Live your best life & take care
Our DNA faces a staggering number of damaging events each day. Estimates suggest that each cell in our body endures approximately 70,000 DNA lesions [1] up to 100.000 per day [2][3]. While this number includes all types of DNA damage, sunlight remains a major culprit, especially for skin cells, which may experience even higher rates of DNA damage. Oxidative stress, another significant contributor, is estimated to cause about 10,000 DNA lesions per cell per day [1][3].
Frequency types of DNA damage: [3] ▌Oxidative damage: 10,000 to 11,500 incidents per cell per day in humans ▌Depurinations: 2,000 to 10,000 per cell per day in mammalian cells ▌Single-strand breaks: About 55,200 per cell per day in mammalian cells ▌Double-strand breaks: 10 to 50 per cell cycle in human cells Factors influencing DNA damage and rates: [4] ▌Environmental factors: UV-radiation, pollution and lifestyle choices (e.g., smoking) can increase oxidative stress ▌Frequency of exposure: repeated UV exposure can overwhelm repair mechanisms ▌Age: DNA repair efficiency declines with age ▌Skin phototype: individuals with fair skin are more susceptible to UV-induced damage ▌Cell type and location in the body ▌Individual factors: like genetics and epigenetics SUNLIGHT INDUCED DNA DAMAGE UVA, UVB, and High Energy Visible Light (HEVIS) harm our genetic material in different ways. UVA makes up the majority of UV radiation reaching the Earth's surface, and both UVA and blue light are used in artificial UV exposure settings [5][6]. 50% of the damaging oxidative stress in human skin is generated in the VIS spectrum and the other 50% by UV light [7]. UVB-Induced DNA damage UVB (280-315 nm) is generally considered the most harmful due to its higher energy content and efficient absorption by DNA [6], and is known to directly interact with DNA, primarily causing the formation of cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs) [8]. These lesions can distort the DNA helix, potentially leading to mutations if left unrepaired. ▌Direct formation of cyclobutane pyrimidine dimers (CPDs): Most abundant UVB-induced lesion, formed between adjacent pyrimidines [6][5] ▌Formation of 6-4 photoproducts (6-4PPs): Second most common UVB-induced lesion [6][5] ▌Generation of Dewar valence isomers: Derived from 6-4PPs upon further UVB exposure [6] ▌Oxidative DNA damage: Through generation of reactive oxygen species (ROS), though less prominent than with UVA [9][10] ▌DNA-protein crosslinks: Formed between DNA and nearby proteins [6] ▌Single-strand breaks: Can occur as a result of UVB exposure [11] ▌Pyrimidine hydrates: Minor UVB-induced lesions [12] ▌Oxidative DNA-lesions, such as 8-oxodeoxyguanosine, when they are in proximity or on opposite DNA-strands, may generate double-strand breaks [5] UVB radiation is considered more genotoxic than UVA due to its direct absorption by DNA and efficient formation of mutagenic CPDs and 6-4PPs. However, both UVA and UVB contribute to solar UV-induced DNA damage and mutagenesis. UVA-Induced DNA damage UVA-induced (315-400 nm) DNA damage occurs through various mechanisms, primarily involving indirect effects but also some direct damage. ▌Photosensitization: Interaction with endogenous photosensitizers like riboflavin and porphyrins, leading to reactive oxygen species (ROS) generation [13] ▌Oxidative stress: ROS-induced oxidative DNA damage, with 8-oxo-7,8-dihydroguanine (8-oxoG) as a primary lesion [13][6][5] ▌Indirect cyclobutane pyrimidine dimer (CPD) formation: Through photosensitized triplet energy transfer, less efficient than UVB [13] ▌Direct DNA damage: Formation of CPDs, particularly at TT sequences [5][6] ▌Genomic instability [6] ▌Single-strand and double-strand DNA breaks [6][14] UVA-induced DNA double-strand breaks result from the repair of clustered oxidative DNA damages [6]. This means UVA doesn't directly cause DSBs, but rather creates oxidative damage that can lead to DSBs during