędź-Masłowska, Anna
Paw, Milena
Madeja, Zbigniew
Czyż, Jarosław
Powiązania:
https://bibliotekanauki.pl/articles/1038754.pdf
Data publikacji:
2016
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
carcinosarcoma
mitoxantrone
curcumin
apoptosis
motility
Opis:
Numerous adverse effects limit the applicability of mitoxantrone for the treatment of drug-resistant tumors, including carcinosarcoma. Here, we estimated the additive effects of mitoxantrone and curcumin, a plant-derived biomolecule isolated from Curcuma longa, on the neoplastic and invasive potential of carcinosarcoma cells in vitro. Curcumin augmented the cytostatic, cytotoxic and anti-invasive effects of mitoxantrone on the Walker-256 cells. It also strengthened the inhibitory effects of mitoxantrone on the motility of drug-resistant Walker-256 cells that had retained viability after a long-term mitoxantrone/curcumin treatment. Thus, curcumin reduces the effective doses of mitoxantrone and augments its interference with the invasive potential of drug-resistant carcinosarcoma cells.
Źródło:
Acta Biochimica Polonica; 2016, 63, 3; 397-401
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Changes in the mitochondrial network during ectromelia virus infection of permissive L929 cells
Autorzy:
Gregorczyk, Karolina
Szulc-Dąbrowska, Lidia
Wyżewski, Zbigniew
Struzik, Justyna
Niemiałtowski, Marek
Powiązania:
https://bibliotekanauki.pl/articles/1039359.pdf
Data publikacji:
2014
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
mitochondrial network
ECTV-MOS
apoptosis
Opis:
Mitochondria are extremely important organelles in the life of a cell. Recent studies indicate that mitochondria also play a fundamental role in the cellular innate immune mechanisms against viral infections. Moreover, mitochondria are able to alter their shape continuously through fusion and fission. These tightly regulated processes are activated or inhibited under physiological or pathological (e.g. viral infection) conditions to help restore homeostasis. However, many types of viruses, such as orthopoxviruses, have developed various strategies to evade the mitochondrial-mediated antiviral innate immune responses. Moreover, orthopoxviruses exploit the mitochondria for their survival. Such viral activity has been reported during vaccinia virus (VACV) infection. Our study shows that the Moscow strain of ectromelia virus (ECTV-MOS), an orthopoxvirus, alters the mitochondrial network in permissive L929 cells. Upon infection, the branching structure of the mitochondrial network collapses and becomes disorganized followed by destruction of mitochondrial tubules during the late stage of infection. Small, discrete mitochondria co-localize with progeny virions, close to the cell membrane. Furthermore, clustering of mitochondria is observed around viral factories, particularly between the nucleus and viroplasm. Our findings suggest that ECTV-MOS modulates mitochondrial cellular distribution during later stages of the replication cycle, probably enabling viral replication and/or assembly as well as transport of progeny virions inside the cell. However, this requires further investigation.
Źródło:
Acta Biochimica Polonica; 2014, 61, 1; 171-177
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Apoptosis of peripheral blood leucocytes in rabbits infected with different strains of rabbit haemorrhagic disease virus
Autorzy:
Niedźwiedzka-Rystwej, Paulina
Hukowska-Szematowicz, Beata
Tokarz-Deptuła, Beata
Trzeciak-Ryczek, Alicja
Działo, Joanna
Deptuła, Wiesław
Powiązania:
https://bibliotekanauki.pl/articles/1039609.pdf
Data publikacji:
2013
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
granulocytes
RHDV
lymphocytes
apoptosis
RHDVa
Opis:
The pathogenicity of RHDV (rabbit haemorrhagic disease virus) is mainly associated with its affinity to blood vessels, with causing disseminated intravascular coagulations (DIC), and with the stimulation of the host immune system. Moreover, there are implications suggesting that apoptosis may be a pivotal process in understanding the basis of viral haemorrhagic disease in rabbits - a serious infectious disease causing mortality to wild and domestic rabbits. The aim of this study is to evaluate, by means of flow cytometry, the dynamics of apoptosis in peripheral blood granulocytes and lymphocytes in rabbits experimentally infected with seven different strains of RHDV and so-called antigenic variants of RHDV denominated as RHDVa, i.e.: Hungarian 24V/89, 1447V/96, 72V/2003; Austrian 01-04, 237/04, V-412 and French 05-01. The results showed that all of the RHDV and RHDVa strains cause an increase in the number of apoptotic cells throughout the infection, which might indicate the need for further analysis of the importance of this process.
Źródło:
Acta Biochimica Polonica; 2013, 60, 1; 65-69
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Direct tumor damage mechanisms of photodynamic therapy.
Autorzy:
Nowis, Dominika
Makowski, Marcin
Stokłosa, Tomasz
Legat, Magdalena
Issat, Tadeusz
Gołąb, Jakub
Powiązania:
https://bibliotekanauki.pl/articles/1041411.pdf
Data publikacji:
2005
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
photosensitizer
tumor
photodynamic therapy
apoptosis
Opis:
Photodynamic therapy (PDT) is a clinically approved and rapidly developing cancer treatment regimen. It is a minimally invasive two-stage procedure that requires administration of a photosensitizing agent followed by illumination of the tumor with visible light usually generated by laser sources. A third component of PDT is molecular oxygen which is required for the most effective antitumor effects. In the presence of the latter, light of an appropriate wavelength excites the photosensitizer thereby producing cytotoxic intermediates that damage cellular structures. PDT has been approved in many countries for the treatment of lung, esophageal, bladder, skin and head and neck cancers. The antitumor effects of this treatment result from the combination of direct tumor cell photodamage, destruction of tumor vasculature and activation of an immune response. The mechanisms of the direct photodamage of tumor cells, the signaling pathways that lead to apoptosis or survival of sublethaly damaged cells, and potential novel strategies of improving the antitumor efficacy of PDT are discussed.
