Oxypower: Herbal Supplement for Mitochondrial Efficiency and Cardiovascular Health

by Tsu-Tsair Chi, NMD, PhD

Introduction

The mitochondrion plays an important role in health. Its dominant role in the body is to produce adenosine triphosphate (ATP) or energy. Besides energy production, it is also associated with processes such as regulating the cell cycle and cell growth. Damage to the mitochondrial or to the mitochondrial DNA has been linked to conditions like cardiovascular disease, neurological disorders, diabetes, and aging.

Many factors have been implicated in mitochondrial dysfunction, including oxidative stress, vascular endothelial cell impairment and DNA damage. When there is an overabundance of reactive oxygen species (ROS) or free radicals and the body is unable to clear these toxins fast enough, then oxidative stress and mitochondrial damage results. Cells are normally able to defend themselves against ROS damage, but in many cases, a supplement is needed as aid. Natural antioxidants can help clean free radicals from the system.

There are many plants in existence that have antioxidant properties. OxyPower contains the herbs Hippophae rhamnoides¹ and Rhodiola rosea², both of which can effectively protect cells against oxidative stress, promote mitochondrial efficacy as well as protect and repair DNA.

Oxypower Research

Cell Oxidative Damage Study

There are many factors that cause oxidative stress. One is the oxidation and reduction in cells due to free radicals producing substances that cause cell damage. For instance, hydrogen peroxide, one of the most powerful oxidizers, can penetrate through cell membrane and can be catalyzed into hydroxyl compounds (OH). These free radical compounds cause oxidative stress to the cells and hamper the efficacy of the mitochondria. This can eventually contribute to atherosclerosis, diabetes, hypertension and coronary heart disease.

Antioxidants are widely used to protect cells from damage and to combat oxidative stress. Coenzyme Q10 (CoQ10) is one of the more common antioxidant supplements in the market today. In the following in vitro study on human umbilical vascular endothelial cells (HUVECs), CoQ10 was used as a point of comparison for OxyPower’s antioxidant and cell protection properties.

In the study, hydrogen peroxide (H₂O₂) was used to induce damage to HUVECs (positive control). CoQ10 or OxyPower, at varying doses, was given to their respective groups to determine how much cell protection each of these substances offers. Based on Table 1, HUVEC proliferation increased with an increasing dose of OxyPower. Comparing it to CoQ10, the 100 μg CoQ10 + H₂O₂ group provided 60% cell growth while 75 μg OxyPower + H₂O₂ group provided over 63% cell growth. To calculate how much better OxyPower protects the cells, the following formula was used:

(% proliferation_{OxyPower+H2O2 group} – % proliferation _{positive control} )

x 100

(% proliferation _{OxyPower+H2O2 group} – % proliferation _{positive control} )

According to the results, 75μg OxyPower provides 26% higher cell protection than 100μg CoQ10 from free radical cell damage.

Table 1: In vitro: OxyPower vs. CoQ10 on Cell Protection

A value is the spectrometric measurement for cell proliferation; *p < 0.05

OxyPower: Antioxidant Function

OxyPower’s antioxidant properties were further tested in animal studies by measuring the activities of superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA). These are biomarkers for oxidative stress.

SOD counteracts the damaging effects of free radicals, protecting the cell from toxicity. GSH protects cells from oxidation by free radicals and peroxides. In Table 2, both of these markers increased with an increasing dose of OxyPower, suggesting that it protects the cells from oxidative damage.

Table 2: In vivo study:

OxyPower vs. CoQ10: Antioxidant Properties

MDA, on the other hand, is an end product of the degradation of lipids by reactive oxygen. This biomarker is used to measure the level of oxidative stress in an organism: a lower MDA level indicates lesser cell damage. In Table 2, the MDA level progressively decreased with an increasing dose of OxyPower.