the repair process. While UVA was originally not expected to induce DSBs due to its relatively low photonic energy, several studies have shown that UVA can induce DSBs in a replication-independent manner [6]. Oxidative DNA-lesions, such as 8-oxodeoxyguanosine, when they are in proximity or on opposite DNA-strands, may generate double-strand breaks [5]. Blue Light (HEViS)-induced DNA damage Blue light or high-energy visible light (HEVIS)-induced (400-700 nm) DNA damage occurs through mechanisms similar to UVA, primarily involving indirect effects mediated by reactive oxygen species (ROS). ▌Photosensitization: Interaction with endogenous photosensitizers like riboflavin and porphyrins, leading to ROS generation [15] ▌Oxidative stress: ROS-induced oxidative DNA damage, with 8-oxo-7,8-dihydroguanine (8-oxoG) as a primary lesion [5][16][17] ▌Mitochondrial DNA damage: Blue light can penetrate into cells and damage mitochondrial DNA, leading to mitochondrial dysfunction [6] ▌Indirect formation of cyclobutane pyrimidine dimers (CPDs): Through photosensitized triplet energy transfer, though less efficient than UVA or UVB [5][18] ▌Single-strand DNA breaks: Caused by ROS-induced oxidative damage [19] ▌Lipid peroxidation: ROS-induced damage to cellular membranes, indirectly affecting DNA integrity [20] ▌Protein oxidation: Damage to DNA repair enzymes and other proteins involved in maintaining genomic stability [21] ▌Chromosome aberrations (clastogenic/aneugenic effects) [5] ▌DNA double-strand breaks (DSBs), through indirect mechanisms Double-Strand Breaks (DSBs) While DSBs are less common than other types of UV-induced DNA damage, they are particularly dangerous because they affect both strands of the DNA helix and can lead to genomic instability if not properly repaired [14][22]. ▌UVA-induced DSBs: These often result from the repair of clustered oxidative DNA lesions. When repair enzymes attempt to fix closely spaced lesions on opposite strands simultaneously, it can lead to DSBs [6]. Some studies have found that UVA radiation can induce DSBs, particularly through oxidative stress mechanisms [6][23]. Other research suggests that UVA alone may not directly cause significant DSB formation or activate certain DNA damage response pathways associated with DSBs [24] ▌UVB-induced DSBs: UVB can cause DNA double-strand breaks. These can occur directly or as a result of replication fork collapse at sites of unrepaired lesions [22][25] ▌ROS-induced DSBs: UVA, UVB and Blue Light can generate reactive oxygen species (ROS), which can cause various types of DNA damage, including DSBs [5][6][14][23] The dose and wavelength of UV radiation can influence the types and extent of DNA damage, including DSB formation [25][26]. Cellular specificity of DNA damage Different skin cell types exhibit varying susceptibilities to DNA damage: 1. Keratinocytes: Most numerous and most exposed, they bear the brunt of UV-induced CPDs [6]. Blue light has been shown to cause DNA damage in human keratinocytes, potentially contributing to premature skin aging [5] 2. Melanocytes: Particularly vulnerable to oxidative damage due to melanin production [27] 3. Fibroblasts: While less directly exposed, they can accumulate damage over time, contributing to photoaging [27] Mitochondria, the powerhouses of the cell, have their own DNA and are particularly susceptible to DNA damage due to their proximity to reactive oxygen species (ROS) production. While oxidative stress in mitochondria can lead to damage, a certain level of ROS is actually necessary for proper cellular signaling and adaptation. Other types of DNA damage Beyond UV-induced damage, our DNA faces threats from various sources: 1. Hydrolytic Damage: Spontaneous hydrolysis can lead to depurination and depyrimidination [1] 2. Alkylation: Endogenous and exogenous alkylating agents can modify DNA bases [1] 3. Mismatch Errors: During DNA replication, incorrect nucleotides may be incorporated [1] MECHANISMS OF DNA REPAIR Cells have sophisticated DNA repair mechanisms, however, some damage may escape repair, potentially leading to mutations or cellular dysfunction over time. 1. Nucleotide Excision Repair (NER): ▌Primary mechanism for repairing UV-induced DNA damage, particularly cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs)[25][28][29] ▌Involves recognition of DNA distortion, excision of the damaged segment, and synthesis of new DNA to fill the gap [30]. 