Antioxidant cream guards skin from UV damage - Yahoo! News: "Thu Sep 18, 2008
"(Reuters Health) - A cream containing vitamin C, vitamin E and ferulic acid protects the skin from sun damage and reduces cancer-associated mutations in skin cells, new research shows...The cream's "mechanism of action is different from sunscreens and would be expected to supplement the sun protection provided by sunscreens,"...The active cream almost completely blocked the production of thymine dimers, a type of UV-related genetic damage, as well as the induction of the tumor suppressor gene p53...While unprotected skin exposed to UV radiation produced substances called cytokines that promote inflammation and suppress immune system function, protected skin did not..."
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Showing posts with label p53. Show all posts
Showing posts with label p53. Show all posts
Thursday, September 18, 2008
Monday, May 19, 2008
Herbal Medicine (thymoquinone, an extract of nigella sativa seed oil) Kills Pancreatic Cancer Cells, Researchers Report
Traditional Herbal Medicine Kills Pancreatic Cancer Cells, Researchers Report - ScienceDaily
2008.05.19
"...thymoquinone, an extract of nigella sativa seed oil, blocked pancreatic cancer cell growth and killed the cells by enhancing the process of programmed cell death...nigella sativa helps treat a broad array of diseases, including some immune and inflammatory disorders. Previous studies also have shown anticancer activity in prostate and colon cancers, as well as antioxidant and anti-inflammatory effects...thymoquinone triggered programmed cell death in the cells, and that a number of important genes, including p53, Bax, bcl-2 and p21, were affected. The researchers found that expression of p53, a tumor suppressor gene, and Bax, a gene that promotes programmed cell death, was increased, while bcl-2, which blocks such cell death, was decreased. The p21 gene, which is involved in the regulation of different phases of the cell cycle, was substantially increased...thymoquinone caused "epigenetic" changes in pancreatic cancer cells, modifying the cells' DNA. She explains that these changes involve adding acetyl groups to the DNA structure, specifically to blocks of proteins called histones. This "acetylation" process can be important for genes to be read and translated into proteins. In this case, it could involve the genes that are key to initiating programmed cell death..."We looked at the status of the histones and found surprisingly that thymoquinone increased the acetylation process," Dr. Arafat says. "We never anticipated that."...At the same time, adding thymoquinone to pancreatic cancer cells reduced the production and activity of enzymes called histone deacetylases (HDACs), which remove the acetyl groups from the histone proteins, halting the gene transcription process. Dr. Arafat notes that HDAC inhibitors are a "hot" new class of drugs that interfere with the function of histone deacetylases, and is being studied as a treatment for cancer and neurodegenerative diseases. Finding that thymoquinone functions as an HDAC inhibitor, she says, "was very remarkable and really exciting."..."
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2008.05.19
"...thymoquinone, an extract of nigella sativa seed oil, blocked pancreatic cancer cell growth and killed the cells by enhancing the process of programmed cell death...nigella sativa helps treat a broad array of diseases, including some immune and inflammatory disorders. Previous studies also have shown anticancer activity in prostate and colon cancers, as well as antioxidant and anti-inflammatory effects...thymoquinone triggered programmed cell death in the cells, and that a number of important genes, including p53, Bax, bcl-2 and p21, were affected. The researchers found that expression of p53, a tumor suppressor gene, and Bax, a gene that promotes programmed cell death, was increased, while bcl-2, which blocks such cell death, was decreased. The p21 gene, which is involved in the regulation of different phases of the cell cycle, was substantially increased...thymoquinone caused "epigenetic" changes in pancreatic cancer cells, modifying the cells' DNA. She explains that these changes involve adding acetyl groups to the DNA structure, specifically to blocks of proteins called histones. This "acetylation" process can be important for genes to be read and translated into proteins. In this case, it could involve the genes that are key to initiating programmed cell death..."We looked at the status of the histones and found surprisingly that thymoquinone increased the acetylation process," Dr. Arafat says. "We never anticipated that."...At the same time, adding thymoquinone to pancreatic cancer cells reduced the production and activity of enzymes called histone deacetylases (HDACs), which remove the acetyl groups from the histone proteins, halting the gene transcription process. Dr. Arafat notes that HDAC inhibitors are a "hot" new class of drugs that interfere with the function of histone deacetylases, and is being studied as a treatment for cancer and neurodegenerative diseases. Finding that thymoquinone functions as an HDAC inhibitor, she says, "was very remarkable and really exciting."..."
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Friday, July 27, 2007
Cancer-fighting gene also delays ageing
Cancer-fighting gene also delays ageing: study Reuters/Scientific American 7/18/07 "...The findings could also one day lead to new drugs that prevent or fight cancer while extending healthy youth and lifespan, said Manuel Serrano...Serrano said researchers genetically engineered mice to have an extra copy of a key cancer-fighting gene called p53 and found it also played an important role in delaying ageing..."Everyone agrees that the ageing is produced by the accumulation of faulty cells," Serrano said. "In other words, p53 delays ageing for exactly the same reason that it prevents cancer."...Previous cancer studies have shown that p53 can actually cause premature ageing symptoms by killing too many cells when it goes into overdrive, but Serrano said his research strictly regulated the gene so that it turned on only when needed..."The mice lived 16 percent longer in their average lifespan."...Serrano also said that other research has shown that mice and worms that eat less have slower metabolisms and live longer. But his study offers evidence that the mice can benefit from the extra copy of the genes without having to be starved..."There are a number of chemical compounds that have been developed by the big pharmaceutical companies and these compounds are able to boost p53 in the organism," he said...."These compounds are being tested now for their possible anti-cancer activity and hopefully in the light of our study also for their possible anti-ageing activity.""