OxyPower on Lipid Metabolism and Cardiovascular Health

Endothelial cells line the entire circulatory system, facilitating normal blood flow throughout the body as well as vasoconstriction and vasodilation, among other processes. VEC damage plays a vital role in many cardiovascular diseases. This is why understanding how to protect and repair VECs is at the forefront of cardiovascular research.

Abnormal lipid metabolism results in hyperlipidemia and oxidative stress which, in turn, can lead to vascular endothelial cell (VEC) damage. One of OxyPower’s functions is to facilitate lipid metabolism by regulating cholesterol and triglyceride levels. This reduces oxidative stress and helps protect VECs from damage.

In an in vivo study, hyperlipidemia was induced in rats³. There were 60 healthy male rats in the study, equally divided into five groups. The rats in the positive control group were given an ordinary diet. The rats in negative control group were fed a high-cholesterol diet to induce hyperlipidemia. The rats in the OxyPower groups were also given a high-cholesterol diet and then given OxyPower at different doses of 83, 250, and 750 mg/kg and CoQ10 at the dose of 83 mg/kg.

After four weeks, the effects of OxyPower and CoQ10 on lipid levels, the antioxidant system and the endothelial system were evaluated through the measurement of total cholesterol, triglyceride, very low density lipoprotein, atherogenic index, plasma endothelin and nitric oxide.

Table 3: In Vivo Study: OxyPower on Lipid Levels after Four Weeks

*p < 0.01

The first set of results compared the effect of OxyPower and CoQ10 on lipid levels and on the atherogenic index. In Table 3, OxyPower reduced cholesterol levels by 11.32%, 20.09%, 30.41% at the dose of 83 mg/kg, 250 mg/kg, and 750 mg/kg, respectively, compared to the negative control group. OxyPower also reduced triglyceride levels in all three groups at an average rate of 30.59% after four weeks.

As part of the study, the low density lipoprotein (LDL) level was also measured. LDL transports cholesterol and triglycerides in the bloodstream. In this study, the LDL-C indicates the amount of cholesterol in LDL and is a measure of how much LDL is driving the development of atherosclerosis. Very low density lipoprotein (VLDL) is a precursor to LDLs. Similar to LDL, VLDL is also a marker for atherosclerosis progression.

In Table 4, as expected, both LDL-C and VLDL-C are high in the negative control group. In the OxyPower groups, both indicators progressively decreased with an increasing dose of OxyPower.

Table 4: In Vivo Study: OxyPower vs. CoQ10 on LDL-C and Atherogenic Index

The atherogenic index (AI) is another marker for the formation of fat deposits in the vascular walls. Looking at Table 4 again, OxyPower performed better at reducing the AI than CoQ10. Compared with the negative control group, OxyPower reduced AI by 29.47%, 38.95%, and 53.42% at doses of 83 mg/kg, 250 mg/kg and 750 mg/kg, respectively.

These results demonstrate that OxyPower can regulate the lipid metabolism in hyperlipidemic rats, inhibit oxidative modification and protect the vascular endothelial system.

OxyPower on Nitric Oxide and Endothelin

Cardiovascular health can also be determined through the nitric oxide (NO) and endothelin (ET) levels. Both are produced in the vascular endothelial cells but their functions are opposite. NO has antithrombosis properties. It relaxes the blood vessels, making it more flexible. It can also inhibit involuntary muscle contractions and reduce blood platelet adhesion. ET, on the other hand, is a vasoconstrictor and aids in platelet agglutination. Higher NO levels and lower ET levels are obviously ideal for the prevention of atherosclerosis. However, when VEC damage is present, NO decreases while ET increases.

Results of the study demonstrate that rats on a high lipid diet (negative control group) have low NO and high ET levels (Table 5). When OxyPower was given, their NO levels increased and their ET levels decreased.

Table 5: In Vivo Study: OxyPower vs. CoQ10 on Nitric Oxide and Endothelin

OxyPower on Mitochondrial Function and Energy

It has already been shown that OxyPower reduces oxidative stress by increasing biomarkers that protect the cells and lowering factors that contribute to cell damage. This allows OxyPower to improve mitochondrial efficiency, specifically in the better utilization of oxygen and glucose in cells (Figure 1).

