Broccoli Protects Against UV Radiation

Broccoli sprout-derived extract protects against ultraviolet radiation

A team of Johns Hopkins scientists reports in this week’s issue of the Proceedings of the National Academy of Sciences that humans can be protected against the damaging effects of ultraviolet (UV) radiation — the most abundant cancer-causing agent in our environment — by topical application of an extract of broccoli sprouts.
The results in human volunteers, backed by parallel evidence obtained in mice, show that the degree of skin redness (erythema) caused by UV rays, which is an accurate index of the inflammation and cell damage caused by UV radiation, is markedly reduced in extract-treated skin.

Importantly, notes investigator Paul Talalay, M.D., professor of pharmacology, this chemical extract is not a sunscreen. Unlike sunscreens, it does not absorb UV light and prevent its entry into the skin. Rather, the extract works inside cells by boosting the production of a network of protective enzymes that defend cells against many aspects of UV damage. Consequently, the effects are long-lasting; the protection lasts for several days, even after the extract is no longer present on or in the skin.

As skin cancer incidence is rising dramatically due to the escalating exposure of aging populations to the UV rays of the sun, Talalay says that “treatment with this broccoli sprout extract might be another protective measure that alleviates the skin damage caused by UV radiation and thereby decreases our long-term risk of developing cancer.”

The protective chemical agent in the broccoli sprout extracts is sulforaphane. It was first identified by Talalay and his colleagues more than 15 years ago and has been shown to prevent tumor development in a number of animals treated with cancer-causing chemicals.

After first testing mouse models of skin cancer to confirm sulforaphane’s protective effects, Talalay and his team tested six healthy volunteers. Each one was exposed to a pulse of UV radiation on small patches of their skin (less than 1 inch in diameter) that were either treated or untreated with different doses of broccoli extract.

At the highest doses, UV-induced redness and inflammation were reduced by an average of 37 percent. The extracts were protective even when applied three days prior to UV exposure. The protection did vary considerably among the subjects, ranging from 8 percent to 78 percent, which Talalay notes may be due to genetic differences among individuals, local differences in the skin, or other factors such as dietary habits. He also points out that conventional sunscreens were essentially ineffective in these experiments.

Source: Johns Hopkins Medical Institutions

The Miracle of Cell Repair

UVA researchers explain cell response to skin-damaging UV rays.

CHARLOTTESVILLE, Va., Oct. 1, 2007 -- It’s well known that overexposure to ultraviolet rays from the sun can cause major skin problems, ranging from skin cancer to sunburns and premature wrinkles. A tan, for example, is nature’s own UV protection and an unhealthy sign that your skin is damaged.
But what is not so well known is exactly how UV rays specifically interact with your DNA and the complex organelles and proteins found inside every cell of your body.

Researchers at the University of Virginia Health System have published a new study that helps scientists around the world expand the body of knowledge on how cells protect themselves (or not) from DNA damage caused by UV rays.

Their study reveals part of a “simple switch” mechanism inside cells, triggered by UV exposure from the sun, that helps our cells survive and thrive after being exposed. This mechanism involves an unanticipated connection between several proteins in the cell, the researchers discovered.

Their findings, published in the September 7th online issue of the journal Cell, describe part of a pathway inside human cells that regulates when and how cells repair damage to their DNA when irradiated with UV rays. The research was conducted by Ian Macara, PhD, professor of microbiology at UVa’s Center for Cell Signaling, along with two MD/PhD students at UVa, Brandon Kremer and Laura Adang.

“When cells get DNA damage, normally they stop moving and stop responding to stimuli until they are repaired,” Macara explains. “We detail in this paper how a certain protein, called SOCS7, moves from the cytoplasm into the cell nucleus and essentially instructs the cell to stop dividing via a protein called NCK. The role of SOCS7 is both to stop outside signals from being relayed to the cell and to switch on the cell’s response to radiation damage. Cancer can arise if the repair work is not performed properly.”

The SOCS7 protein is known to be involved in the body’s insulin response to blood glucose levels, but Macara said he was surprised to find SOCS7 involved in the response to cellular DNA damage as well. Macara said it will now be important to study whether the absence of SOCS7 in cells would make a person more susceptible to skin cancer.

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The paper was supported by grants from the National Institutes of Health. Titled “Septins Regulate Actin Organization and Cell Cycle Arrest Through SOCS7-Mediated Nuclear Accumulation of NCK”, this research can be found online at: http://tinyurl.com/38pe2d.