The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 17 No. 7 • August 2014


Reduced Systolic Blood Pressure (BP) With Tomato Extract Supplementation, Especially for Those with Baseline Systolic BP > 120 mm Hg

A recent meta-analysis that examined the effect of tomato extract supplementation on blood pressure included 241 subjects in six studies. One limit of the meta-analysis was that, although the amount of lycopene that was contained in the supplement ingested by subjects was known, the authors could not ascribe the results only to lycopene, since tomato extract contains many other bioactive components than just lycopene. The results, therefore, can be ascribed to tomato extract, but are not all necessarily due to lycopene.

The researchers reported that the tomato extract supplementation showed a significant reduction of systolic blood pressure, with subgroup analysis finding that a higher dosage of lycopene (>12 mg/day) derived from the supplement lowered systolic blood pressure more significantly, especially for participants whose baseline systolic blood pressure was greater than 120 mm Hg, such as Asians.

Midlife Blood Pressure Is a Significant Predictor of Reduced Cognitive Function in Later Life

An earlier paper2 reported that, among 3735 Japanese-American subjects (surviving cohort members of the prospective Honolulu Heart Program that began in 1965 – 68) living in Hawaii with an average age of 78 years (at the time of their examination for this study), there was a progressive increase in the risk of intermediate and poor cognitive function with increasing level of midlife systolic blood pressure. For every 10 mm. Hg increase in systolic blood pressure, the authors calculated an increase of 7% (95% confidence interval, 3% to 11%) in the risk for intermediate cognitive function and an increase of 9% (95% confidence interval, 3% to 16%) in the risk for poor cognitive function. The researchers reported finding no association between later cognitive function and midlife diastolic blood pressure.

The results suggest that a relatively small reduction in systolic blood pressure in middle age can provide physiologically important protection against age-associated cognitive decline.


  1. Li and Xu. Lycopene supplement and blood pressure: an updated meta-analysis of intervention trials. Nutrients. 5:3696-712 (2013).
  2. Launer, Masaki, Petrovitch, et al. The association between midlife blood pressure levels and late-life cognitive function. JAMA. 274(23):1846-51 (1995).


The Tomato Carotenoid LYCOPENE is a Powerful Scavenger of Hypochlorous Acid (HOCl)

Protects Against Inflammation

Considerable evidence supports the involvement of the enzyme myeloperoxidase (MPO) in inflammatory processes. Indeed, a very recent paperA notes that “[t]he serum levels of MPO and its by-products have potential as predictors of outcome in patients with severe inflammation.” For example, in atherosclerosis, the enzyme promotes the oxidation of LDL1—and oxidized LDL causes macrophages to turn into foam cells in atherosclerotic plaques. MPO has also been reported to cause extensive damage to double stranded DNA, and to attack the double bonds of unsaturated fatty acids and cholesterol (where it has been reported to function as a major enzymatic catalyst for initiation of lipid peroxidation at sites of inflammation).2 Hypochlorous acid (HOCl)—released by MPO—can react with superoxide to generate highly toxic hydroxyl radicals.3

MPO Accelerates the Aging of Oocytes (Mammalian Egg Cells)

Interestingly, MPO has been shown to play an important role in accelerating the aging of mouse oocytes through a mechanism that appears to involve oocyte fragmentation and degradation.6 (Paper #6 was an earlier one published by the group that published paper #3.) This could be of particular importance in the case of women wanting to conceive at a relatively late age because of the increased potential for birth defects in offspring derived from older, more-likely-to-be-damaged oocytes. The researchers6 explain: “[a]ging of the unfertilized oocyte inevitably occurs following ovulation, limiting its fertilizable life span.” They studied the effects of major reactive oxygen species (superoxide, hydrogen peroxide, and hypochlorous acid) on the aging of young and of relatively old mouse oocytes. They report that their “results clearly demonstrate that HOCl [hypochlorous acid] produced by mammalian peroxidases [including myeloperoxidase] is a much more powerful oxidant in accelerating oocyte aging than either [superoxide] or H2O2 [hydrogen peroxide] and may easily be formed internally in oocytes or provided by the neighboring follicular cells through the reaction of MPO with H2O2 in the presence of chloride ions. Indeed, young oocytes exposed to lower concentrations (1 – 10uM) accelerate aging phenomena, while higher concentrations (0.1 – 1mM) caused lysis of the cell membrane and death of the oocyte. In contrast, the older oocytes underwent lysis even on exposure to 1 μM HOCl.”6