Figure 1: OxyPower Improves Mitochondrial Efficiency

In the mitochondrial electron transport chain, OxyPower improves the mechanism that transports fatty acids, glucose, and protons across mitochondrial membrane to produce ATP, the form of energy used by cells. Since the factors that hinder mitochondrial efficiency (e.g., oxidative factors) have been reduced or eliminated, OxyPower is able to work very quickly in producing energy as well as in preventing fatigue.

Unlike coffee and other drinks that provide energy temporarily, OxyPower provides a more lasting effect by helping the body to use stored energy more efficiently at different levels.

First, it increases the oxygen-carrying capacity of red blood cells, making more oxygen available to different organs and tissues. As a result, energy increases. In this capacity, OxyPower may be beneficial for individuals with fatigue, anemia and cancer.

Second, OxyPower increases serum glycogen levels. Glycogen is the storage form of carbohydrates in the liver and muscle tissues. When energy is needed, it is converted readily into glucose. When glycogen levels are low, fatigue occurs during exertions such as in exercise. In a mice study, glycogen in the OxyPower group was 20.35%, 35.6%, and 53.2% higher than the control group at doses of 2.5, 5.0, and 10 ml/kg, respectively. This means OxyPower increases the body’s energy storage, helping to combat fatigue.

In another mice study, liver glycogen in mice was tested. Since there is no significant difference in glycogen level in this test (Table 6), it means that OxyPower is able to utilize energy longer and much more efficiently, without burning much glycogen. This further illustrates OxyPower’s antifatigue function.

Table 6. In Vivo Study: OxyPower on Liver Glycogen in Mice

Third, OxyPower works at a much deeper level, the mitochondrial level, to be exact. Since the mitochondria are the cells’ principal source of energy, they have to be working efficiently to produce optimal energy. Mitochondrial damage or dysfunction will obviously hamper energy production and lead to fatigue. It has already been demonstrated that OxyPower improves mitochondrial efficiency by reducing oxidative stress and VEC damage.

Serum Lactic Acid Study

Lactate (lactic acid) is the end product of the glycolysis (the metabolic breakdown of carbohydrates and sugars to produce energy) under anaerobic conditions. In a condition called lactic acidosis, the production of too much lactic acid causes damage to the mitochondria. Acidosis can occur when there is inadequate oxygenation in the tissues. During bursts of vigorous activity, such as exercise, oxygen supply to the tissues can become depleted. Lactate then escapes from muscle cells into the blood and is rebuilt into glucose in the liver during recovery. However, if it is not cleared fast enough, acidification can result in fatigue and muscle soreness. In order to prevent this from happening, there should be adequate oxygen supply to the tissues and the accumulation of too much lactic acid should be avoided.

An animal study demonstrates that OxyPower reduces serum lactic acid. In the study, forty mice were divided equally into four groups: the control group and three groups given 0.25 ml/kg, 0.125 ml/kg and 0.0625 ml/kg OxyPower, respectively, for eight weeks. At the end of the study, the serum lactic acid level was measured.

Table 7: In Vivo Study: OxyPower on Serum Lactic Acid after 8 Weeks

** p<0.01, * p<0.05

Results of the study (Table 7) revealed that the dosage of OxyPower was inversely proportional to the level of lactic acid in the serum. Since serum lactic acid is a determinant of anaerobic metabolism, this means that an elevated level signifies insufficient oxygen delivery to meet organ and tissue demands, especially during vigorous activity. Since lactic acid levels decreased with an increasing dose of OxyPower, this suggests that OxyPower is able to improve oxygen delivery in the organ and tissues, promote mitochondrial efficacy and prevent cell damage.

