Sun Damage: Skin Cells’ Inner Workings Revealed

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The fact that too much exposure to UVA and UVB radiation from the sun harms skin cells has been known for a long time. However, scientists are still exploring the underlying mechanisms of sun damage. Skin has a number of defense mechanisms that make it hardy and resistant to many environmental factors. However, these are not a foolproof defense against radiation – especially after a lifetime of sun exposure.

Inside the Cell

A 2007 studyrep on the inner workings of skin cells has revealed what happens when UV exposure causes DNA damage. Cells have a protective mechanism that basically shuts down operations until repairs can be completed. A protein labeled SOCS7 migrates into the cell nucleus and signals it to stop dividing until the DNA is fixed. SOCS7 also blocks the cell from receiving signals from outside and activates the parts of the cell that handle repair work for radiation damage.

If the cell kept multiplying while it was damaged, each new cell would contain the abnormal DNA. So, by preventing this from happening, SOCS7 helps ensure that only healthy skin cells multiply. Unfortunately, the DNA injury caused by UVA and UVB can’t always be repaired. When there is too much sun damage and the cell’s self-protective mechanisms break down, cancer may develop.

Enzyme Activity Linked to Cancer

Scientists have found that an enzyme called protein kinase D may play a role in both normal cell regeneration and the survival of cancerous cells. This enzyme assists the body in regulating the rate of skin cell replacement. Dead skin cells slough off over time in response to changes in the immediate environment. New cells must be formed by mitosis (the division of healthy cells into equal parts that then grow to the same size as the original cell).

The body also has the ability to repair minor amounts of DNA damage in skin cells. Kinase D enzyme activity signals the body to keep skin cells alive for attempted repair instead of allowing them to die off and be replaced. Under normal circumstances, this is a beneficial effect since it helps keep too much skin from dying at one time.

However, cancer cells can also benefit from a high level of protein kinase D. That’s because the enzyme foils the body’s natural tendency to break down skin cells that have damaged or abnormal DNA. UV radiation is one of the triggers for increasing the activity of this enzyme which may allow cancer cells to proliferate instead of being destroyed. The effects are cumulative which helps explain why skin cancer becomes more common with increasing age.

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