MPO and Stroke

MPO is also widely distributed in ischemic tissues, as occurs in stroke or heart attack, where it was shown to correlate positively with infarct size (the volume of cells killed in a stroke).4

MPO and Neurodegenerative Diseases

A recent hypothesis5 proposed a model in which the interaction of microglia (immune cells in the brain) and MPO may be important in the generation of inflammatory cytokines as seen in neurodegenerative diseases.

Lycopene Identified as Potential Scavenger of HOCl (an MPO end product)

Multiple Molecules of HOCl May Be Consumed Per Molecule of Lycopene

A recent paper reviewed extensive evidence and results of experiments performed by the authors supporting a role for lycopene to act as a potent scavenger of HOCl.3 The researchers found that “[t]he degree of degradation of lycopene (as assessed by the number and chain lengths of the different oxidative metabolites of lycopene) depends mainly on the ratio between HOCl to lycopene, suggesting that multiple molecules of HOCl are consumed per molecule of lycopene.” This points to a superior protective effect of lycopene in comparison to other agents reportedly able to protect against MPO and its end product HOCl.3 In its interaction with HOCl, lycopene can be attacked at its many double bonds, resulting in degradation into a variety of breakdown products, of which a number have been identified to have biological activity.3

The authors’ experiments show that “lycopene can function as a potent scavenger of HOCl at a wide range of concentrations that span various pathophysiological and supplemental ranges.”

The researchers interpreted the disappearance of the red lycopene color as an indication of the oxidation of lycopene in interactions with HOCl. “The oxidation of lycopene by a slight excess of HOCl was accompanied by a marked change from red color to colorless.”

As the authors explain, “[i]ncreased levels of HOCl, a potent oxidant, are typically observed in the plasma and tissues of individuals with inflammatory diseases … a functional deficiency of taurine, a potent HOCl scavenger, is a defining feature of diabetes, obesity, depression, hypertension, gout, kidney failure, and autism, among other conditions.” The need for additional protection against HOCl is indicated. The authors conclude: “[i]n summary, inhibition of MPO or removing its downstream final product, HOCl, is an attractive target for preventing HOCl-mediated tissue injury and progression of inflammatory diseases. In this study we … show for the first time that lycopene may serve as a potent scavenger of HOCl. The interplay between lycopene and HOCl may have a broad implication in the function of inflammatory biological systems throughout the body.” The authors propose that lycopene “could represent an interventional approach to minimize the deleterious effects associated with inflammation.”

We take 20 mg (Sandy) or 40 mg (Durk) of lycopene a day as a dietary supplement.


A. Patterson, Fraser, Capretta, et al. Carbon monoxide-releasing molecule 3 inhibits myeloperoxidase (MPO) and protects against MPO-induced vascular endothelial cell activation/dysfunction. Free Radic Biol Med. 70:167-73 (2014).
1. Van Antwerpen, Boudjeltia, Babar, et al. Thiol-containing molecules interact with the myeloperoxidase/H2O2/chloride system to inhibit LDL oxidation. Biochem Biophys Res Commun. 337:82-8 (2005).
2. Zhang, Brennan, Shen, et al. Myeloperoxidase functions as a major enzymatic catalyst for initiation of lipid peroxidation at sites of inflammation. J Biol Chem. 277(48):46116-22 (2002).
3. Pennathur, Maitra, Byun, et al. Potent antioxidative activity of lycopene: a potential role in scavenging hypochlorous acid. Free Radic Biol Med. 49(2):205-13 (2010).
4. Breckwoldt, Chen, Stangenberg, et al. Tracking the inflammatory response in stroke in vivo by sensing the enzyme myeloperoxidase. Proc Natl Acad Sci USA. 105(47):18584-9 (2008).
5. Lefkowitz and Lefkowitz. Microglia and myeloperoxidase: a deadly partnership in neurodegenerative diseases. Free Radic Biol Med. 45:726-31 (2008).
6. Goud, Goud, Diamond, et al. Reactive oxygen species and oocyte aging: role of superoxide, hydrogen peroxide, and hypochlorous acid. Free Radic Biol Med. 44:1295-304 (2008).