OxyPower on Energy (Antifatigue)

In another animal study, a swimming test was utilized to determine the effect of OxyPower on endurance of mice. Forty mice were divided into four groups of ten mice each. Mice in the OxyPower groups were given 0.0625 ml/kg, 0.125 ml/kg and 0.25ml/kg OxyPower, respectively, for 8 weeks. At the end of 8 weeks, the mice were given weights and allowed to swim. Their endurance was then measured by calculating the length of time the mice stayed afloat.

Table 8:

In Vivo Study: OxyPower on Swimming Endurance after 8 Weeks

** p<0.01, * p<0.05

It is clear from the results in Table 8 that higher doses of OxyPower provide greater effect on endurance. Even mice given the lowest OxyPower dose were able to swim longer than mice in the control group.

OxyPower on Muscle Strength

In another study, the muscle strength of mice with or without OxyPower was measured using the climbing test. The same number of mice was involved. Mice in the OxyPower groups were given 0.0625 ml/kg, 0.125 ml/kg and 0.25 ml/kg OxyPower, respectively. At the end of 8 weeks, the mice were placed in a pool of water with a pole to which they can climb and hold. To gauge their muscle strength, the time it took for the mice to hold on to the pole without falling into the water was measured.

Table 9:

In Vivo Study: OxyPower on Muscle Strength after 8 Weeks

** p<0.01, * p<0.05

The study clearly shows that with increasing dosage of OxyPower, the mice were able to hold on to the pole much longer (Table 9). This indicates that OxyPower increased muscular strength, allowing the mice to hold on to the pole longer without falling back into the water.

Antihypoxia Study

In this study, it will be demonstrated that OxyPower prevents oxygen deprivation in tissues (antihypoxia). Preventing hypoxia plays an important role in mitochondrial efficiency. As mentioned, lactic acidosis occurs when oxygen supply to the tissues is not adequate during vigorous activity. Since acidosis can eventually cause damage to the mitochondria, it is important to avoid this occurrence by ensuring that there is enough oxygen supply to the tissues.

An in vivo study compared OxyPower with the extract of Rhodiola algida, an herb known for its antihypoxia effects. There were 50 mice involved in the study, divided equally into five groups. Mice in the Rhodiola group were given 0.125 g/kg Rhodiola. Mice in the OxyPower groups were given 0.0625 ml/kg, 0.125 ml/kg and 0.25 ml/kg OxyPower, respectively. At the end of 8 weeks, the mice were placed in a water-filled chamber with progressively decreasing oxygen content to simulate a hypoxic environment. Their survival time in the chamber was then measured.

Table 10. In Vivo Study: Antihypoxia effect of OxyPower vs. Rhodiola

** p<0.01, * p<0.05

As the results show (Table 10), OxyPower at the dose of 0.0625 ml/kg, which is half the dose of Rhodiola, produced comparable results with Rhodiola in terms of survival time. At the same dose as Rhodiola (0.125 ml/kg), mice in the OxyPower group survived 15.9% longer. With 0.25 ml/kg of OxyPower, survival time was 31.8% higher than the Rhodiola group and 48.7% higher than the control group.

Clearly OxyPower has a more effective antihypoxic function than Rhodiola alone, making it beneficial for those with lung problems and those with oxygen deficiency conditions.

Informal Human Experiment on the AntiHypoxia Function of OxyPower

An informal experiment was performed to determine OxyPower’s effect on respiratory function, fatigue and general well-being at high altitudes. In the experiment, 15 men and women (ages 7 to 69) participated in a mountain hike. All the participants stayed at an elevation of 12,500 feet for three nights. Various doses of OxyPower were given at varying time lengths before and during the hike.

Six of the participants (a 7-year-old girl, a 34-year-old female, two 36-year-old females, a 24-year-old male and a 51-year-old male) were nauseous and suffered from headaches by the time they climbed up. They were given two 250 mg soft gels of OxyPower. After only 13 minutes, the 34-year-old female’s headache had alleviated. Within two hours, headaches were alleviated and nausea was relieved in all six participants. With continued use of the OxyPower, they did not feel any symptoms during their three-day stay at 12,500 feet.