So this seems to be evidence that the p53 vs longevity framing is wrong. It isn't an either/or relationship, but rather a when/where/how much question. More p53 at the right times and at the right places appears to reduce cancer and increase lifespan. However too much p53 at the wrong time and wrong places appears to shorten lifespan. At least this is the case for mice and fruit flies.
Probably one of the safest ways to increase p53 is through exercise - that's assuming our bodies can get the balance right. Which might be assuming too much. On the diet side, which might be riskier, ellagic acid and quercetin can both increase p53. Curcumin and resveratrol also might increase p53. Milk thistle increases p53 expression. EGCG increases it. Alpha lipoic acid appears to increase it as well. The leaves of ashwagandha does. Triptolide does through an alternate p53 pathway (a plus if certain p53 pathways are inactivated such as in some prostate cancer).
And to complicate matters there's this research from 2005 on fruit flies showing that if you reduce p53 activity in neurons you increase their lifespan by as much as 58%. This seems to be an example of the importance of the location and amount of p53 protein. An interesting part to this research is the connection the scientists made to caloric restriction ""We believe that p53 is part of the caloric restriction life span extension pathway," Helfand said. "It's not the entire explanation, but it appears to play a major role." "
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So this seems to be evidence that the p53 vs longevity framing is wrong. It isn't an either/or relationship, but rather a when/where/how much question. More p53 at the right times and at the right places appears to reduce cancer and increase lifespan. However too much p53 at the wrong time and wrong places appears to shorten lifespan. At least this is the case for mice and fruit flies.
Probably one of the safest ways to increase p53 is through exercise - that's assuming our bodies can get the balance right. Which might be assuming too much. On the diet side, which might be riskier, ellagic acid and quercetin can both increase p53. Curcumin and resveratrol also might increase p53. Milk thistle increases p53 expression. EGCG increases it. Alpha lipoic acid appears to increase it as well. The leaves of ashwagandha does. Triptolide does through an alternate p53 pathway (a plus if certain p53 pathways are inactivated such as in some prostate cancer).
And to complicate matters there's this research from 2005 on fruit flies showing that if you reduce p53 activity in neurons you increase their lifespan by as much as 58%. This seems to be an example of the importance of the location and amount of p53 protein. An interesting part to this research is the connection the scientists made to caloric restriction ""We believe that p53 is part of the caloric restriction life span extension pathway," Helfand said. "It's not the entire explanation, but it appears to play a major role." "
DogVitals dog supplement - helping dogs live a younger, healthier life
Friday, April 13, 2007
How curcumin might fight cancer
Curcumin's anti-cancer mechanism proposed NutraIngredients.com 4/13/07 "The study, published in the journal Cancer Research, adds weight to the growing body of science linking consumption of the spice to decreased risk of certain cancers, like colorectal and prostate cancer...The anti-cancer effects of spices from curcumin to red chili pepper capsaicin have been consistently researched. The lowest incidence of both colorectal and prostate cancers is observed in Asia and the Far East, in particular India and China, and this has been linked to high dietary intake of compounds like turmeric...curcumin decreased the expression of a protein associated with malignant tumor formation called MDM2. The turmeric extract was also found to increase the expression of a protein that increases programmed cell death (apoptosis) of the cancer cells....Curcumin inhibited growth of PC3 xenografts and enhanced the antitumor effects of gemcitabine and radiation. In these tumors, curcumin reduced the expression of MDM2," wrote the researchers. "Down-regulation of the MDM2 oncogene by curcumin is a novel mechanism of action that may be essential for its chemopreventive and chemotherapeutic effects," ..."
In our bodies MDM2 usually acts as a brake on the p53 protein. P53 is a cancer preventing protein. The ratio between these two is crucial. Obviously we know what happens when the ratio tips in favor of MDM2, but what happens when it tips toward P53? It appears longevity is decreased. It's an interesting balance. On the one hand longevity, the other protection from mutations.
Half of all cancers have the p53 protein inactivated.
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In our bodies MDM2 usually acts as a brake on the p53 protein. P53 is a cancer preventing protein. The ratio between these two is crucial. Obviously we know what happens when the ratio tips in favor of MDM2, but what happens when it tips toward P53? It appears longevity is decreased. It's an interesting balance. On the one hand longevity, the other protection from mutations.
Half of all cancers have the p53 protein inactivated.
