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kupik [55]
3 years ago
11

Why does prolonged exposure to UV light from the sun or tanning beds increase the risk for getting skin cancer?

Biology
2 answers:
LenKa [72]3 years ago
8 0

Answer:

Option B, increased exposure to UV light increases the risk of a mutation occurring

Explanation:

Ultraviolet radiations (UV) coming from the sun are radioactive waves that affect the skin. They not only cause skin infection, irritation, but are are also potential source of cancer causing agent . Some times these radiations on prolonged exposure  causes genetic mutations in the skin cells which continues though ages.

Ultraviolet rays are short wavelength radiations and the shorter is the wavelength of any radiation, the greater is the potential harm caused by it.

Hence, UV rays are harmful.

Option B is correct

Lilit [14]3 years ago
7 0
B. Increased exposure to UV light increases the risk of mutation occurring.
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Photosynthesis happens in the leaves of a plant.

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I HOPE THIS HELPED YOU :)

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Which statement would most likely be found in an advertisement from a cell phone provider
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What are tissues made of?
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Cells - Tissue - Organ ...

If you want to know more - look for "Biological Organisation"
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4 years ago
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The CFTR protein is a ABC transporter protein that functions at the plasma membrane of epithelial cells. Numerous mutations in t
kap26 [50]

Answer and Explanation:

  • The normal function of the CFTR protein is to transport Cl- ions as it works as a chlorine channel regulated by AMPc and by protein kinase K (PKA). CFTR is also a regulator for other ionic channels. The CFTR protein expresses in the luminal portion of the secretory and absorptive epithelial membranes and they have an important role in the secretion of electrolytes activated by AMPc and intracellular calcium. This protein constitutes the way out of Cl-from the lumen. Apart from its secretory function, CFTR protein also regulates the function of the electrolyte by inhibiting the epithelial Na+ channel activity in absorptive epithelial cells from the colon and aerial vias, and by activating the Na+ channel in sudoriparous conducts.
  • Given that defects on the CFTR protein take to a defective regulation in the Na+ channel, the cystic fibrosis characterizes for alterations in electrolytes secretions and absorption.  There are two important physiopathological mechanisms:

1) altered Cl- secretion in submucous glands,

2) increased Na+ absorption and consequent electrolytes hyperabsorption in the superficial epithelium.  

Patients with cystic fibrosis are incapable of increasing their secretory transport. On the contrary, the increased epithelial Na+ conductance in apical membranes, the paracellular permeability to Cl- and elevated permeability to water, all together, do not allow a higher osmotic transepithelial gradient, which leads to a hyperabsorption in the patient epitheliums.  The superficial liquid layer in the aerial vias decrease, mucous glands are not released from the mucus and the mucociliary clearance is strongly altered in aerial vias.

  • The Lumacaftor (VX-809) is a drug directed to type II mutations. These mutations are present in an elevated number of patients with CF and include Phe508del that is the most frequent mutation. Ivacaftor (VX-770), is a drug directed to type III mutations in homozygote patients for Phe508del.

Given that lumacaftor helps the movement of Phe508del CFTR to the cell surface and the ivacaftor increases the opening time and the Cl- conductance through the epithelial cell, the treatment can be possible with a combination of the two drugs.

Another alternative compound is VX-661 that <u>is being studied</u>. Its efficiency is being evaluated by itself and together with ivacaftor.

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JulsSmile [24]

Answer:

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