What component does alpha-1 antitrypsin inhibit?

What component does alpha-1 antitrypsin inhibit?

• A. Elastin
• B. Elastase
• C. Collagen
• D. Protease

Answer: (B)

Alpha-1 antitrypsin (AAT) is a serine protease inhibitor that primarily inhibits the activity of elastase, an enzyme released by neutrophils that breaks down elastin found in connective tissues. Elastin is a protein that provides elasticity to various tissues, particularly in the lungs and blood vessels. When elastase is unchecked due to insufficient alpha-1 antitrypsin levels, it can lead to the destruction of elastin in the lung tissue, resulting in conditions such as emphysema. This makes alpha-1 antitrypsin crucial for maintaining lung integrity and function. In individuals with alpha-1 antitrypsin deficiency, there is an increased risk of pulmonary diseases because elastase can excessively degrade elastin leading to structural damage in the lungs. To summarize, alpha-1 antitrypsin's primary role is as an inhibitor of elastase, thus protecting the lungs from excessive degradation of elastin. This aligns with the role of AAT as a protective mechanism against tissue damage caused by proteolytic enzymes.

Alpha-1 antitrypsin (AAT) is a serine protease inhibitor that primarily inhibits the activity of elastase, an enzyme released by neutrophils that breaks down elastin found in connective tissues. Elastin is a protein that provides elasticity to various tissues, particularly in the lungs and blood vessels.

When elastase is unchecked due to insufficient alpha-1 antitrypsin levels, it can lead to the destruction of elastin in the lung tissue, resulting in conditions such as emphysema. This makes alpha-1 antitrypsin crucial for maintaining lung integrity and function. In individuals with alpha-1 antitrypsin deficiency, there is an increased risk of pulmonary diseases because elastase can excessively degrade elastin leading to structural damage in the lungs.

To summarize, alpha-1 antitrypsin's primary role is as an inhibitor of elastase, thus protecting the lungs from excessive degradation of elastin. This aligns with the role of AAT as a protective mechanism against tissue damage caused by proteolytic enzymes.