2. Base Excision Repair (BER): ▌Repairs oxidative DNA damage caused by UVA and HEViS-induced reactive oxygen species (ROS) [30][31] ▌Involves removal of damaged bases (including oxidative lesions like 8-oxoG [29], creation of an apurinic/apyrimidinic (AP) site, and DNA synthesis to fill the gap [29][30] 3. Homologous Recombination Repair (HRR): ▌Repairs double-strand breaks that can result from UV exposure, particularly during DNA replication [32] ▌Uses an undamaged DNA template (usually a sister chromatid) to accurately repair the break [32] 4. Mismatch Repair (MMR): ▌Corrects errors in DNA replication that result in mismatched base pairs and small insertion/deletion loops [29][30][33] ▌Important for maintaining genomic stability and preventing mutations [30] 5. Double-Strand Break Repair: Includes homologous recombination and non-homologous end joining [29] 6. Non-Homologous End Joining (NHEJ): [32] ▌An alternative mechanism for repairing double-strand breaks ▌Directly ligates broken DNA ends without the need for a homologous template NER is particularly crucial for UV-induced damage, while the repair of oxidative lesions through BER can be challenging due to the persistent nature of oxidative stress. Additionally, research has highlighted the role of the AMPK pathway in promoting UVB-induced DNA repair by increasing the expression of XPC, a key protein in the NER pathway [28]. OTHER DNA REPAIR MECHANISMS In addition to the mechanisms primarily responsible for repairing sunlight-induced damage, our bodies have several other DNA repair pathways: 1. Direct Reversal Repair: ▌Includes mechanisms like O6-methylguanine-DNA methyltransferase (MGMT), which directly removes alkyl groups from guanine bases [25] 2. Translesion Synthesis (TLS): ▌Not a repair mechanism per se, but allows DNA replication to bypass damaged sites [30] ▌Can be error-prone but prevents replication fork collapse and more severe DNA damage [30] 3. Interstrand Crosslink Repair: ▌Repairs covalent links between DNA strands that can block replication and transcription [30] ▌Involves a complex interplay of multiple repair pathways, including NER and homologous recombination [30] 4. Single-Strand Break Repair: ▌Repairs breaks in one strand of the DNA double helix [30] ▌Often involves components of the BER pathway [30] These repair mechanisms often work in concert, and there can be significant overlap and interaction between different pathways. The choice of repair mechanism depends on factors such as the type of damage, the cell cycle stage, and the availability of repair proteins [28][30]. CONSEQUENCES OF UNREPAIRED DNA DAMAGE When DNA repair mechanisms fail or are overwhelmed, several outcomes can occur: 1. Skin Aging: Accumulation of damage in epidermal keratinocytes and dermal fibroblasts leads to reduced collagen production and elastin degradation [34] 2. Hyperpigmentation: DNA damage in melanocytes can trigger increased melanin production [34] 3. Skin Cancer: Mutations in key genes like p53 can lead to uncontrolled cell growth [34] CORRELATION INCREASE DAMAGE, INCREASED RISK OF PREMATURE AGING & CANCER While a large amount of DNA damage does increase the workload on repair mechanisms and can potentially lead to more errors, it's not a simple direct relationship. The body has multiple layers of protection, including cell death pathways for severely damaged cells. The balance between efficient repair, controlled cell death, and mutation accumulation is crucial in determining outcomes related to cancer and aging. Both cancer and aging are complex, multifactorial processes influenced by many factors beyond DNA damage and repair. 