China
Africa
Explore chapters and articles related to this topic
Sleep-Promoting Substance (SPS) and Nucleosides
Published in Shojiro Inoué, Biology of Sleep Substances, 2020
Deoxyguanosine (see Figure 14, right) caused a significant prolongation of SWS episodes and a slight reduction of their number. Both compounds increased considerably the amount of PS as compared to the control, but the difference was statistically insignificant. Deoxycytidine (see Figure 15) at a dose of 10 pmol/10 h resulted in a significant increase in PS
Purine nucleoside phosphorylase deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
The abnormality in purine metabolism in purine nucleoside phosphorylase deficiency resembles that of adenosine deaminase deficiency in that each leads to the accumulation of nucleosides and deoxynucleosides (Figure 70.2). These are rapidly converted to nucleotides and the major increases in purine products observed are the trinucleotides. Thus, as in adenosine deaminase deficiency dATP accumulates, in PNP deficiency dGTP accumulates [25, 26]. Deoxyguanosine, like deoxyadenosine, kills cultured T lymphoblasts, but B lymphoblasts are relatively resistant to deoxyguanosine [27–29]. The association of the toxicity of deoxyguanosine and the accumulation of high concentrations of dGTP is thought to result from the fact that dGTP is a potent inhibitor of ribonucleotide reductase [30–32]. This is thought to inhibit the synthesis of DNA [33]. Disordered immune function in these conditions is considered to result from the death of immunocompetent cells.
Primary Immunodeficiencies
Published in Gérard Chaouat, The Immunology of the Fetus, 2020
Alain Fischer, Durandy Anne, Claude Griscelli
Similarly, another purine metabolism disorder, purine nucleoside Phosphorylase (PNP) deficiency, provokes a progressive T-cell deficiency.2’ In addition, neurological abnormalities are often observed. PNP deficiency provokes the accumulation of deoxyguanosine triphosphate, which inhibits ribonucleotide reductase in T-lymphocytes. Rare diseases involving pyrimidine synthesis (oroticuria) folate metabolism (methionine synthase deficiency) or carboxylases (biotin-dependent multicarboxylase deficiency) can also lead on some occasions to T- and B-cell deficiencies.
Verbascoside inhibits paraquate-induced pulmonary toxicity via modulating oxidative stress, inflammation, apoptosis and DNA damage in A549 cell
Published in Drug and Chemical Toxicology, 2022
Nastaran Khorashadizadeh, Ali Neamati, Mohammad Moshiri, Leila Etemad
Superoxide dismutase (SOD), CAT (Catalase), GPX (Glutathione peroxidase) activities were determined using a kit supplied by Cayman (Cat. No. 706002, 707002, and 703102, respectively, Cayman, USA). The levels of IL-6 (Interleukin 6) and TNF-α (Tumor necrosis factor) were measured using commercially available ELISA kits (CA: ab46027 and ab181421; Abcam, Cambridge, MA, USA). The 8-hydroxy-2′-deoxyguanosine (8-OHdG) was quantified with an ELISA kit (CA: ab201734; Abcam, Cambridge, MA, USA). Measurements were performed according to the manufacturer's guidelines. Microplates were read at 440–460nm for SOD, 540 for CAT, 340 for GPX, 450 for TNF-α and IL-6, and 450nm for 8-OHdG using an automated reader (Biohit- BP800, Finland). The levels of antioxidant enzymes and inflammatory markers, as well as 8-OHdG, were expressed as units/mg protein or pg/mL.
Oxidative nucleic acid damage as a biomarker for preeclampsia
Published in Journal of Obstetrics and Gynaecology, 2022
Chandrakala Nagarajappa, Sheela Shikaripur Rangappa, Sharath Balakrishna
Preeclampsia is highly heterogeneous with respect to the gestational age of onset and severity (Yung et al. 2014). Therefore, determining the impact of clinical subtypes is important in order to understand the scope of application of the biomarker and its role in disease pathogenesis. Herein, we have shown that the urinary levels of oxidised guanine species are not affected by severity and but by the gestational age of onset. The non-relevance of severity may indicate the involvement of oxidative stress in the early stages of preeclampsia development. Another interesting finding of this study is the differential impact of the gestational age of onset on the urinary levels of oxidised guanine species. This is in contrast to the report of Fukushima et al. (2011) who observed a higher frequency of 8-hydroxy-2-deoxyguanosine in the placenta of early-onset preeclampsia. The discrepancy between the studies may add to our understanding of preeclampsia development. There are certain differences between the two studies. Fukushima et al. (2011) measured 8-hydroxy-2-deoxyguanosine under in situ conditions in the placental tissue. In contrast, we have measured the products of the DNA repair process initiated by this damage and its excreted form in the urine. The differential impact of the gestational age may hold a clue to the likely source of oxidised guanine species in the urine.
Attenuation of experimentally induced atopic dermatitis in mice by sulforaphane: effect on inflammation and apoptosis
Published in Toxicology Mechanisms and Methods, 2022
A major cause for cell membrane destruction is lipid peroxidation that resulted from the deteriorating effect of free radicals especially hydrogen peroxide and superoxide anion (Sivaranjani et al. 2013). Under physiological conditions, these lipid hydroperoxides are decomposed to produce highly cytotoxic aldehydes, especially MDA. However, we found a significant increase in hydrogen peroxide and MDA associated with a significant reduction in catalase activity in AD mice. Of note treatment with sulforaphane significantly reduced AD-induced oxidative stress that was associated with inhibition of the severity of AD symptoms. We found that sulforaphane significantly increased the gene expression of Nrf2. In line with our study, it was reported previously that the antioxidant effects of sulforaphane are attributed to its ability to activate the Nrf2 protective pathway (Ren et al. 2021). The subsequent effect on DNA oxidative damage was investigated by measuring the levels of 8-hydroxy2′-deoxyguanosine in the skin of mice. We found that sulforaphane significantly reduced AD-induced expression of 8-hydroxy2′-deoxyguanosine without affecting the control mice leading to DNA protection. No previous study investigated 8-hydroxy2′-deoxyguanosine in AD induced in mice.