Apo-10’-Lycopenoic Acid, a Lycopene Metabolite, Increases Sirtuin 1 (SIRT1) mRNA and Protein Levels and Decreases Liver Fat Accumulation in Mice

Here we describe recent research on a lycopene metabolite (one of the “lycopenoids”), apo-10’-lycopenoic acid.1 There are a lot of metabolites, but only a limited amount of research has been done in this area so far. Like so many other nutrients, including vitamin E,A metabolites may play a far larger role in the biological effects of these substances than has been previously realized. Conversion of the parent molecules to metabolites is likely to play an important role in determining how long the parent compounds can be detected in the bloodstream and their peak concentrations.

In one paper,1B researchers noted that “[a]n indication of how essential these secondary metabolites are to plants’ survival can be seen in the energy invested in their synthesis, which is usually far in excess of that required to synthesize primary metabolites.”

Take apo-10’-lycopenoic acid, for example. The recent discovery of carotene 9,10-oxygenase, a mammalian enzyme that catalyzes the cleavage of lycopene (and other carotenoids) into metabolites has opened the door to a larger world of hitherto unknown effects of lycopene. “A series of apo-lycopenals, including apo-10’-lycopenal, has recently been identified in human plasma.”1 The researchers1 decided that there might be something important going on here and have followed up on it. The work was supported by grants from the NIH, the USDA, and from Kyung Hee University in Korea.

The researchers first calculated a dose of the apo-10’-lycopenoic acid (synthesized at BASF, it had a purity of >99%) based on a number of factors to be approximately equivalent to 14.4 mg lycopene/day in a 60 kg. adult male human and, therefore, the authors concluded, to be “physiologically relevant.” The apo-10’-lycopenoic acid was used to treat ob/ob mice, a strain susceptible to the development of obesity and fatty liver on a high fat diet. The authors1 cited two studies (one of which their group published), that had found lycopene to reduce these adverse effects in rodents on a high fat diet. They wondered whether apo-10’-lycopenal was wholly or partially responsible for that effect.

The results showed, first, that apo-10’-lycopenal accumulated in the liver and decreased the fatty liver seen in the untreated controls on the high fat diet. Previous work cited in the paper1 reported that suppression of or knockout of SIRT1 resulted in the accumulation of fat in mouse livers in mice on a high fat diet as a result of changes in lipid metabolism. In this study,1 the authors report that not only did ALA decrease fat accumulation in the liver but the liver expression of SIRT1 was “greatly induced by ALA [apo-10’-lycopenoic acid] supplementation.”

SIRT1 May Be a Longevity Gene

The increased expression of SIRT1 with apo-10’-lycopenal supplementation is of interest beyond the prevention of fatty liver because SIRT1 is a gene that has been extensively studied and found to have life-extending effects in animal models of aging.2–4 A human study5 reported that a single nucleotide polymorphism (SNP) of the SIRT1 gene was associated with better cognitive functioning.


A. Jiang, Yin, Lill, et al. Long-chain carboxychromanols, metabolites of vitamin E, are potent inhibitors of cyclooxygenases. Proc Natl Acad Sci USA. 105(51):20464-9 (2008).
1. Chung, Koo, Lian, et al. Apo-10’-Lycopenoic acid, a lycopene metabolite, increases sirtuin 1 mRNA and protein levels and decreases hepatic fat accumulation in ob/ob mice. J Nutr. 142:405-10 (2012).
1B. Kennedy and Wightman. Herbal extracts and phytochemicals: plant secondary metabolites and the enhancement of human brain function. Adv Nutr. 2:32-50 (2011).
2. Milne, Lambert, Schenk, et al. Small molecule activators of SIRT1 as therapeutics for the treatment of type 2 diabetes. Nature. 450(7170):712-6 (2007).
3. Morselli, Maiuri, Markaki, et al. The life span-prolonging effect of sirtuin-1 is mediated by autophagy. Autophagy. 6(2);186-8 (Jan, 2010).
4. Smith, Kenney, Gagne, et al. Small molecule activators of SIRT1 replicate signaling pathways triggered by calorie restriction in vivo. BMC Syst Biol. 3:31 (March 2009) doi:10.1186/1752-0509-3-31.
5. Kuningas, Putters, Westendorp, et al. SIRT1 gene, age-related diseases, and mortality: the Leiden 85-Plus Study. J Gerontol A Biol Sci Med Sci. 62(9):960-5 (2007).