All the other participants had similar results even with the variety of doses they have taken. A 39-year-old male took 4 250 mg soft gels daily for a month while a 43-year-old male only took two soft gels. An 8-year-old and a 13-year-old male only took one OxyPower soft gel. A 69-year-old male took OxyPower for 3 months but stopped taking it 10 days before the trip. Despite stopping 10 days before the trip, the effect of OxyPower still lingered because he did not have breathing problems or other high altitude symptoms.

It is also worth mentioning two similar cases:

M. C., a 50-year-old female, has been mountain hiking twice in the past two years. Both times, she went up to 10,000 ft in elevation and suffered from altitude sickness. During her last trip, she took OxyPower for four days prior to the hike. She reported having no symptoms of illness for the entire three days of her trip, even at 13,000 ft.

T. C., a 55-year-old male, had gone to Tibet (elevation 12,500 ft) about 12 years ago. During that trip, he had to have an oxygen tank to help him breathe because of the high elevation. For the present hike, he took two OxyPower soft gels twice per day before and during the trip. For the entire time he was in Tibet, he did not even have any breathing difficulty except when he walked fast.

All of the above cases illustrate that the antihypoxia function of OxyPower is very beneficial for reducing symptoms of altitude sickness.

OxyPower on DNA

In the last 20 years, numerous studies have unearthed the mysteries of the DNA, shedding light on how DNA is changed in cancer, aging and other health conditions. It has become a consensus among scientists that diseases occur because of damage to DNA. Normally, the cells’ DNA genes are able to naturally repair mutations and other changes. However, in cases like cancer, the DNA repair genes are unable to do so.

According to animal studies, genetic deficiencies in DNA repair can lead to increased incidence of cancer, premature onset of aging-related diseases and a shorter lifespan. This is because the rate of DNA damage exceeds the ability of the cell to repair it. Eventually, the accumulation of damage can overwhelm the cell, causing the above-mentioned conditions.^4–7

Furthermore, mitochondrial DNA damage increases susceptibility to aging and neurodegenerative diseases, including Alzheimer’s disease and age-related macular degeneration (AMD), according to a report by Frank Shallenberger, MD. Apparently, a deficiency in repairing mitochondrial DNA damage contributes to the development of retinal degeneration.⁸ Antioxidant therapies have been shown to delay the progression of AMD.⁹

Mitochondrial DNA mutations may also underlie Alzheimer’s disease, Parkinson’s disease, and other disorders that are common among senior citizens, says Doug Wallace, Director of the University of California, Irvine’s new Center for Molecular and Mitochondrial Medicine and Genetics. “If we could find a way to protect mitochondrial DNA, either with drugs or by using gene therapy to transplant it to the nucleus, it could not only extend our life spans but prevent many of the diseases we associate with aging as well.”^10–12

Studies have shown that protection against oxidative stress and repair of mitochondrial DNA damage may have a strong impact on the prevention and treatment of Alzheimer’s Disease.¹³ In this regard, OxyPower may have a viable application.

An in vitro study demonstrates that OxyPower may have protective and reparative functions on the DNA. The single cell gel electrophoresis assay, also known as the Comet assay, was used in this instance to detect DNA damage. Thymidine kinase DNA of TK6 human lymphoblast cells were analyzed using electrophoresis. To induce DNA damage, K₂Cr₂O₇ was added to the cells.

Figure 2: In Vitro Study: OxyPower Repairs Mitochondrial DNA Damage

A

B

Figure 2A. Damaged TK6 human lymphoblast cell, tail is evident.

Figure 2B. Twenty-four hours after OxyPower administration, DNA damage is repaired, shown as the absence of the tail.

DNA damage was evident in the TK6 human lymphoblast cell without OxyPower, shown as the comet tail (Figure 2A). Twenty four hours after adding OxyPower, it is clear from the results that DNA damage was repaired, as evidenced by the absence of the comet tail (Figure 2B).

