scholarly journals Effect of thymoquinone administration on erythrocyte fragility in diethylnitrosamine administered rats

2017 ◽  
Vol 3 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Hawar Ahmad Muhammed Amin ◽  
Okan Arihan ◽  
Murat Cetin Ragbetli
Keyword(s):  
Erythrocyte Fragility

Interactions among Antioxidant Defenses in Liver of Rainbow Trout (Oncorhynchus mykiss) Exposed to Cadmium

1993 ◽  
Vol 50 (1) ◽  
pp. 156-162 ◽  
Author(s):  
V. P. Palace ◽  
H. S. Majewski ◽  
J. F. Klaverkamp
Keyword(s):  
Ascorbic Acid ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Blood Cells ◽  
Physiological Saline ◽  
Antioxidant Defenses ◽  
Glutathione Peroxidase Activity ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Cd Exposure ◽  
Erythrocyte Fragility

Rainbow trout (Oncorhynchus mykiss) (mean weight 180 ± 10 g) fed diets deficient in ascorbic acid, tocopherol, both, or neither were exposed to one of three cadmium concentrations (0, 2, or 4 μg Cd/L). After 181 d of exposure, liver and whole blood were sampled. Cadmium exposure was found to significantly increase the Cd content in liver, especially in fish fed a diet deficient in ascorbic acid. Hepatic stores of ascorbic acid decreased in fish exposed to Cd and in fish fed diets deficient in tocopherol and ascorbic acid. Depletion of tocopherol in liver occurred only in those fish fed a diet deficient in tocopherol and exposed to Cd. Superoxide dismutase activity in liver increased with Cd exposure and with dietary deficiencies of tocopherol and ascorbic acid, while catalase was inhibited by exposure to Cd alone. Glutathione peroxidase activity was unaffected by Cd but was lower in fish fed a diet deficient in both tocopherol and ascorbic acid. Erythrocyte fragility, measured by spontaneous hemolysis of red blood cells in physiological saline, was increased by Cd exposure and the deficiencies of dietary tocopherol and ascorbic acid.

scholarly journals Seasonal Variation in the Haematological Parameters of the Adult Mallard Duck in a Tropical Environment

2020 ◽  
pp. 30-37
Author(s):  
O. S. Olawuwo ◽  
O. I. Azeez ◽  
J. O. Oyewale
Keyword(s):  
Seasonal Variation ◽  
Osmotic Fragility ◽  
Dry Season ◽  
Tropical Environment ◽  
Haematological Parameters ◽  
Mallard Duck ◽  
Corpuscular Haemoglobin ◽  
Erythrocyte Osmotic Fragility ◽  
Mean Corpuscular Haemoglobin ◽  
Erythrocyte Fragility

Duck production is a growing poultry enterprise in Nigeria and they are mostly reared in extensive management system. However, the haematological profiles as influenced by the tropical environment have not been well documented. The objective of the present study was to examine the seasonal variation in the haematological parameters of the adult Mallard duck in the tropical environment of Nigeria; as they effects duck production adversely. The Erythrocyte, leucocyte and platelet counts, as well as the erythrocyte osmotic fragility of the domestic duck of the mallard breed during the wet and dry seasons in the hot humid tropical environment of the Experimental Animal Unit of the Department of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, Ibadan, Nigeria was investigated. The study showed that the values of the packed cell volume (PCV), mean corpuscular haemoglobin (MCH) and platelet were significantly higher in the dry season than in the wet season, but the red blood cell (RBC), haemoglobin (Hb), mean corpuscular volume (MCV), mean corpuscular haemoglobin concentration (MCHC), total and differential leucocyte values were similar in the two seasons. The erythrocyte fragility was also higher in the dry season. In conclusion the higher PCV, MCH and platelet values in the dry season might have resulted from haemoconcentration occasioned by higher evaporative heat loss, which is a common occurrence in the dry season. The higher erythrocyte fragility could have been the result of stress induced by the high ambient temperature during the dry season, or higher metabolic rate associated with lactic acid accumulation, which has been shown to increase erythrocyte osmotic fragility.

scholarly journals THE DISTRIBUTION CURVE OF ERYTHROCYTE FRAGILITY

Blood ◽  
1949 ◽  
Vol 4 (2) ◽  
pp. 172-178 ◽  
Author(s):  
J. H. BOLTON
Keyword(s):  
Distribution Curve ◽  
Simple Method ◽  
Erythrocyte Fragility ◽  
Marrow Activity

Abstract 1. A simple method of representing erythrocyte fragility as a distribution curve of actual cellular fragility is described. 2. The importance of deciding the form of a distribution before using summarizing statistics is emphasized. 3. The danger of concluding that abnormal fragility is present in the presence of increased marrow activity is pointed out. 4. Possible applications in diagnosis are suggested.