Mechanisms of Cell Growth Inhibition That May Be Involved in Lycopene’s Anticancer Effects

A number of mechanisms through which lycopene and tomato products providing lycopene might reduce the risk of developing various types of cancer include (as found in in vitro and some in vivo animal models) were reviewed in a recent paper:1 “upregulation of connexin 43 and consequent enhancement of gap junction communication; modulation of growth factors and growth factor receptors, including insulin-like growth factor-1 and platelet-derived growth factor; immunoenhancement and decrease in inflammation; modulation of cyclo-oxygenase pathways and xenobiotic metabolism and gene methylation.” A year later, however, another paper found that lycopene and apo-10’-lycopenal did not alter DNA methylation of the gene for GSTP1 (a selenoprotein) in cancer cell lines as reported in the paper cited in reference #1.2

Figure 1.
(click on thumbnail for full sized image)

The researchers1 sought to further investigate the inhibitory effect of lycopene on the synthesis of cholesterol, which is increased in many types of cancer cells. This inhibitory effect is produced by lycopene’s interference in the Mevanolate Pathway by inhibition of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. (See Fig. 1.) HMG-CoA reductase catalyzes the synthesis of cholesterol production. (Statins work, in a major—but not the only—way by inhibiting HMG-CoA reductase.) The scientists treated cancer cell lines with lycopene in which the oncogene ras was activated (including LNCaP prostatic carcinoma and colon carcinoma HT-29) as well as squamous carcinoma BEN cells and other cell lines in which ras was not activated.

In the prostatic LNCaP carcinoma cells, total cholesterol was progressively decreased by adding increasing concentrations of lycopene (2.5 – 10 μM) to the culture media. At concentrations below 2.5 μM, lycopene had no effect in reducing cholesterol levels or inhibiting HMG-CoA reductase expression. Interestingly, lycopene reduced Ras activity (as indicated by markedly decreased translocation from the cytosol to cell membranes). At concentrations above 2.5 μM, lycopene inhibited cancer cell growth, by decreasing cell proliferation and by increasing apoptosis (programmed cell death).

The researchers also tested the effect of mevalonate on lycopene’s ability to inhibit cancer cell growth by adding mevalonate to the cell culture medium. Mevalonate is a fatty acid derivative that results from the conversion of HMG-CoA into cholesterol via the Mevalonate Pathway. With the addition of 100 μM mevalonate to the culture medium, even 10 μM of lycopene was ineffective in inhibiting cancer cell growth. This strongly suggests that the effect of lycopene on the mevalonate pathway (via inhibition of HMG-CoA reductase) was responsible for the reduced cancer cell growth in these lines of cancer cells.

Why Do Data for Lycopene Treatment of Cancer Show Inconsistent Results?

Despite strong support for important anti-cancer effects of lycopene, the totality of the evidence for in vitro and in vivo studies with lycopene treatment is not consistent though, overall, supporting anticancer activity. There are several reasons: There is not just one mechanism causing cancer. Cancer is a complex FAMILY of diseases where many pathways are dysfunctional, where each cancer differs from another (in fact, the cancer cells change from one stage of growth to another and what therapy works at one stage may not work at another). Hence, it is unrealistic to expect any single agent to be effective for all cancers at all times in all individuals. That is one reason cancer still remains a challenging disease to treat and why it is also challenging to dissect the results of clinical studies to determine what caused beneficial effects when they are observed, as well as determining why beneficial effects of treatment often do not persist, allowing cancer cells to become resistant and cancers to recur.3 (And be sure to keep in mind that the cancer that recurs is not quite the same cancer that you had in the first place …)

As the authors3 pointed out, “[w]e now know that cellular functions are regulated by a network of effector pathways. These pathways interact with each other and maintain cellular stability, but also trigger proliferation, differentiation, migration, and survival.” “The acquired resistance of cancer cells has to be approached from a signaling network perspective and take into account the insights into the regulatory mechanisms which establish interconnections and adaptations between effector pathways.”

