Glucose-6-phosphate dehydrogenase, reduced glutathione and heinz bodies in congenital haemolytic anaemia

1976 ◽  
Vol 43 (9) ◽  
pp. 272-277
Author(s):  
N. Joshi ◽  
I. N. Ramdeo ◽  
K. N. Sachdev
Keyword(s):  
Haemolytic Anaemia ◽  
Reduced Glutathione ◽  
Heinz Bodies ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Glucose 6-phosphate dehydrogenase Palermo R257M: a novel variant associated with chronic non-spherocytic haemolytic anaemia

2010 ◽  
Vol 149 (2) ◽  
pp. 296-297 ◽  
Author(s):  
Paolo Rigano ◽  
Carmelo Fabiano ◽  
Fannj Pojero ◽  
Marcello Niceta ◽  
Alice Pecoraro ◽  
...  
Keyword(s):  
Haemolytic Anaemia ◽  
Novel Variant ◽  
Glucose 6 Phosphate Dehydrogenase

Aspirin-Induced Acute Haemolytic Anaemia in Glucose-6-Phosphate Dehydrogenase-Def icient Children with Systemic Arthritis

1989 ◽  
Vol 81 (4) ◽  
pp. 208-209 ◽  
Author(s):  
Tullio Meloni ◽  
Gavino Forteleoni ◽  
Augusto Ogana ◽  
Vannina Franca
Keyword(s):  
Haemolytic Anaemia ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Systemic Arthritis

Glucose-6-phosphate dehydrogenase deficiency

2020 ◽  
pp. 5472-5479
Author(s):  
Lucio Luzzatto
Keyword(s):  
Haemolytic Anaemia ◽  
Viral Infections ◽  
Selective Advantage ◽  
Screening Tests ◽  
Lumbar Pain ◽  
Dark Urine ◽  
Direct Demonstration ◽  
Life Saving ◽  
High Doses ◽  
Glucose 6 Phosphate Dehydrogenase

Deficiency of the enzyme glucose-6-phosphate dehydrogenase (G6PD) in red blood cells is an inherited abnormality due to mutations of the G6PD gene on the X chromosome that renders the cells vulnerable to oxidative damage. The condition is widespread in many populations living in or originating from tropical and subtropical areas of the world because it confers a selective advantage against Plasmodium falciparum malaria. Clinical features—G6PD deficiency is mostly an asymptomatic trait, but it predisposes to acute haemolytic anaemia in response to exogenous triggers, including (1) ingestion of fava beans—favism; (2) certain bacterial and viral infections; and (3) some drugs—notably some antimalarials (e.g. primaquine), some antibiotics (e.g. sulphanilamide, dapsone, nitrofurantoin), and even aspirin in high doses. Other manifestations include (1) severe neonatal jaundice; and (2) chronic nonspherocytic haemolytic anaemia—the latter is only seen with rare specific genetic variants. The acute haemolytic attack typically starts with malaise, weakness, and abdominal or lumbar pain, followed by the development of jaundice and passage of dark urine (haemoglobinuria). Most episodes resolve spontaneously. Diagnosis relies on the direct demonstration of decreased activity of G6PD in red cells: a variety of screening tests are available, with (ideally) subsequent confirmation by quantitative assay. Prevention is by avoiding exposure to triggering factors of previously screened subjects. Prompt blood transfusion is indicated in severe acute haemolytic anaemia and may be life-saving.

Dexamethasone causes defective glucose-6-phosphate dehydrogenase dependent antioxidant barrier through endoglin in pregnant and nonpregnant rats

2020 ◽  
Vol 98 (10) ◽  
pp. 667-677
Author(s):  
Olufunto O. Badmus ◽  
Lawrence A. Olatunji
Keyword(s):  
Cell Adhesion Molecule ◽  
Antioxidant Defense ◽  
Tissue Injury ◽  
Reduced Glutathione ◽  
Antioxidant Defenses ◽  
Vascular Cell Adhesion ◽  
Metabolic Disturbances ◽  
Per Oral ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Cell Adhesion Molecule 1

