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Cancer Biology and Genetics for Non-Biologists
Published in Trevor F. Cox, Medical Statistics for Cancer Studies, 2022
A deoxyribose sugar molecule and a phosphate molecule are attached to each base, forming a nucleotide (structure not shown). The nucleotides join together in pairs (base-pairs) so that Adenine always joins with Thymine (A-T) and Guanine always with Cytosine (G-C). DNA is a very long sequence (32 billion) of these pairs of nucleotides, joined by the deoxyribose sugar/phosphate molecules, as shown in Figure 2.3. The two strands of nucleotides run anti-parallel with the phosphate end of each strand denoted by 5′ and the deoxyribose sugar end denoted by 3′. By convention, the base sequence is read from the 5′ end to the 3′ end.
Hormesis
Published in T. D. Luckey, Radiation Hormesis, 2020
The production of alarmones readily fits the hypothesis of Ehrenberg that certain kinds of shock, such as ionizinig radiation, restrict metabolic production of ribose and deoxyribose from the pentose phosphate shunt.251 Their experiments suggest the pentose phosphate shunt is one of the most radiosensitive areas of metabolism. Single electron reactions are initiated or augmented by free radical formation; this helps to govern redox reactions by supplying proton acceptors within cell organelles such as mitochondria. Radiation hormesis probably involves the production of disulfide bonds, RSSR, at the expense of thiols, RSH. The decreased RSH/RSSR ratio evokes increased glutathione peroxidase and decreases pentose and nucleotide production from the hexose monophosphate shunt. Zykova et al. noted increased leukocyte enzyme activity, particularly redox enzymes, in humans working with radioactive material; exposures averaged 18 mGy/year.1018 A decrease in ribose and deoxyribose synthesis would lead to insufficient RNA and DNA, lowered levels of the reduced coenzyme, a signal for alarmone production, and a partial deficiency of cAMP, an intracellular messenger. This hypothesis was supported by research in bacteria and rat liver enzymes by Brown and associates.105–109 It is not, however, supported by the increased glucose oxidation in exposed spleen cells.353,709
The Genetics of Alzheimer Disease:
Published in Robert E. Becker, Ezio Giacobini, Alzheimer Disease, 2020
The ultimate biological marker would be determination of the AD genotype or genotypes. Ultimately, this would allow deoxyribose nucleic acid (DNA) diagnosis. The genetics of AD may well turn-out to be extremely complex. Yet, genetic marker techniques would allow more definitive testing of potential mechanisms of genetic transmission.
Clinical pharmacology of siRNA therapeutics: current status and future prospects
Published in Expert Review of Clinical Pharmacology, 2022
Ahmed Khaled Abosalha, Jacqueline Boyajian, Waqar Ahmad, Paromita Islam, Merry Ghebretatios, Sabrina Schaly, Rahul Thareja, Karan Arora, Satya Prakash
Chemical modification acts as a significant strategy to optimize the delivery of naked siRNAs to overcome some delivery obstacles. The negatively charged phosphodiester skeleton of siRNA represents a powerful barrier to its cellular uptake through the anionic lipid bilayers of the cell membrane. Furthermore, the original structure of siRNA candidates makes them highly susceptible to degradation by endonucleases with a poor pharmacokinetic profile. Also, hazardous off-target side effects such as the unintended block of expression of other genes have been reported besides triggering the host immune response [48]. Consequently, chemically modified siRNA therapeutics can offer a high degree of cellular uptake and resistance against endonucleases in addition to minimizing the harmful off-target effects and antigenicity. Generally, both DNA and RNA are composed of nucleotides as building blocks. Nucleotides compromise a ribose or 2′-deoxyribose sugar moiety with 1′-nucleobase and 3′-phosphate groups. Four sites of chemical modifications to siRNA molecules were previously proposed, including the ribose sugar, nucleobase, phosphate link, and strand terminus [17].
Liposome-encapsulated glycyrrhizin alleviates hyperglycemia and glycation-induced iron-catalyzed oxidative reactions in streptozotocin-induced diabetic rats
Published in Journal of Liposome Research, 2022
Table 3 represents the iron-catalyzed free radical-mediated lipid peroxidation in the absence or presence of H2O2. Lipid peroxidation was found to be higher in DC + H2O2 samples in comparison to that of NC + H2O2. Treatment of diabetic rats with liposome-encapsulated glycyrrhizin prevented lipid peroxidation and the degree of inhibition was more prominent in DTbd + H2O2 samples compared to that of DTG + H2O2 (NC + H2O2 vs. DC + H2O2 and DC + H2O2 vs. DTbd + H2O2p < .05). Table 4 represents the iron-catalyzed free radical-mediated deoxyribose degradation in the absence or presence of H2O2. TBA reactivity expressed in terms of fluorescence arbitrary units was found to be significantly higher in DC samples compared to that of controls (NC). Deoxyribose degradation was found to be higher in DC + H2O2 samples in comparison to that of NC + H2O2. Treatment of diabetic rats with free glycyrrhizin or liposome-encapsulated glycyrrhizin prevented deoxyribose degradation though the degree of inhibition was more prominent in DTbd + H2O2 samples compared to that of DTG + H2O2 (NC + H2O2 vs. DC + H2O2 and DC + H2O2 vs. DTbd + H2O2p < .05).
In silico and in vitro antioxidant activity profiles of urea and thiourea derivatives of 5-hydroxytryptophan
Published in Journal of Receptors and Signal Transduction, 2019
Hasti Sudhamani, Gandavaram Syam Prasad, Chintha Venkataramaiah, Chamarthi Naga Raju, Wudayagiri Rajendra
The hydroxyl radical scavenging capability of the title compounds was determined according to the procedure described by Particia et al. [24] with slight modification. The assay is based on quantification of the degradation product of 2-deoxyribose by condensation with TBA. Hydroxyl radical was generated by the Fe3+-ascorbate-EDTA-H2O2 system (the Fenton reaction). The reaction mixture containing 450 µL of 0.2 M sodium phosphate buffer (pH 7.0), 150 µL of 10 mM 2-deoxy ribose, 150 µL of 10 mM FeSO4-EDTA, 525 µL of distilled water and 75 µL of 3a-l (5 µg–25 µg). The reaction was started by the addition of 150 µL of 10 mM hydrogen peroxide. The reaction mixture was kept for incubation at 37 °C for 4 h and stopped the reaction by addition of 750 µL 2.8% trichloroacetic acid. The contents were cooled and the absorbance was measured at 535 nm against reagent blank. Epicatechin was used as a positive control. The ability to scavenge the hydroxyl radical activity was calculated by using the following equation.