A key insight from the study of the regulatory networks of cancer cells is that a single agent is generally inadequate to restore a cancer cell to normality or to kill it without also doing irreparable damage to a large number of normal cells. (As an extreme example, you could certainly destroy every cancer cell in your body by a high enough dose of whole body irradiation, but guess what? It wouldn’t do you any good because you’d also have killed every normal cell in your body.) You need to simultaneously target as many known cancer-supporting pathways as you can. That is one reason why it is important to identify particular mechanisms by which a substance with substantial anticancer properties such as lycopene can block a cancer-inducing pathway.

The breakthrough in treating AIDS came about when it was realized that if you treat somebody infected with HIV with a single drug they might respond for a period of time but would eventually stop responding. You might even get a second remission using a second rank drug—but people died because the HIV virus was very good at mutating and, hence, adapting, to treatment with a single drug. Nowadays they use a few to several different drugs to hit the virus at different targets. A person infected with HIV can typically live for 20 years or more. That’s what happens when you go from an acute disease that is likely to kill you within a few years to one that is a chronic disease that probably won’t kill you at all because you will live long enough to die from something else.

We suggest including lycopene in your cancer prevention kit. You don’t need a magic (and nonexistent) silver bullet if you have enough bullets of different types. As a BONUS, you get the lycopene metabolites at NO EXTRA CHARGE!!

Lycopene Metabolites May Have Anti-Cancer Activity

A group that has done quite a bit of work on lycopene metabolites reported a recent paper of theirs4 in which they found that apo-10’-lycopenal and apo-12’-lycopenal treatment reduced the proliferation of DU145 prostate cancer cells in a dose-dependent manner in part by affecting the cell cycle. A study5 by a different group found apo-10’-lycopenoic acid reduced the proliferation of a human bronchial epithelial cell line as well as tumor promotion of an in vivo lung tumor mouse model by inducing Nrf2-mediated induction of protective phase II detoxifying/antioxidant enzymes. In the latter paper, the researchers found ALA to increase expression of enzymes that included heme oxygenase-1, glutathione-S-transferases, NAD(P)H:quinone oxidoreductase 1, and glutamate-cysteine ligases in the bronchial (BEAS-2B) cells. Moreover, apo-10’-lycopenoic acid treatment was reported to increase total intracellular glutathione levels as well as to reduce reactive oxygen species generation and hydrogen peroxide-mediated cell damage.

We wondered whether the stock solutions of lycopenoids that were prepared in tetrahydrofuran that contained 0.025% BHT (butylated hydroxytoluene) were affected in the experiments reported in paper #5 by the included BHT, which is a powerful antioxidant (probably added to prevent autooxidation). That appears not to be a problem as it was reported in a later paper by a different group6 that also used tetrahydrofuran containing 0.025% BHT that the vehicles had no effect on the parameters measured in that study, which examined the effect of oxidized lycopenoids in the activation of phase II enzymes.

Interestingly, the last paper6 reported that the apo­carotenals (oxidized derivatives of lycopene) “inhibited breast and prostate cancer cell growth with a similar order of potency to the activation of EpRE/ARE [electrophile/antioxidant response element].” The researchers suggested that this “may provide a mechanistic explanation for the cancer preventive effect of carotenoids.” EpRE/ARE regulates a system of protective antioxidant defenses including phase II detoxifying enzymes, “a major cellular strategy for reducing the risk of cancer, inflammation, and other chronic degenerative diseases.”6 In that same paper, the researchers mention that “lycopene is more active than beta carotene in stimulating the EkpRE/ARE activity and thus may be more effective in cancer prevention.” [Emphasis added.]

A Message to Those Who Have Read This Far

We include these detailed descriptions of how scientists follow the pathways from starting material (lycopene) to metabolites (lycopenoids) and the intercommunication with other pathways along the way to show how complex it is to unravel something as seemingly “simple” as lycopene, a tomato carotenoid that makes tomatoes red, and to get a grasp on why the tomato plant bothers to make it in the first place. A wondrous story and a true inspiration to those with a love for solving/understanding the many mysteries of life.