Glucocorticoid therapy has been associated with adverse cardiometabolic effects during pregnancy. Inflammation-mediated cardiac dysfunction, an independent risk factor for morbidity and mortality, has been linked to defective glucose-6-phosphate dehydrogenase (G6PD) dependent antioxidant defenses and increased endoglin expression. We therefore sought to investigate the effects of dexamethasone (DEX) on cardiac endoglin and G6PD-dependent antioxidant defense. Twenty-four rats were randomly assigned to nonpregnant (PRE(–)), DEX-exposed nonpregnant (PRE(–) + DEX), pregnant (PRE(+)), and DEX-exposed pregnant (PRE(+) + DEX) rats, respectively (n = 6 per group). PRE(–) and PRE(+) rats received vehicle (per oral (po)), while PRE(–) + DEX and PRE(+) + DEX groups were administered DEX (0.2 mg/kg po) between gestational days 14 and 19, respectively. Results showed that DEX caused increased cardiac pro-inflammatory markers (adenosine deaminase (ADA) activity, endoglin, vascular cell adhesion molecule-1 (VCAM-1), tissue injury markers (LDH, GGT, AST, ALT, and ALP), metabolic disturbances (elevated fasting plasma glucose, free fatty acid (FFA), lactate, cardiac FFA, and lactate) and depressed G6PD-dependent antioxidant defenses (G6PD activity, reduced glutathione/oxidized glutathione ratio, and nitric oxide) in pregnant and nonpregnant rats. The present study demonstrates that DEX led to increased cardiac endoglin and VCAM-1 that is accompanied by defective G6PD-dependent antioxidant defenses but not cardiac lipid accumulation in both pregnant and nonpregnant rats.

Glutathione metabolism in heart and liver of the aging rat

1994 ◽  
Vol 72 (1-2) ◽  
pp. 58-61 ◽  
Author(s):  
M. Stio ◽  
T. Iantomasi ◽  
F. Favilli ◽  
P. Marraccini ◽  
B. Lunghi ◽  
...  
Keyword(s):  
Rat Heart ◽  
Reduced Glutathione ◽  
Age Groups ◽  
Glutathione Metabolism ◽  
Oxidized Glutathione ◽  
Glutathione S Transferase ◽  
Age Related ◽  
Glutamylcysteine Synthetase ◽  
Old Rats ◽  
Glucose 6 Phosphate Dehydrogenase

A comprehensive study on glutathione metabolism in rat heart and liver as a function of age was performed. In the heart, reduced glutathione, total glutathione, and the glutathione redox index showed a decrease during aging, while oxidized glutathione levels increased in 5-month-old rats with respect to the young animals and remained quite constant in 14- and 27-month-old rats. In the liver, the highest levels of reduced glutathione were found in the 2-month-old rats, while oxidized glutathione reached a peak at 5 months. Glutathione-associated enzymes showed age-related changes. Glutathione peroxidase, unaffected by aging in the heart, decreased in the liver of the 27-month-old rats. In the heart and the liver, the highest values of glutathione S-transferase were found at 5 months and 27 months, respectively. Glucose-6-phosphate dehydrogenase followed a similar trend in both heart and liver. Glutathione reductase also showed the same behaviour in heart and in liver, increasing in old rats with respect to the other age groups. A decrease in γ-glutamylcysteine synthetase was found in the heart and liver of 27-month-old rats in comparison with the 2-month-old ones. In conclusion, a decreased antioxidant capability has been demonstrated in both heart and liver of old rats.Key words: glutathione metabolism, age, rat heart, rat liver.

Red blood cells

2016 ◽  
Author(s):  
Shaun R. McCann
Keyword(s):  
Bone Marrow ◽  
Blood Loss ◽  
Red Blood Cells ◽  
Haemolytic Anaemia ◽  
Blood Cells ◽  
G6pd Deficiency ◽  
Paroxysmal Nocturnal Haemoglobinuria ◽  
Globin Chains ◽  
Glucose 6 Phosphate Dehydrogenase

Red blood cells, erythrocytes, are unique in that they do not contain a nucleus. This fact facilitates the study of their metabolism. Erythrocytes contain the protein pigment haemoglobin, which is in solution in the cells and consists of globin chains and iron. In this chapter, the development of the understanding of erythrocytes is linked to the blood conditions haemolytic anaemia and paroxysmal nocturnal haemoglobinuria. Premature destruction of erythrocytes, in the absence of blood loss, is termed haemolysis. If the bone marrow is unable to compensate adequately, then anaemia ensues and the condition is called haemolytic anaemia. The underlying defect is a deficiency in the activity of the enzyme glucose-6-phosphate dehydrogenase, termed G6PD deficiency.

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