Editor's note: Please note
that just because your skin has a tendency to repair or protect against damage
caused by ultraviolet rays does not mean UV rays won’t cause any harm. In
a word, UV causes damage to the skin and people need to avoid excessive
exposure to ultraviolet rays no matter they come from the sun or not.
There is a reason for the skin to become dark brown after it’s
exposed to the sunshine.
Tanning induced
by ultraviolet rays plays a role in protecting against the development of skin
cancer, namely melanoma, the fastest growing form of cancer in the world, according
to a new study.
Early studies have linked exposure to sunshine rays to increased risk of skin cancer. But the new study suggests that when the skin is exposed to sun rays, a protein known as the
“master watchman of the genome” is triggered to guard against cancer-causing
DNA damage, which would otherwise lead to the development of skin cancer.
In addition, the study reported in the March 9 issue of the
journal Cell by researchers from Dana-Farber Cancer Institute suggested that
the protein, p53 also may play a role in people’s desire to be exposed to the
sunshine, which can reduce one’s risk of melanoma by promoting tanning.
A scientist with foodconsumer.org said that the role
of the sunshine or Ultraviolet rays may be more than just protecting against
melanoma as early studies have associated sun exposure to reduced risk of a
number of other cancers although some researchers attribute such a protective
effect to the increased level of vitamin D.
“The number
one risk factor for melanoma is an inability to tan; people who tan easily or
have dark pigmentation are far less likely to develop the disease,” says the
study’s senior author, David E. Fisher, MD, PhD, director of the Melanoma
Program at Dana-Farber and a professor in pediatrics at Children's Hospital
Boston.
“This study
suggests that p53, one of the best-known tumor-suppressor proteins in our body,
has a powerful role in protecting us against sun damage in the skin.”
Earlier last year, Fisher and his colleagues published a
study revealing that ultraviolet (UV) radiation from the sun triggers the secretion
of a hormone called α-MSH in skin cells, which attaches to nearby skin cells
called melanocytes, promoting the production of a skin-darkening pigment called
melanin.
But it has been unknown how production of α-MSH is increased
although investigators knew it is created when another protein known as opiomelanocortin
or POMC was split apart.
They also knew
sun rays increase POMC in cells. But what causes the increase in POMC remained
unclear.
The answer might be protein P53, according to Fisher and
colleagues.
A gene analysis showed that
PMOC proteins meshed well with p53, leading the researchers to speculate that
there was a possibility that when p53 docks well, POMC production increases.
Studies of human and mouse keratinocytes showed that 6-hour
exposure of the cells to UV radiation drastically increased both POMC and p53,
leading to an increase in α-MSH by a factor of 30 times compared to the cells
unexposed.
Further evidence supported the p53's role in tanning.
When p53 was inserted into keratinocytes,
POMC increased drastically.
In contrast,
mice without p53 in the cells did not experience POMC increase and the mice did
not tan.
The p53 theory may also explain the common skin condition or
the development of small dark spots, which is caused by stress or irritation of
the skin, but not ultraviolet rays and is common among elderly people.
The condition is not dangerous, but renders a
negative cosmetic effect.
“Our research
offers a potential explanation of how this condition – known as
post-inflammatory hyper-pigmentation, or age spots – occurs,” Fisher says.
“We know that
it occurs as a result of stress, and p53 is a classic ‘stress’ protein, going
into action when cells experience stress-related DNA damage. What we’ve learned
about p53 suggests that it may trigger the hyperpigmentation process.”
The researchers also said that the same process that causes
PMOC to increase production of α-MSH, which leads to the protection against
melanoma, may also causes the production of β-endorphin, which binds to the
body's opiate receptor associated with perception of feelings of pleasure.
This theory explains why people often get addicted to
exposure to sunshine.
“Even as p53
is causing skin to tan during sunlight exposure, it may also affect neuronal
circuits,” Fisher says.
“These proteins may provide an explicit link between the regulation
of tanning and of mood. It raises the question of whether p53-mediated induction
of β-endorphin is involved in sun-seeking behavior, which often increases skin
cancer risk.”
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