  1. Palozza et al. Lycopene induces cell growth inhibition by altering mevalonate pathway and Ras signaling in cancer cell lines. Carcinogenesis. 31(10):1813-21 (2010).
  2. Liu and Erdman. Lycopene and apo-10’-lycopenal do not alter DNA methylation of GSTP1 in LNCaP cells. Biochem Biophys Res Commun. 412:479-82 (2011).
  3. von Manstein, Yang, Richter, et al. Resistance of cancer cells to targeted therapies through the activation of compensating signaling loops. Curr Sig Transduction Therapy. 8:193-202 (2013).
  4. Ford, Elsen, Zunga, Lindshield, Erdman. Lycopene and apo-12’-lycopenal reduce cell proliferation and alter cell cycle progression in human prostate cancer cells. NUTRI CANCER. 63:256-63 (2011).
  5. Lian and Wang. Enzymatic metabolites of lycopene induce Nrf2-mediated expression of phase II detoxifying/antioxidant enzymes in human bronchial epithelial cells. Int J Cancer. 123(6):1262-8 (2008).
  6. Linnewiel, Ernst, Caris-Veyrat, et al. Structure-activity relationship of carotenoid derivatives in activation of the electrophile/antioxidant response element transcription system. Free Radic Biol Med. 47:659-67 (2009).

The Safety of Lycopene Depends, Like That of All
Natural Substances, on the Dose

As a rule of thumb, “the dose makes the poison” can hardly be beat. It provides the basic guidance to the safe use of a natural substance, which, at amounts found in a diet, are quite safe—but at high doses (more than you could get in a diet even highly enriched in the substance) could have adverse effects.

With respect to carotenoids, taking the data all together, you generally observe protection against cancer at low doses, with sometimes increased risk of cancer at high doses. Beta carotene surprised many when it increased the risk of lung cancer in smokers in a large intervention trial. Scientists who published on this effect1 explained it this way:

… we have shown that high doses of beta carotene in an oxidative environment (such as the lungs of smokers) may result in excess levels of polar metabolites, which can promote carcinogenesis, whereas lower doses of beta carotene have been shown to be protective.

In a very recent study,2 we observed that high dose lycopene supplementation in the presence of alcohol* ingestion increased hepatic [liver] inflammation and TNFalpha [tumor necrosis factor alpha, an inflammatory cytokine]. While no apparent adverse effects—such as a decrease in body weight or tissue damage—were observed in our recent study of apo-10’-lycopenoic acid-supplemented NNK-treated A/J mice, an earlier study showed enhancement of benzo[a]pyrene [a polynuclear aromatic hydrocarbon constituent of smoke]-induced mutagenesis in mouse lung and colon tissues after lycopene supplementation.

* In the experiment referred to here (involving high dose lycopene in the presence of alcohol), the alcohol dose amounted to 36% of the caloric intake. This is roughly equivalent to a human on a 2400 kcal/day diet (including the alcohol) consuming 120 grams of pure ethanol per day or about 1½ bottles of 12% alcohol-containing wine per day. The lower dose of lycopene was roughly equivalent to 15 mg per day while the high dose was roughly equivalent to 45 mg per day for a 70 kg adult human.

Further research is needed to determine the mechanisms involved in whether a carotenoid will, at a particular dose, act to protect against cancer or to increase the risk of cancer—particularly under conditions involving smoke exposure and/or alcohol ingestion.

Taking lycopene at an amount that could be ingested by people eating a diet enriched in tomato products would, therefore, likely, be safe and reduce the risk of cancer, while it would be unclear how safe it would be to take a lot more than this.

The principle is the same with other dietary supplements. You see a similar effect with turmeric, a spice used in fairly large amounts on a daily basis in Indian food. Taking turmeric root as a supplement in amounts that are consumed by Indians eating a traditional turmeric-spiced diet is associated with a reduced risk of Alzheimer’s disease (though this is an association, not proof of cause and effect) and has not been associated with increased risk of diseases. On the other hand, taking very large doses of turmeric might not be safe for some people, though turmeric and its contained curcumin and curcuminoids are remarkably safe and are being used experimentally to try to prevent Alzheimer’s disease.3


