proteins lecture 1
Copd - enlargement of the aveoli and destruction of the cell walls
4th most common cause of death in middle aged men in western world
Caused by - absence of the normal inhibitor of human neutrophil leukocyte elastase- a proteolytic enzyme in our bodies
One key aspect of COPD is an imbalance of enzymes in the lungs. The lungs have enzymes COPD, there's an excess of these enzymes, leading to destruction of lung tissue and loss of elasticity, making it harder to breathe
COPD can be linked to a genetic condition where the body doesn't produce enough of a protein called alpha-1 antitrypsin AAT). AAT is crucial for protecting the lungs from the destructive effects of enzymes like elastase. Without enough AAT, the lungs are more susceptible to damage, leading to COPD.
In the context of the lungs, elastase is mainly produced by certain white blood cells, such as neutrophils, which are part of the immune system. Elastase is released by these cells as a defense mechanism to help break down foreign substances like bacteria and debris during an immune response. However, when elastase is not properly regulated or controlled, it can lead to damage of lung tissue.
Elastase is a serine protein - breaks down other proteins into smaller proteins
Antitrypsin- bigger molecules - blocks the enzymes active sites preventing putting up elastin- compounds in cigarette smoke block this antitrypsin so therefore it cannot block the elastase and therefore u have higher levels of elastase and thus u have inflammation
Drugs used to treat copd block some of the enzymes active sites - essentially artificially replacing antitrypsin
Alpha-1 antitrypsin is a natural inhibitor of elastase. In individuals with a deficiency of AAT, augmentation therapy involves providing them with AAT derived from human plasma to augment their levels and inhibit excessive elastase activity
Proteins
50% of dry weight of a cell
Building blocks and molecular tools
In functional scheme of life - more important than genes
Large variety of functions