1. DNA damage accumulation and cancer/aging risk ▌DNA damage does accumulate over time in cells, with estimates of 10,000 to 100,000 DNA lesions per cell per day [3] ▌This accumulated damage, if not properly repaired, ca n lead to mutations that contribute to both cancer development and aging [35][36] 2. DNA repair and mutation risk ▌While DNA repair mechanisms are generally beneficial, they are not perfect and can occasionally introduce errors [30] ▌High levels of DNA damage can overwhelm repair systems, potentially leading to more errors during the repair process [37] 3. Connection to cancer and premature aging ▌Defects in DNA repair pathways are associated with increased cancer risk and premature aging syndromes [37][38] ▌Some inherited mutations in DNA repair genes (like POLE/POLD1) can lead to higher mutation rates and increased cancer risk, though not necessarily premature aging in all aspects [36] 4. Balance between repair and consequences ▌There's a delicate balance between DNA repair, cell death, and mutation accumulation [38] ▌Excessive DNA damage can lead to increased cell death and stem cell exhaustion, potentially promoting premature aging [38] ▌However, if mutations accumulate without triggering cell death, this can increase cancer risk [38] 5. Stem cell considerations ▌Stem cells have special mechanisms to maintain low mutation rates, but when mutations do occur, clonal expansion can contribute to both aging and cancer risk [38] PREVENTION AND SUPPORT OF DNA REPAIR 1. Sun Protection: Broad-spectrum sunscreens (preferably including blue light protection), protective clothing, and avoiding peak UV hours remain the most effective strategies [39]. 2. Antioxidants: Both topical and oral antioxidants can help combat oxidative stress, though their efficacy in preventing DNA damage is still debated [40]. 3. Glycyrrhetinic Acid (GA): has protective effects against DNA damage and enhances DNA repair mechanisms both topical or as supplement. 3. DNA repair enzymes: Topical applications of enzymes like T4 endonuclease V have shown promise in enhancing repair [39]. 4. Lifestyle factors: Adequate sleep, a balanced diet, and stress management can support overall cellular health and DNA repair processes. 5. Supplements: ▌Vitamin C: Dose: 500 mg [41]. .Vitamin C has been shown to potentially induce nucleotide excision repair (most important for sun damage) through anti-oxidant properties, however in high concentrations may be acting as pro-oxidant. ▌Folic Acid and Vitamin B12: Dose 15 mg folic acid and 1 mg vitamin B12 thrice weekly [42] Folic acid has show promise in markers for genomic instability, but does not significantly affect DNA strand breakage and excess may even increase DNA mutations and affect DNA repair gene expression. Vitamin B12 plays a role in DNA synthesis and methylation, which are important for genomic stability. ▌Selenium (as selenomethionine): Dose: 100 μg/day [43] promising, not conclusive. ▌Zinc: Dose: 22 mg/day Molecular Nutrition & Food Research. A small increase in dietary zinc can reduce oxidative stress and DNA damage as shown by reduced leukocyte DNA strand breaks, however more comprehensive human studies are necessary to be conclusive. ▌Coenzyme Q10: Dose: 100 mg/day Associated with reduced baseline DNA damage [44]. Ubiquinol-10 may enhance DNA resistance to oxidative damage and reducing strand breaks in vitro. Further research is needed to be conclusive. ▌Taurine: Taurine supplementation has been shown to reduce DNA damage in several studies [45][46][47]. In one study, taurine (20 mM) reduced formation of DNA base adducts like 5-OH-uracil, 8-OH adenine, and 8-OH guanine by 21-49% [45]. Taurine (2 g three times daily) decreased DNA damage associated with exercise [49][50]. Taurine suppresses DNA damage and improves