  1. Mein, Lian, Wang. Biological activity of lycopene metabolites: implications for cancer prevention. Nutr Rev. 66(12):667-83 (2008).
  2. Veeramachaneni, Ausman, Choi, Russell, Wang. High dose lycopene supplementation increases hepatic cytochrome P4502E1 protein and inflammation in alcohol-fed rats. J Nutr. 138:1329-35 (2008).
  3. Frautschy, Hu, Kim, et al. Phenolic anti-inflammatory antioxidant reversal of amyloid beta-induced cognitive deficits and neuropathology. Neurobiol Aging. 22:993 – 1005 (2001). In this study, one experiment involved 22 month old Sprague-Dawley female rats; a group of these rats were treated with 500 ppm dietary curcumin, which prevented amyloid beta-infusion induced spatial memory deficits in the Morris Water Maze and post-synaptic density (PSD)-95 loss and reduced amyloid beta deposits.


Famous Radiation-Resistant Bacterium Relies on Defensive System That Includes Potent Carotenoid

Deinococcus radiodurans, the famously radiation resistant bacterium, is able to tolerate gamma-ray and UV radiation, cold, vacuum, acid, oxidants and desiccation. Versions of it were even produced by genetic engineering to recover radionuclides/heavy metals from nuclear wastes! Radiodurans can survive radiation doses 2,000 times what would fry a human being, and is reportedly even better at resisting radiation than cockroaches. (The bacterium was actually discovered in a batch of irradiated meat.) Radiodurans is even listed as the world’s toughest bacterium in “The Guinness Book of World Records!”A Here is a bug whose ability to thrive under hostile conditions would be nice to emulate!

Carotenoid Protection Against Protein Oxidation in radiodurans

Substantial Protection by Lycopene as Compared to Deinoxanthin in Chemical Assay

Just for fun, we report here that a study of carotenoids in D. radiodurans1 found that the bug synthesizes a unique carotenoid, deinoxanthin, as its major carotenoid and that the compound “was shown to protect DNA against damage as it is a more efficient scavenger of H2O2 [hydrogen peroxide] and singlet oxygen than lycopene, beta carotene, and lutein.”1 At a concentration of 0.05 mmol/liter, deinoxanthin inhibited protein oxidation by 29.7% as compared to 16.8% for lycopene, 14.3% for beta carotene, and 6.59% for lutein. At 0.1 mmol/liter, protein oxidation was inhibited by 45.1% by deinoxanthin, 37.6% by lycopene, 22.7% by lutein, and 50.3% by beta carotene (not significantly different from deinoxanthin).

The numbers above were obtained in an experimental system in which oxidative damage to bovine serum albumin was determined in the presence or absence of carotenoids.1 As protein oxidation is believed to be an important part of the aging process, preventing this (especially in long-lived proteins) is a desirable part of any longevity regimen. Another paper1B proposes that it is the oxidation of protein, rather than DNA, that is the principal target of ionizing radiation in bacteria, and resistance to that oxidation is the basis for radioresistance in bugs such as radiodurans.

The authors of another paper2 on the properties of deinoxanthin conclude that the ROS-scavenging ability of radiodurans “plays an important role in the radioresistance of D. radiodurans.”

Keeping in mind that D. radiodurans has a lot more in its damage resistance tool kit than just carotenoids and/or ROS-scavenging,3 the numbers above from paper #1 are still pretty impressive. It would be interesting to see what deinoxanthin would do in mammalian cells.


A. “Deinococcus radiodurans,” WIKIPEDIA (In their writeup here, it is said that the bug has been nicknamed “Conan the Bacterium.”)
1. Tian, Sun, Shen, et al. Effects of carotenoids from Deinococcus radiodurans on protein oxidation. Lett Appl Microbiol. 49:689-94 (2009).
1B. Daly, Gaidamakova, Matrosova, et al. Protein oxidation implicated as the primary determinant of bacterial radioresistance. PLoS Biol. 5(4):e92 (Apr 2007).
2. Hong-Fang Ji. Insight into the strong antioxidant activity of deinoxanthin, a unique carotenoid in Deinococcus radiodurans. Int J Mol Sci. 11:4506-10 (2010).
3. Slade and Radman. Oxidative stress resistace in Deinococcus radiodurans. Microbiol Mol Biol Rev. 75(1):133-91 (Mar. 2011).

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