INTERACTING EFFECTS OF THYROID ACTIVITY AND DIETARY LEVEL OF VITAMIN A ON ERYTHROCYTE FRAGILITY IN THE CHICKEN

1966 ◽  
Vol 44 (2) ◽  
pp. 295-300 ◽  
Author(s):  
B. E. March ◽  
Viona Coates ◽  
Jacob Biely
Keyword(s):  
Vitamin A ◽  
Indirect Effect ◽  
Fragility Curves ◽  
Osmotic Fragility ◽  
Dietary Vitamin ◽  
Thyroid Activity ◽  
Dietary Level ◽  
Osmotic Stability ◽  
Consequent Increase ◽  
Erythrocyte Fragility

The level of dietary vitamin A is shown to affect the osmotic stability of chick erythrocytes in hypotonic solutions. In chicks fed an excess of vitamin A, induced hyperthyroidism shifts the osmotic fragility curves, which indicates that an increase in the proportion of more stable cells has occurred. When the level of dietary vitamin A is normal, induced hyperthyroidism does not appreciably alter the osmotic fragility curve. It is concluded that the increased fragility of erythrocytes from chicks fed an excess of vitamin A may be an indirect effect of suppression of thyroid activity with a consequent increase in the proportion of older, more fragile cells in the blood.

Comparison of four erythrocyte fragility tests as indicators of vitamin E status in adult dogs

1992 ◽  
Vol 107 (4) ◽  
pp. 399-410 ◽  
Author(s):  
S.R. Pillai ◽  
Janet E. Steiss ◽  
Maret G. Traber ◽  
H.J. Kayden ◽  
J.C. Wright
Keyword(s):  
Vitamin E ◽  
Erythrocyte Fragility ◽  
Vitamin E Status

scholarly journals A new erythrocyte fragility test. A simple procedure utilizing stirring.

2000 ◽  
Vol 25 (3) ◽  
pp. 161-165
Author(s):  
Yoshie MANABE ◽  
Norifumi MATSUSHITA ◽  
Yasufumi KONDOU ◽  
Kazuo HAKOI ◽  
Taiji HAYASHI ◽  
...  
Keyword(s):  
Simple Procedure ◽  
Erythrocyte Fragility

Enhanced Erythroblast Mobilization in Nix-Deficient Mice Confers Resistance to Phenylhydrazine-Induced Anemia Despite Accelerated Erythrocyte Turnover.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3659-3659
Author(s):  
Abhinav Diwan ◽  
Andrew G. Koesters ◽  
Amy M. Odley ◽  
Theodosia A. Kalfa ◽  
Gerald W. Dorn
Keyword(s):  
Bone Marrow ◽  
Steady State ◽  
Half Life ◽  
Hematopoietic Cells ◽  
Dynamic Regulation ◽  
Genetic Ablation ◽  
Deficient Mice ◽  
Erythrocyte Fragility

Abstract Steady-state and dynamic regulation of erythrocyte production occurs by altering the balance of cell-survival versus apoptosis signaling in maturing erythroblasts. Previously, the pro-apoptotic factor Nix was identified as a critical death signal in normal erythropoietic homeostasis, acting in opposition to erythroblast-survival signaling by erythropoietin and Bcl-xl. However, the role of Nix in stress-erythropoiesis is not known. Here, by comparing the consequences of erythropoietin administration, acute phenylhydrazine-induced anemia, and aging in wild-type and Nix-deficient mice, we show that complete absence of Nix, or its genetic ablation specifically in hematopoietic cells, mimics the effects of erythropoietin (Epo). Both Nix ablation and Epo treatment increase early erythroblasts in spleen and bone marrow and increase the number of circulating reticulocytes, while maintaining a pool of mature erythroblasts as an “erythropoietic reserve”. As compared with WT, Nix null mice develop polycythemia more rapidly after Epo treatment, consistent with enhanced sensitivity to erythropoietin observed in vitro. After phenylhydrazine administration, anemia in Nix-deficient mice is less severe and recovers more rapidly than in WT mice, despite lower endogenous Epo levels. Anemic stress depletes mature erythroblasts in both WT and Nix null mice, but Nix null mice with basal erythroblastosis are resistant to anemic stress. These findings show that Nix null mice have greatly expanded erythroblast reserve and respond normally to Epo- and anemia-stimulated induction of erythropoiesis. However, the hematocrits of young adult Nix null mice are not elevated, and these mice paradoxically develop anemia as they age with decreased hemoglobin content (10g/dl) and hematocrit (36%; at 80±3 weeks of age) compared to WT mice (13g/dl and 46%; 82±5 weeks of age), inspite of persistent erythoblastosis observed in the bone marrow and spleen. Nix null erythrocytes, which are macrocytic and exhibit membrane abnormalities typically seen in immature cells or with accelerated erythropoiesis, demonstrate shorter life span with a half life of 5.2±0.6 days in the peripheral circulation by in vivo biotin labeling (as compared with a half life of 11.7±0.9 days in WT), and increased osmotic fragility as compared with normal erythrocytes. This suggests that production and release of large numbers of reticulocytes in Nix null mice can decrease erythrocyte survival. To rule out a non-hematopoietic consequence of Nix ablation that contributes to or causes increased erythrocyte fragility and in vivo consumption, such as primary hypersplenism, we undertook Tie2-Cre mediated conditional Nix gene ablation. Nixfl/fl + Tie2-Cre mice (hematopoietic-cell specific Nix null) develop erythroblastosis with splenomegaly, reticulocytosis, absence of polycythemia and increased erythrocyte fragility; suggesting that erythroblastosis and accelerated erythrocyte turnover are a primary consequence of Nix ablation in hematopoietic cells. Hence, dis-inhibition of erythropoietin-mediated erythroblast survival pathways by Nix ablation enhances steady-state and stress-mediated erythropoiesis.

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