survival of mice after oxidative DNA damage [52]. Most studies used doses between 1-6 g per day [51]. A proposed safe level of taurine consumption is 3 g/day [49]. Doses as high as 10 g/day for 6 months have been tested [51]. For exercise benefits, 2 g three times daily was effective [49][50]. Taurine acts as an antioxidant and can protect against oxidative DNA damage [45][46]. It may activate DNA repair pathways involving p53 [48][53]. Taurine deficiency is associated with increased DNA damage and cellular senescence [52]. ▌ Magnesium: Plays a crucial role in DNA repair and recommended dose varies by gender and age. Magnesium Malate and Citrate or Orotate are good for energy, while Glycinate and Threonate have an additional bonus as both support sleep quality, DNA repair processes are influenced by circadian rhythms and more active overnight. Sleep enhances the repair over double-strand breaks. Dark chocolate and deep green vegetables contain Magnesium. The studies cited come mostly from reputable peer-reviewed journals. Supplements have shown benefits in specific studies, their effects may vary depending on individual factors, correct dose and overall health status. Always consult with a healthcare professional before starting any new supplement regimen. PARP (Poly ADP-ribose polymerase) plays a crucial role in DNA repair, particularly in the base excision repair (BER) pathway. PARP acts like a cellular "first responder" for DNA damage, initiating the repair process to keep our genetic material intact. 1. DNA damage sensing: PARP1, the most abundant PARP enzyme, acts as a DNA damage sensor, quickly binding to single-strand breaks (SSBs) in DNA [54][55]. 2. Recruitment of repair factors: Once bound to damaged DNA, PARP1 catalyzes the synthesis of poly(ADP-ribose) (PAR) chains on various proteins, including itself. This PARylation helps recruit other DNA repair factors to the site of damage [54][56]. 3. Base Excision Repair (BER): PARP is a key component of the BER complex, which also includes DNA ligase III, DNA polymerase beta, and the XRCC1 protein [55]. 4. Chromatin relaxation: PARylation of histones by PARP leads to chromatin relaxation, allowing better access for repair enzymes to the damaged DNA [55][56]. This is moreover an epigenetic mechanism. 5. Regulation of other repair pathways: PARP is also involved in other DNA repair pathways, including nucleotide excision repair (NER) and double-strand break repair [55][56]. Boosting PARP activity for enhanced DNA repair: 1. Raising NAD+ levels: PARP activation will decrease NAD+ levels. Increasing NAD+ levels through precursors like nicotinamide riboside or nicotinamide mononucleotide might support PARP activity [57], especially in response to oxidative stress and DNA damage [58][59]. .Although NMN supplementation does raise NAD+ levels and it´s health benefits are hyped by longevity experts, some scientists are skeptical as they find the data in humans not very convincing to date, with minor benefits for unhealthy and older volunteers in 14 publications. Fact is that NAD+ levels decrease as we age as a result of declining levels or activity of the NAD+ recycling enzyme NAMPT in the biosynthetic salvage pathway and other NAD+ consuming enzymes like CD38 and as mentioned before PARPs. 1. Lifestyle factors: Regular exercise and calorie restriction have been shown to increase NAD+ levels, which could indirectly support PARP function [57]. Both aerobic and resistance exercise have been shown to increase NMAPT levels, reversing age related declines [66][61]. 