Źródło:
Acta Biochimica Polonica; 2005, 52, 2; 339-352
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The DFF40/CAD endonuclease and its role in apoptosis.
Autorzy:
Widłak, Piotr
Powiązania:
https://bibliotekanauki.pl/articles/1044225.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
caspase
nuclease
DNA fragmentation
apoptosis
Opis:
The sequential generation of large-scale DNA fragments followed by internucleosomal chromatin fragmentation is a biochemical hallmark of apoptosis. One of the nucleases primarily responsible for genomic DNA fragmentation during apoptosis is called DNA Fragmentation Factor 40 (DFF40) or Caspase-activated DNase (CAD). DFF40/CAD is a magnesium-dependent endonuclease specific for double stranded DNA that generates double strand breaks with 3'-hydroxyl ends. DFF40/CAD is activated by caspase-3 that cuts the nuclease's inhibitor DFF45/ICAD. The nuclease preferentially attacks chromatin in the internucleosomal linker DNA. However, the nuclease hypersensitive sites can be detected and DFF40/CAD is potentially involved in large-scale DNA fragmentation as well. DFF40/CAD-mediated DNA fragmentation triggers chromatin condensation that is another hallmark of apoptosis.
Źródło:
Acta Biochimica Polonica; 2000, 47, 4; 1037-1044
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Cytostatic and cytotoxic effects of (E)-2'-deoxy-2'-(fluoromethylene)-cytidine on a solid tumor and a leukemia cell line.
Autorzy:
Grieb, Paweł
Koronkiewicz, Mirosława
Skierski, Janusz
Powiązania:
https://bibliotekanauki.pl/articles/1044427.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
cytotoxicity
flow cytometry
fluoromethylenedeoxycytidine
apoptosis
Opis:
(E)-2'-deoxy-2'-(fluoromethylene)-cytidine (FMdC), a deoxycytidine analog displaying a very high toxicity toward a variety of solid tumor cell lines and xenografts, is activated intracellularly by deoxycytidine kinase (dCK). We have compared cytotoxicity of FMdC towards a human promyeolocytic leukemia line HL-60 and a human colorectal carcinoma line COLO-205. Despite dCK activity being by far the highest in cells of lymphoid origin, the effects of FMdC were detectable at the lowest drug concentration only in a solid tumor cell line, and at higher concentrations they were qualitatively similar in the two tumor lines (increased cell protein content, cell cycle block and apoptosis). Apparently, low dCK activity in solid tumor cells sufficiently activates FMdC to yield cytotoxic effects, while high dCK activity in leukemia cells does not increase its cytotoxicity.
Źródło:
Acta Biochimica Polonica; 2000, 47, 1; 165-171
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Antiproliferative effect of β-escin - an in vitro study
Autorzy:
Mojžišová, Gabriela
Kello, Martin
Pilátová, Martina
Tomečková, Vladimíra
Vašková, Janka
Vaško, Ladislav
Bernátová, Silvia
Mirossay, Ladislav
Mojžiš, Ján
Powiązania:
https://bibliotekanauki.pl/articles/1038845.pdf
Data publikacji:
2016
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
escin
apoptosis
mitochondria
fluorescence fingerprint
Opis:
This study examined the antiproliferative effects of β-escin (E) in cancer cells. The study showed that E inhibited cancer cells growth in a dose-dependent manner. The flow cytometric analysis revealed an escin-induced increase in the sub-G1 DNA content, which is considered to be a marker of apoptosis. Apoptosis was also confirmed by annexin V staining and DNA fragmentation assay. These effects were associated with increased generation of reactive oxygen species (ROS), caspase-3 activation and decreased mitochondrial membrane potential (MMP). Moreover, escin decreased mitochondrial protein content and mitochondrial fluorescence intensity as well as caused depletion of glutathione (GSH). However, activity of glutathione peroxidase (GPx) and glutathione reductase (GR) was not significantly changed in escin-treated cells. In conclusion, our results demonstrated that E has apoptotic effects in human cancer cells through the mechanisms involving mitochondrial perturbation. Although the exact mechanism needs to be investigated further, it can be concluded that E may be a useful candidate agent for cancer treatment.
Źródło:
Acta Biochimica Polonica; 2016, 63, 1; 79-87
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Alteration of Cytomorphology of Peritoneal Macrophages of Albino Rat Exposed to Mercuric Compound
Autorzy:
Srikanta, Guria
Powiązania:
https://bibliotekanauki.pl/articles/1158129.pdf
Data publikacji:
2018
Wydawca:
Przedsiębiorstwo Wydawnictw Naukowych Darwin / Scientific Publishing House DARWIN
Tematy:
Apoptosis
Blebbing
Macrophage
Mercury
Rat
Opis:
Mercury is among the heavy metals that have been reported to cause devastating health problems worldwide. The present work was aimed at investigating the effects of mercury chloride on the cytomorphology of the peritoneal macrophages of rat. The current study characterizes the mechanism by which mercury, a toxic metal, induces death in rat macrophages. In mercury treated group significant numbers of peritoneal macrophages were found to be pyknotic. The cellular death was confirmed by membrane blebbing and membrane rupture. Percentages of cells showing membrane blebbing was increased significantly after treatment. The result indicated mercury induced toxicity may affect macrophage mediated immunity. So macrophage activation during heavy metal mediated reaction is an interesting area to be explored in future researches.
Źródło:
World Scientific News; 2018, 92, 2; 392-399
2392-2192
Pojawia się w:
World Scientific News
Dostawca treści:
Biblioteka Nauki
Artykuł
Wyświetlanie 1-15 z 134

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