Deficiency erythrocyte fragility

Erythrocyte fragility, hemolysis, and anemia were described as vitamin E deficiency symptoms in various animals fed diets devoid of vitamin E. Additionally, studies in experimental animals have shown that a deficiency of both selenium (a required component of glutathione peroxidases) and vitamin E causes a more rapid and severe onset of debilitating deficiency symptoms. Hypothetically, a deficiency of both vitamins E and C should also cause more severe antioxidant deficiency symptoms, but most animals make their own vitamin C, so this interaction has not been unequivocally demonstrated in humans or animals. 

In experimental animals, vitamin E deficiency results in resorption of femses and testicular atrophy. Dietary deficiency of vitamin E in humans is unknown, though patients with severe fat malabsorption, cystic fibrosis, and some forms of chronic fiver disease suffer deficiency because they are unable to absorb the vitamin or transport it, exhibiting nerve and muscle membrane damage. Premamre infants are born with inadequate reserves of the vitamin. Their erythrocyte membranes are abnormally fragile as a result of peroxidation, which leads to hemolytic anemia. 

The red blood cell has no mitochondria and is totally dependent on anaerobic glycolysis for ATP. In pyruvate kinase deficiency, the decrease in ATP causes the erythrocyte to lose its characteristic biconcave shape and signals its destruction in the spleen. In addition, decreased ion pumping by Na /K -ATPase results in loss of ion balance and causes osmotic fragility, leading to swelling and lysis. 

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