2. Avoiding PARP inhibitors: Certain medications and supplements (interestingly these include polyphenols like resveratrol, favonoids and Vitamin D) can inhibit PARP activity [62]. Avoiding these could help maintain normal PARP function, although PARP inhibition can also have significant therapeutic benefits too. 3. Managing oxidative stress: Reducing oxidative stress through antioxidant-rich diets and lifestyle modifications may help preserve PARP function, as excessive oxidative damage can lead to PARP overactivation and subsequent depletion [56]. VITAMIN D The biggest benefit of sunlight for humans, next to enhancing our mood, is that sunlight is the primary source of vitamin D3 synthesis for most people. UVB radiation (290-315 nm) converts 7-dehydrocholesterol in the skin to previtamin D3, which then isomerizes to vitamin D3 [1]. Click here to read more about Vitamin D. A study published in the International Journal of Molecular Medicine demonstrated that the active form of vitamin D inhibits PARP. The most effective protection against UV-induced DNA damage is avoiding excessive sun exposure and using protective clothing. Sunscreens help, however their efficacy depends on the formula, applied amount, distribution evenness and reapplication. Some research is exploring the topical delivery of repair enzymes [39], while the efficacy of Glycyrrhetinic Acid to enhance DNA repair is well established. Always consult a qualified healthcare professional to determine what the most suitable approach is for your health and beauty goals. Take care Anne-Marie
References
[1] Chatterjee N, Walker GC. Mechanisms of DNA damage, repair, and mutagenesis. Environ Mol Mutagen. 2017;58(5):235-263. [2 ] Markiewicz E, Idowu OC. DNA damage in human skin and the capacities of natural compounds to modulate the bystander signalling. Open Biol. 2019 [3] Wikipedia, DNA repair Journal (peer reviewed [4] Gilchrest BA. Photoaging. J Invest Dermatol. 2013;133(E1):E2-6. [5] Cécile Chamayou-robert, Olivier Brack, Olivier Doucet, Carole Di Giorgio. Blue light induces DNA damage in normal human skin keratinocytes. Photodermatology, Photoimmunology & Photomedicine, 2022 [6] Greinert R, Volkmer B, Henning S, Breitbart EW, Greulich KO, Cardoso MC, Rapp A. UVA-induced DNA double-strand breaks result from the repair of clustered oxidative DNA damages. Nucleic Acids Res. 2012 [7] Exp Dermatol. Skin Pigmentation and its Control: From Ultraviolet Radiation to Stem Cells Joseph Michael Yardman-Frank et al. 2021 [8 ] Yarosh DB. DNA damage and repair in skin aging. Textbook of Aging Skin. 2016:1-7. [9] Rajeshwar P. Sinhaa Photochemical & Photobiological Sciences UV-induced DNA damage and repair: a review 2002 [10] André Passaglia Schuch, Natália Cestari Moreno, Natielen Jacques Schuch, Carlos Frederico Martins Menck, Camila Carrião Machado Garcia, Sunlight damage to cellular DNA: Focus on oxidatively generated lesions, Free Radical Biology and Medicine, 2017 [11] Jones Daniel L. , Baxter Bonnie K. Frontiers in Microbiology, DNA Repair and Photoprotection: Mechanisms of Overcoming Environmental Ultraviolet Radiation Exposure in Halophilic Archaea 2017 [12] Frauke Pescheck, Kai T. Lohbeck, Michael Y. Roleda, Wolfgang Bilger, UVB-induced DNA and photosystem II damage in two intertidal green macroalgae: Distinct survival strategies in UV-screening and non-screening Chlorophyta, Journal of Photochemistry and Photobiology B: Biology, Volume 132, 2014 [13] Cadet J, Douki T. Formation of UV-induced DNA damage contributing to skin cancer development. Photochem Photobiol Sci. 2018;17(12):1816-1841. [14] Rastogi RP, Richa, Kumar A, Tyagi MB, Sinha RP. Molecular mechanisms of ultraviolet radiation-induced DNA damage and repair. J Nucleic Acids. 2010 Dec 16;2010:592980. doi: 10.4061/2010/592980. PMID: 21209706; PMCID: PMC3010660. [15] Cadet J, Douki T, Ravanat JL. Oxidatively generated damage to cellular DNA by UVB and UVA radiation. Photochem Photobiol. 2015;91(1):140-55. [16] Mouret S, Baudouin C, Charveron M, Favier A, Cadet J, Douki T. Cyclobutane pyrimidine dimers are predominant DNA lesions in whole human skin exposed to UVA radiation. Proc Natl Acad Sci U S A. 2006;103(37):13765-70. [17] Ikehata H, Ono T. The mechanisms of UV mutagenesis. J Radiat Res. 2011;52(2):115-25. [18] Jin SG, Padron F, Pfeifer GP. UVA Radiation, DNA Damage, and Melanoma. ACS Omega. 