DogVitals dog supplement - helping dogs live a younger life
Friday, February 9, 2007
Theory on why women live longer than men
Why Do Women Tend To Live Longer Than Men? ScienceDaily 2/8/07
In short: "Because the mitochondrial genome (as well as the X chromosome) is inherited from the mother, evolutionary pressures might have selected for versions optimized for the female body. If the mitochondrial genome is better adapted to the female environment, the mitochondria in females just may work better, and longer, than those in males. "
A bit more:
"A provocative new model proposed by molecular biologist John Tower of the University of Southern California...genes known to increase longevity always affect male and female flies differently...a gene for the antioxidant enzyme Cu/Zn-superoxide dismutase (SOD) led to a longer life span in male flies, but had a less dramatic impact in females...a new way to link the regulation of life span to the biological mechanisms that trigger a fertilized egg's development into a male or female. The model suggests that sexual differentiation may exact a high biological cost -- reduced function of the cell's mitochondria, the energy-producing components of the cell...In recent years, much of Tower's research on aging has focused on extending life span by manipulating genes that produce the cell's most powerful and ancient antioxidants -- the superoxidase dismutase (SOD) enzymes. Antioxidants protect cells from the toxic effects of oxygen free radicals, which are produced when cells burn their oxygen fuel during normal metabolism. Free radicals are destructive to DNA, protein and the other complex, delicate molecules that carry out life's every function. In the so-called "oxidative stress" theory of aging, biologists surmise that the whips and scorns of time -- arthritis, dementia, cancer and all the rest -- are caused in part by a steady accumulation of such damage...The mitochondria, thousands of which populate every cell, are the body's largest producers of free radicals. The mitochondria also are unique in that they evolved from free-living bacteria and contain their own complete set of genes, or genome, which has remained distinct from the cell's genome (stored in the nucleus) over millions of years of evolution. While both parents contribute to their offspring's cellular genetic inheritance, only the female passes on the mitochondrial genome to the next generation. Why, and how, this asymmetrical inheritance happens is not clear, but Tower thinks understanding it may be key to understanding sex differences in aging...Because the mitochondrial genome (as well as the X chromosome) is inherited from the mother, evolutionary pressures might have selected for versions optimized for the female body. If the mitochondrial genome is better adapted to the female environment, the mitochondria in females just may work better, and longer, than those in males. ...Mitochondria play a key role in regulating the programmed cell death pathway, or apoptosis. In flies and humans, apoptosis works during normal embryonic development and sexual differentiation, sculpting the body by killing unwanted cells. But the cell death pathway, in which the p53 gene is a central player, also appears to malfunction more frequently over an organism's lifetime, thereby contributing to aging and aging-related diseases like Parkinson's. This might happen more often or differently in males, Tower speculates, leading to a shorter life span"
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In short: "Because the mitochondrial genome (as well as the X chromosome) is inherited from the mother, evolutionary pressures might have selected for versions optimized for the female body. If the mitochondrial genome is better adapted to the female environment, the mitochondria in females just may work better, and longer, than those in males. "
A bit more:
"A provocative new model proposed by molecular biologist John Tower of the University of Southern California...genes known to increase longevity always affect male and female flies differently...a gene for the antioxidant enzyme Cu/Zn-superoxide dismutase (SOD) led to a longer life span in male flies, but had a less dramatic impact in females...a new way to link the regulation of life span to the biological mechanisms that trigger a fertilized egg's development into a male or female. The model suggests that sexual differentiation may exact a high biological cost -- reduced function of the cell's mitochondria, the energy-producing components of the cell...In recent years, much of Tower's research on aging has focused on extending life span by manipulating genes that produce the cell's most powerful and ancient antioxidants -- the superoxidase dismutase (SOD) enzymes. Antioxidants protect cells from the toxic effects of oxygen free radicals, which are produced when cells burn their oxygen fuel during normal metabolism. Free radicals are destructive to DNA, protein and the other complex, delicate molecules that carry out life's every function. In the so-called "oxidative stress" theory of aging, biologists surmise that the whips and scorns of time -- arthritis, dementia, cancer and all the rest -- are caused in part by a steady accumulation of such damage...The mitochondria, thousands of which populate every cell, are the body's largest producers of free radicals. The mitochondria also are unique in that they evolved from free-living bacteria and contain their own complete set of genes, or genome, which has remained distinct from the cell's genome (stored in the nucleus) over millions of years of evolution. While both parents contribute to their offspring's cellular genetic inheritance, only the female passes on the mitochondrial genome to the next generation. Why, and how, this asymmetrical inheritance happens is not clear, but Tower thinks understanding it may be key to understanding sex differences in aging...Because the mitochondrial genome (as well as the X chromosome) is inherited from the mother, evolutionary pressures might have selected for versions optimized for the female body. If the mitochondrial genome is better adapted to the female environment, the mitochondria in females just may work better, and longer, than those in males. ...Mitochondria play a key role in regulating the programmed cell death pathway, or apoptosis. In flies and humans, apoptosis works during normal embryonic development and sexual differentiation, sculpting the body by killing unwanted cells. But the cell death pathway, in which the p53 gene is a central player, also appears to malfunction more frequently over an organism's lifetime, thereby contributing to aging and aging-related diseases like Parkinson's. This might happen more often or differently in males, Tower speculates, leading to a shorter life span"
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