Rats were fed a diet deficient in pyridoxine until they developed a microcytic, hypochromic, pyridoxine-responsive anemia. Studies of red cell survival time demonstrated that there was a hemolytic factor involved in this anemia; and the more severe the anemia, the more rapid the destruction of red cells. It also demonstrated that the defect was intracorpuscular. Blood regeneration studies confirmed findings by others that erythropoiesis was impaired in pyridoxine deficiency, particularly when the accompanying anemia was severe. These studies indicate that a dual mechanism may be operating in these anemic rats.

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