In another in vitro study, OxyPower was compared with Mitomycin C (MMC), a chemotherapeutic agent.¹⁴ Similar to the previous study, the Comet assay was again used to detect DNA damage to the cells with or without OxyPower. The percentage of cells with tailing signifies the amount of damage while the length of the tailing signifies the degree of damage.

Table 11: In Vitro Study:

Effect of OxyPower on Mitomycin C-induced DNA Damage

As illustrated in Table 11, MMC alone induced significant DNA damage, with tailing in 46.8% of the TK6 human lymphoblast cells and an average tail length of 17.65 μm after 24 hours. As expected, there was very minimal damage in the OxyPower only group. In fact, the percentage of cells with tailing in this group (3.6%) is less than even the negative control group (7.4%), signifying cell protection. In the OxyPower + MMC group, only 4% of the cells had damage while the average tail length was only 4.55 μm. This means that even in the presence of a substance that harms the DNA, OxyPower’s DNA protection property is still potent. Overall, this study indicates that OxyPower has both protective and reparative functions on the cells.

Discussion

With the many studies behind its different functions, OxyPower proves to be a wide-ranging supplement, with applications in cardiovascular disease, energy, mitochondrial health, and DNA protection and repair.

All these different functions have a common link: the mitochondrion. Mitochondria are the power plants of cells, containing enzymes, ribosomes, tRNA and mitochondrial DNA. While the major role of the mitochondria is energy production, it also contains reactive oxygen species (ROS) that may potentially cause damage. Mitochondrial dysfunction has been associated with conditions such as cardiovascular disease, neurological disorders, and diabetes. Moreover, impaired mitochondrial function and loss of efficiency are related to fatigue and aging.

Preserving the integrity of the mitochondria and minimizing oxidative stress that contributes to mitochondrial damage are viable goals to minimizing the risk of developing cardiovascular disease and other disorders.

Oxidative stress is considered one of the major factors of mitochondrial and vascular endothelial damage. Minimizing this stress is vital to preventing many cardiovascular diseases such as atherosclerosis as well as neurological disorders like Alzheimer’s disease. In recent years, the application of antioxidants for these conditions has been the subject of many studies.

In the in vivo antioxidant study, it is clear that OxyPower increases biomarkers (SOD and GSH) that protect cells from damage caused by free radicals. This is evident in the cell protection study where, even in the presence of a reactive oxygen species like hydrogen peroxide, the addition of OxyPower still enabled the cells to proliferate.

Antioxidants are especially beneficial in cardiovascular health because damage to vascular endothelial cells occurs when there is oxidative stress. Besides free radicals, lipids can also pose a risk for cardiovascular health. It is widely known that high cholesterol and high triglycerides are risk factors for atherosclerosis and stroke. Additionally, there is a feedback loop that occurs among lipids, oxidative stress and mitochondrial damage. When lipids accumulate, their oxidized forms are more easily retained in the cells and cause oxidative stress, leading to mitochondrial damage. Mitochondrial damage, in turn, causes more lipid accumulation.

OxyPower blocks this feedback loop through all three paths: reducing lipid levels, minimizing oxidative stress and preventing mitochondrial DNA damage.

In the hyperlipidemia mice study, OxyPower clearly reduced cholesterol level by an average of 20.61% and triglyceride level by an average of 30.59% after four weeks. The study also tested the atherogenic index (AI), a measure of fat deposits in the blood vessel walls. Results show that with an increasing dose of OxyPower, the AI value decreases, suggesting the reduction of fat deposits in vascular walls.

Moreover, OxyPower increases nitric oxide (NO) levels and reduces endothelin (ET) levels. NO enhances blood vessel flexibility, reduces clumping of platelets, and prevents involuntary muscle contractions while ET increases vascular contractions. These functions have important roles in maintaining cardiovascular health.

