Preventive Role of Specific Dietary Factors and Natural Compounds Against DNA Damage and Oxidative Stress.

1999 ◽  
Author(s):  
Guangyu Wu
2007 ◽  
Vol 30 (3-4) ◽  
pp. 203-210 ◽  
Author(s):  
T. Said ◽  
M. Dutot ◽  
C. Martin ◽  
J.-L. Beaudeux ◽  
C. Boucher ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Uraiwan Panich ◽  
Gunya Sittithumcharee ◽  
Natwarath Rathviboon ◽  
Siwanon Jirawatnotai

Skin is the largest human organ. Skin continually reconstructs itself to ensure its viability, integrity, and ability to provide protection for the body. Some areas of skin are continuously exposed to a variety of environmental stressors that can inflict direct and indirect damage to skin cell DNA. Skin homeostasis is maintained by mesenchymal stem cells in inner layer dermis and epidermal stem cells (ESCs) in the outer layer epidermis. Reduction of skin stem cell number and function has been linked to impaired skin homeostasis (e.g., skin premature aging and skin cancers). Skin stem cells, with self-renewal capability and multipotency, are frequently affected by environment. Ultraviolet radiation (UVR), a major cause of stem cell DNA damage, can contribute to depletion of stem cells (ESCs and mesenchymal stem cells) and damage of stem cell niche, eventually leading to photoinduced skin aging. In this review, we discuss the role of UV-induced DNA damage and oxidative stress in the skin stem cell aging in order to gain insights into the pathogenesis and develop a way to reduce photoaging of skin cells.


2015 ◽  
Vol 1 (3) ◽  
pp. 125 ◽  
Author(s):  
FathiaA Mannaa ◽  
NagiA Ibrahim ◽  
SolimanS Ibrahim ◽  
KhaledG Abdel-Wahhab ◽  
NabilaS Hassan ◽  
...  

2019 ◽  
Vol 124 ◽  
pp. 54-63 ◽  
Author(s):  
Sevtap Aydın ◽  
Merve Bacanlı ◽  
Hatice Gül Anlar ◽  
Tuğbagül Çal ◽  
Nuray Arı ◽  
...  

2013 ◽  
Vol 83 (3) ◽  
pp. 168-175 ◽  
Author(s):  
Agnieszka Greń

Background: The main objective of the study was to analyze the potential ability of vitamins E, C, and D, used as nutritional supplements, in averting inflammation and oxidative stress in the course of diabetes mellitus. Methods: Male mice were divided into eight groups. Diabetes was induced (groups II, VI, VII, and VIII) by an intraperitoneal injection of streptozotocin (STZ). The third and sixth groups were given vitamin C (50 mg/kg) 3 times per week, the fourth and seventh groups were given vitamin E (300 mg/kg) 3 times per week, and the fifth and eight groups were given vitamin D (2000 IU/day). Interleukin-6 levels were measured in serum. Glutathione (GSH) levels and glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activity were measured in the liver tissue. Results: STZ resulted in a significant decrease in all tested enzymes and glutathione levels, and an increase in IL-6 level in comparison to control animals (p < 0.05). Mice treated with vitamins had a significantly (p < 0.05) higher content of enzymes and glutathione in liver than diabetic mice, however IL-6 concentration showed a significant decrease. Concurrent administration of STZ and vitamins caused a significant increase (compared to the diabetes group) in SOD, CAT, GPx, GSH content, and a decrease in IL-6 levels (p < 0.05). Conclusion: These results indicate the preventive role of vitamin C, E, and D against STZ-induced diabetic oxidative stress and inflammation. Hence these vitamins could be used as an adjuvant therapy for the prevention and/or management of diabetes.


2017 ◽  
Vol 10 ◽  
pp. 117863881668466 ◽  
Author(s):  
Carina Ladeira ◽  
Elisabete Carolino ◽  
Manuel C Gomes ◽  
Miguel Brito

The links between diet and genomic instability have been under investigation for several decades, and evidence suggests a significant causal or preventive role for various dietary factors. This study investigates the influence of macronutrients (calories, protein, and glucides) and micronutrients, such as vitamins and minerals, as assessed by a food frequency questionnaire, on genotoxicity biomarkers measured by cytokinesis-blocked micronucleus assay and comet assay. The results found significant positive and negative correlations. Micronucleus frequency tends to increase with higher intake of caffeine, calcium, magnesium, zinc, and protein ( P < .05, Spearman correlation). Calorie and omega-6 intakes are negatively correlated with DNA damage measured by the comet assay. These results are somewhat controversial because some of the correlations found are contrary to dominant views in the literature; however, we suggest that unraveling the association between diet and genetic instability requires a much better understanding of the modulating role of macronutrients and micronutrients.


2020 ◽  
Vol 25 (40) ◽  
pp. 4310-4317 ◽  
Author(s):  
Lichao Sun ◽  
Shouqin Ji ◽  
Jihong Xing

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.


Sign in / Sign up

Export Citation Format

Share Document