Endogenous DNA damage in humans: a review of quantitative data
By academic.oup.com
DNA damage plays a major role in mutagenesis, carcinogenesis and ageing. The chemical events that lead to DNA damage include hydrolysis, exposure to reactive oxygen substances (ROS) and other reactive metabolites. These reactions are triggered by exposure to exogenous chemicals or they can result from metabolic, endogenous processes. The concentrations and mutagenic potentials of known carcinogens to which we are exposed in our environment are insufficient to explain the high incidence of sporadic cancer that is actually seen in our population (Epe, 2002). Innate factors can also not suffice to explain this high incidence. Epidemiology shows that, in developed societies, exogenous factors are a necessary condition in about 75–80% of cancer cases (Doll and Peto, 1981; Trichopoulos et al., 1994). So, mutations due to DNA damage, caused by unidentified exogenous agents, and to an increase in endogenous damage modulated by exogenous factors must play a role in most cases of cancer, in addition to changes in gene expression due to exogenous conditions. A thorough knowledge of the types and prevalence of endogenous DNA damage can be considered essential for an understanding of the interaction of exogenous agents and influences with endogenous processes in the induction of cancer and other diseases. In particular, this is important for risk analysis concerning low dose environmental factors. Endogenous DNA damage occurs at a high frequency compared with exogenous damage and the types of damage produced by normal cellular processes are identical or very similar to those caused by some environmental agents (Jackson and Loeb, 2001). The study of endogenous damage is also of importance to chemoprevention. It is evident that if an approach could be developed leading to a decrease in endogenous DNA damage and endogenous mutations, the incidence of cancer and other diseases might be substantially reduced, even without a reduction in exogenous mutations.
Oxidative DNA damage
In living cells ROS are formed continuously as a consequence of metabolic and other biochemical reactions as well as external factors. These ROS include superoxide (O2–·), hydrogen peroxide (H2O2), hydroxyl radicals (OH·) and singlet oxygen (1O2) and they can oxidize DNA, which can lead to several types of DNA damage, including oxidized bases and single‐ and double‐strand breaks. DNA damage produced by ROS is the most frequently occurring damage.
Oxidatively modified DNA is, despite extensive DNA repair, abundant in many human tissues, especially in tumours (Iida et al., 2001; Li et al., 2002). Many defence mechanisms within the organism have evolved to limit the levels of reactive oxidants and the damage they induce (Slupphaug et al., 2003). Oxidative stress occurs when the production of ROS exceeds the body’s natural antioxidant defence mechanisms, causing damage to macromolecules such as DNA, proteins and lipids. ROS also inactivate antioxidant enzymes (Kono and Fidovich, 1982; Tabatabaie and Floyd, 1994). So, as pointed out by Epe (2002), any change in the endogenous generation of ROS or cellular antioxidants or in the efficiency of DNA repair should cause a corresponding modulation of the steady‐state levels of oxidative DNA modifications, which in turn should modulate the mutation rate and ultimately the cancer incidence. Epidemiological evidence from different studies points to reduced risks for cancer, particularly in the upper gastrointestinal tract and airways, associated with a diet rich in antioxidants and/or a high content of antioxidants in plasma samples (Loft and Poulsen, 1996).
Data suggest that the rate of damage decreases with age, possibly along with the decreasing rate of metabolism, whereas the steady‐state levels increase due to failing repair (Loft and Poulsen, 1996).
Source: https://academic.oup.com/mutage/article/doi/10.1093/mutage/geh025/1482185/Endogenous-DNA-damage-in-humans-a-review-of
Saturday, May 16, 2026
Tetracycline Antibiotic Treatment Protocols That Ensure Effective Infection Clearance and Recovery Success
Tetracycline treatment decisions depend on infection type, bacterial identification, patient age, kidney function, and medication compatibility. Understanding these factors helps explain why your healthcare provider chose tetracycline for your specific infection. Tetracycline belongs to a broad spectrum antibiotic class effective against many bacteria including typical and atypical organisms. This versatility makes tetracycline useful for infections where bacterial identification results remain pending. Complete bacterial identification allows specialized antibiotic selection if needed. Atypical pneumonia caused by Mycoplasma or Chlamydia responds particularly well to tetracycline. These organisms resist many standard antibiotics but remain highly susceptible to tetracycline. Healthcare providers select tetracycline specifically for confirmed or suspected atypical respiratory infections. Sexually transmitted infections including Chlamydia susceptibility makes tetracycline treatment appropriate for uncomplicated urogenital infections. Partner treatment simultaneously prevents reinfection and transmission. Compliance with partner notification and treatment remains essential for successful outcome. Acne treatment represents another common tetracycline use beyond infectious disease. Long term low dose tetracycline addresses acne through anti-inflammatory mechanisms beyond simple bacterial suppression. Dermatologists prescribe tetracycline specifically for acne due to these additional benefits. Rickettsial infections including Rocky Mountain spotted fever respond well to early tetracycline treatment. These serious infections demand rapid diagnosis and treatment initiation. Tetracycline reduces mortality and serious complication rates when started early. Learn more about tetracycline treatment indications when your healthcare provider prescribes this medication. Understanding why tetracycline was chosen builds treatment confidence and supports adherence. Tetracycline dosing varies based on infection type and severity. Shorter courses with higher doses treat acute infections while longer courses with lower doses address chronic conditions. Your healthcare provider determines appropriate dosing for your specific situation. Tooth discoloration represents a significant tetracycline concern particularly in developing children. Tetracycline permanently stains developing tooth enamel when administered during tooth formation years. This effect restricts tetracycline use in young children despite many other advantages. Pregnancy concerns limit tetracycline use because medication crosses placental barrier and affects fetal bone and tooth development. Alternative antibiotics better serve pregnant patients. Women of childbearing age need pregnancy confirmation before tetracycline initiation. Sun sensitivity increases significantly while taking tetracycline. Prolonged sun exposure triggers severe sunburn despite normal precautions. Dermatologists recommend avoiding intense sun exposure and using high SPF protection during tetracycline treatment. Photosensitivity reactions sometimes involve rash and skin inflammation beyond simple sunburn. Severe reactions warrant medication discontinuation and specialist consultation. Protecting skin religiously from sun prevents troublesome photosensitivity reactions. Gastrointestinal side effects including nausea and esophageal irritation occur when tetracycline contact with throat and esophageal tissue happens. Taking medication with full glass of water and remaining upright afterward prevents these irritation effects. For comprehensive guidance on infection treatment and antibiotic selection decisions, explore evidence based approaches to bacterial infection management. Understanding your tetracycline prescription supports effective treatment adherence and successful infection recovery.
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