These results are very significant especially for individuals with cardiovascular disease, such as atherosclerosis, stroke and congestive heart failure.

OxyPower’s reduction of oxidative stress was determined through the indicators superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA). In vivo studies show that OxyPower reduces oxidative damage by increasing SOD and GSH, both cell protective markers, while lowering MDA, a lipid peroxide product that contributes to cell damage.

In vitro studies show that OxyPower protects and repairs DNA. In the two studies, OxyPower was able to minimize DNA damage caused by the DNA-altering substances, K₂Cr₂O₇ and Mitomycin C. OxyPower’s ability to protect and repair DNA as well as its potent antioxidant effect is not only useful for neurodegenerative and aging disorders but also for cardiovascular conditions.

With its many functions, it is not surprising that OxyPower has energy-boosting and antifatigue properties. It works on many different levels, including the mitochondrial level, that it produces lasting energy, not the temporary energy that one gets from coffee, for example. Furthermore, it is able to combat fatigue by preventing the loss of oxygen supply to tissues (as evident in the serum lactic acid and antihypoxia studies) and by utilizing stored energy more efficiently without burning too much glycogen.

While further clinical studies are needed to firmly establish OxyPower’s effects on energy, oxidative stress, and DNA repair, the evidence presented here are compelling enough to warrant a closer look at this supplement.

Notes

1. M Basu, R Prasad, P Jayamurthy et al. Anti-atherogenic effects of seabuckthorn (Hippophae rhamnoides) seed oil. J Phytomedicine. 2007;14(1):770–777.

2. Kurkin VA. The chemical composition and pharmacological properties of rhodiola plants. Pharm Chem J. 1986;20(10):123.7.

3. Ma HY, Chen JY, Zhang LS. Study on protective effect of Tianji soft capsule on blood lipids, internal antioxidant system and vascular endothelial system in hyperlipidemia rats. Submitted for publication.

4. de Boer J et al. Premature aging in mice deficient in DNA repair and transcription. Science. 2002;296(5571):1276–1279.

5. Dollé ME et al. Increased genomic instability is not a prerequisite for shortened lifespan in DNA repair deficient mice. Mutat Res 2006;596(1–2):22–35.

6. Espejel S et al. Shorter telomeres, accelerated ageing and increased lymphoma in DNA-PKcs-deficient mice. EMBO Rep. 2004;5(5):503–509.

7. Helleday T et al. DNA repair pathways as targets for cancer therapy. Nature Reviews Cancer. 2008;8:193–204.

8. Jarrett SG, Lin H, Godley BF, Boulton ME. Mitochondrial DNA damage and its potential role in retinal degeneration. Prog Retin Eye Res. 2008;27(6):596–607.

9. Fehér J et al. [Metabolic therapy for early treatment of age-related macular degeneration]. Orv Hetil. 2007;148(48):2259–2268

10. Wang AL, Lukas TJ, Yuan M, Neufeld AH. Increased mitochondrial DNA damage and down-regulation of DNA repair enzymes in aged rodent retinal pigment epithelium and choroid. Mol Vis. 2008;14:644–651.

11. Pedersen PL. Mitochondrial matters of the brain: amyloid formation and Alzheimer’s disease introduction. J Bioenerg Biomembr. 2009;41(5):403–4-5.

12. Leuner K et al. Mitochondrial dysfunction: the first domino in brain aging and Alzheimer’s disease? Antioxid Redox Signal. 2007;9(10):1659–1675.

13. Müller WE, Eckert A, Kurz C, Eckert GP, Leuner K. Mitochondrial dysfunction: common final pathway in brain aging and Alzheimer’s disease–therapeutic aspects. Mol Neurobiol. 2010;41(2–3):159–171.

14. Chen W, Zou SY, Zhang LS. Evaluation of mutagenicity and anti-mutagenicity of two health foods by Comet Assay. Mod Prev Med. 2008;35(1):1–3.