the form of an iron-protein complex called ferritin. In time, the biliverdin is converted to an orange pigment called bilirubin. Biliverdin and bilirubin are excreted in the bile as bile pigments (fig. 14.5). Table 14.1 summarizes the process of red blood cell destruction.

In an inherited condition called hemochromatosis, the small intestine absorbs too much iron from food. The metal accumulates in the liver, pancreas, heart, and endocrine glands and makes the skin appear bronze. A symptom is increased susceptibility to bacterial infection, because bacteria thrive in the iron-rich tissues, but the condition often goes undiagnosed for many years. Usually women do not develop symptoms until after menopause, when their menstrual periods no longer relieve the condition each month. Treatment for hemochromatosis is simple—periodically removing blood. Without treatment, premature death results from chronic liver disease or heart failure.

Hemochromatosis is common. It affects 0.3 to 0.5% of many populations, and carriers may be as prevalent as 1 in 10 to 1 in 15 individuals.

1. Squeezing through the capillaries of active tissues damages red blood cells.

1. Squeezing through the capillaries of active tissues damages red blood cells.

2. Macrophages in the liver and spleen phagocytize damaged red blood cells.

3. Hemoglobin from the red blood cells is decomposed into heme and globin.

4. Heme is decomposed into iron and biliverdin.

5. Iron is made available for reuse in the synthesis of new hemoglobin or is stored in the liver as ferritin.

6. Some biliverdin is converted into bilirubin.

7. Biliverdin and bilirubin are excreted in bile as bile pigments.

What is the typical red blood cell count for an adult male? For an adult female?

What happens to damaged red blood cells?

What are the products of hemoglobin breakdown?

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