2022;7(1):1169-1178. [19] Alaa El-Din Hamid S, Hiroshi M. Immunostaining of UVA-induced DNA damage in erythrocytes of medaka (Oryzias latipes). [Journal Name]. 2017. [20] Mouret S, Forestier A, Douki T. The specificity of UVA-induced DNA damage in human melanocytes. Photochem Photobiol Sci. 2012;11(1):155–162. [21] Rünger TM, Kappes UP. Mechanisms of mutation formation with long-wave ultraviolet light (UVA). Photodermatol Photoimmunol Photomed. 2008;24(1):2-10. [22] Rolfsmeier ML, Laughery MF, Haseltine CA. Repair of DNA double-strand breaks following UV damage in three Sulfolobus solfataricus strains. J Bacteriol. 2010 [23] Zhivagui, M., Hoda, A., Valenzuela, N. et al. DNA damage and somatic mutations in mammalian cells after irradiation with a nail polish dryer. Nat Commun 14, 276 (2023). [24] Jennifer L. Rizzo, Jessica Dunn, Adam Rees, Thomas M. Rünger, No Formation of DNA Double-Strand Breaks and No Activation of Recombination Repair with UVA, Journal of Investigative Dermatology, Volume 131, Issue 5, 2011 [25] Kciuk M, Marciniak B, Mojzych M, Kontek R. Focus on UV-Induced DNA Damage and Repair-Disease Relevance and Protective Strategies. Int J Mol Sci. 2020 Oct 1;21(19):7264. doi: 10.3390/ijms21197264. PMID: 33019598; PMCID: PMC7582305. [26] M O Bradley and V I Taylor PNAS DNA double-strand breaks induced in normal human cells during the repair of ultraviolet light damage June 15, 1981 [27] Debacq-Chainiaux F, et al. UV, stress and aging. Dermatoendocrinol. 2012;4(3):236-240. [28] Shah P, He YY. Molecular regulation of UV-induced DNA repair. Photochem Photobiol. 2015 [29] Marteijn JA, et al. Understanding nucleotide excision repair and its roles in cancer and ageing. Nat Rev Mol Cell Biol. 2014;15(7):465-481. [30] Chatterjee N, Walker GC. Mechanisms of DNA damage, repair, and mutagenesis. Environ Mol Mutagen. 2017 [31] Karran P, Brem R. Protein oxidation, UVA and human DNA repair. DNA Repair (Amst). 2016 [32] Clancy, S. (2008) DNA damage & repair: mechanisms for maintaining DNA integrity. Nature Education [33] Chen, J.; Potlapalli, R.; Quan, H.; Chen, L.; Xie, Y.; Pouriyeh, S.; Sakib, N.; Liu, L.; Xie, Y. Exploring DNA Damage and Repair Mechanisms: A Review with Computational Insights. BioTech 2024, 13, 3. [34] Rittié L, Fisher GJ. Natural and sun-induced aging of human skin. Cold Spring Harb Perspect Med. 2015;5(1):a015370. [35] Wu HC, Kehm R, Santella RM, Brenner DJ, Terry MB. DNA repair phenotype and cancer risk: a systematic review and meta-analysis of 55 case-control studies. Sci Rep. 2022 [36] Robinson, P.S., Coorens, T.H.H., Palles, C. et al. Increased somatic mutation burdens in normal human cells due to defective DNA polymerases. Nat Genet 53, 1434–1442 (2021) [37] Hakem R. DNA-damage repair; the good, the bad, and the ugly. EMBO J. 2008 [38] Stead ER, Bjedov I. Balancing DNA repair to prevent ageing and cancer. Exp Cell Res. 2021 [39] Jansen R, et al. Photoprotection: part II. Sunscreen: development, efficacy, and controversies. J Am Acad Dermatol. 2013;69(6):867.e1-14. [40] Godic A, et al. The role of antioxidants in skin cancer prevention and treatment. Oxid Med Cell Longev. 2014;2014:860479. [41] Elizabeth D. Kantor et al. Specialty Supplement Use and Biologic Measures of Oxidative Stress and DNA Damage Cancer Epidemiol Biomarkers Prev (2013) [42] Kaźmierczak-Barańska J, Boguszewska K, Karwowski BT. Nutrition Can Help DNA Repair in the Case of Aging. Nutrients. 2020 [43] Tobias Dansen et al. UMC Utrecht Assumption about cause DNA damage debunked 2024 [44] Dr Kara Fitzgerald 12 biological haalmarks of aging functional medicine longevity [45] Messina SA, Dawson R Jr. Attenuation of oxidative damage to DNA by taurine and taurine analogs. Adv Exp Med Biol. 2000 [46] Anand Thirupathi et al. Front. Physiol.,2020 Taurine Reverses Oxidative Damages and Restores the Muscle Function in Overuse of Exercised Muscle [47] Mir Kaisar Ahmad, Aijaz Ahmed Khan, Shaikh Nisar Ali, Riaz Mahmood PLOS ONE Chemoprotective Effect of Taurine on Potassium Bromate-Induced DNA Damage, DNA-Protein Cross-Linking and Oxidative Stress in Rat Intestine March 6, 2015 [48] Lai L, Wang Y, Peng S, Guo W, Li F, Xu S. P53 and taurine upregulated gene 1 promotes the repair of the DeoxyriboNucleic Acid damage induced by bupivacaine in murine primary sensory neurons. Bioengineered. 2022 [49] Chen Q, Li Z, Pinho RA, Gupta RC, Ugbolue UC, Thirupathi A, Gu Y. The Dose Response of Taurine on Aerobic and Strength Exercises: A Systematic Review. Front Physiol. 2021 [50] Qi Chen et al. Front. Physiol., 18 August 2021 Sec. Exercise Physiology Volume 12 - 2021 The Dose Response of Taurine on Aerobic and Strength Exercises: A Systematic Review [51] Drugs.com Taurine Last updated on May 13, 2024. [52] Parminder Singh et al. ,Taurine deficiency as a driver of aging.Science 2023 [53] Centeno, D.; Farsinejad, S.; Kochetkova, E.; Volpari, T.; Gladych-Macioszek, A.; Klupczynska-Gabryszak, A.; Polotaye, T.; Greenberg, M.; Kung, D.; Hyde, E.; et al. Modeling of Intracellular Taurine Levels Associated with Ovarian Cancer Reveals Activation of p53, ERK, mTOR and DNA-Damage-Sensing-Dependent Cell Protection. Nutrients 2024 [54] Li, X., Fang, T., Xu, S. et al. PARP inhibitors promote stromal fibroblast activation by enhancing CCL5 autocrine signaling in ovarian cancer. npj Precis. Onc. 5, 49 (2021) [55] Morales J, Li L, Fattah FJ, Dong Y, Bey EA, Patel M, Gao J, Boothman DA. Review of poly (ADP-ribose) polymerase (PARP) mechanisms of action and rationale for targeting in cancer and other diseases. Crit Rev Eukaryot Gene Expr. 2014 [56] Singh N, Pay SL, Bhandare SB, Arimpur U, Motea EA. Therapeutic Strategies and Biomarkers to Modulate PARP Activity for Targeted Cancer Therapy. Cancers (Basel). 2020 [57] Poljsak B, Kovač V, Milisav I. Healthy Lifestyle Recommendations: Do the Beneficial Effects Originate from NAD+ Amount at the Cellular Level? Oxid Med Cell Longev. 2020 [58] Jyotika Rajawat et al. Indian Journal of Biochemistry & Biophysics October 2022 NAD+ supplementation reverses the oxidative stress induced PARP1 signalling in D. discoideum [59] Lee, JH., Hussain, M., Kim, E.W. et al. Mitochondrial PARP1 regulates NAD+-dependent poly ADP-ribosylation of mitochondrial nucleoids. Exp Mol Med 54, 2135–2147 (2022). [60] de Guia RM, Agerholm M, Nielsen TS, Consitt LA, Søgaard D, Helge JW, Larsen S, Brandauer J, Houmard JA, Treebak JT. Aerobic and resistance exercise training reverses age-dependent decline in NAD+ salvage capacity in human skeletal muscle. Physiol Rep. 2019 [61] Chong MC, Silva A, James PF, Wu SSX, Howitt J. Exercise increases the release of NAMPT in extracellular vesicles and alters NAD+ activity in recipient cells. Aging Cell. 2022 [62] Geraets L, Moonen HJ, Brauers K, et al. Dietary flavones and flavonoles are inhibitors of poly(ADP-ribose)polymerase-1 in pulmonary epithelial cells. J Nutr. 2007;137(10):2190-2195.
Comments
|
CategoriesAll Acne Ageing Aquatic Wrinkles Armpits Autophagy Biostimulators Blue Light & HEVIS Cleansing CoQ10 Cosmetic Intolerance Syndrome Deodorant Dermaplaning Diabetes DNA Damage DNA Repair Dry Skin Epigenetics Evidence Based Skin Care Exfoliation Exosomes Eyes Face Or Feet? Facial Oils Fibroblast Fingertip Units Gendered Ageism Glycation Gua Sha Hair Hair Removal Hallmark Of Aging Healthy Skin Heat Shock Proteins Hormesis Humidity Hyaluron Hyaluronidase Hypo-allergenic Indulging Jade Roller Licochalcone A Luxury Skin Care Lymphatic Vessel Ageing Malar Oedema Menopause Mitochondrial Dysfunction Mood Boosting Skin Care Neurocosmetics Ox Inflammageing PH Balance Skin Photo Biomodulation Polynucleotides Proteasome Psoriasis Regenerative Treatments Review Safety Scarring Sensitive Skin Skin Care Regimen Skin Flooding Skin Hydration Skin Senescence Skip-Care Sleep Slugging Sunscreen Tanning Under Eye Bags Vitamin C Vitamin D Well Ageing Skin Care Wound Healing Wrinkles
Archives
October 2024
|