@article{BankogluTschoppSchmittetal.2016,
  author    = {Bankoglu, Ezgi Eyluel and Tschopp, Oliver and Schmitt, Johannes and Burkard, Philipp and Jahn, Daniel and Geier, Andreas and Stopper, Helga},
  title     = {Role of PTEN in Oxidative Stress and DNA Damage in the Liver of Whole-Body Pten Haplodeficient Mice},
  series = {PLoS One},
  volume    = {11},
  journal   = {PLoS One},
  number    = {11},
  doi       = {10.1371/journal.pone.0166956},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-146970},
  pages     = {e0166956},
  year      = {2016},
  abstract  = {Type 2 diabetes (T2DM) and obesity are frequently associated with non-alcoholic fatty liver disease (NAFLD) and with an elevated cancer incidence. The molecular mechanisms of carcinogenesis in this context are only partially understood. High blood insulin levels are typical in early T2DM and excessive insulin can cause elevated reactive oxygen species (ROS) production and genomic instability. ROS are important for various cellular functions in signaling and host defense. However, elevated ROS formation is thought to be involved in cancer induction. In the molecular events from insulin receptor binding to genomic damage, some signaling steps have been identified, pointing at the PI3K/AKT pathway. For further elucidation Phosphatase and Tensin homolog (Pten), a tumour suppressor phosphatase that plays a role in insulin signaling by negative regulation of PI3K/AKT and its downstream targets, was investigated here. Dihydroethidium (DHE) staining was used to detect ROS formation in immortalized human hepatocytes. Comet assay and micronucleus test were performed to investigate genomic damage in vitro. In liver samples, DHE staining and western blot detection of HSP70 and HO-1 were performed to evaluate oxidative stress response. DNA double strand breaks (DSBs) were detected by immunohistostaining. Inhibition of PTEN with the pharmacologic inhibitor VO-OHpic resulted in increased ROS production and genomic damage in a liver cell line. Knockdown of Pten in a mouse model yielded increased oxidative stress levels, detected by ROS levels and expression of the two stress-proteins HSP70 and HO-1 and elevated genomic damage in the liver, which was significant in mice fed with a high fat diet. We conclude that PTEN is involved in oxidative stress and genomic damage induction in vitro and that this may also explain the in vivo observations. This further supports the hypothesis that the PI3K/AKT pathway is responsible for damaging effects of high levels of insulin.},
  language  = {en}
}
@article{BeheraJainGangulietal.2022,
  author    = {Behera, Ananyaashree and Jain, Preeti and Ganguli, Geetanjali and Biswas, Mainak and Padhi, Avinash and Pattanaik, Kali Prasad and Nayak, Barsa and Erg{\"u}n, S{\"u}leyman and Hagens, Kristine and Redinger, Natalja and Saqib, Mohd and Mishra, Bibhuti B. and Schaible, Ulrich E. and Karnati, Srikanth and Sonawane, Avinash},
  title     = {Mycobacterium tuberculosis acetyltransferase suppresses oxidative stress by inducing peroxisome formation in macrophages},
  series = {International Journal of Molecular Sciences},
  volume    = {23},
  journal   = {International Journal of Molecular Sciences},
  number    = {5},
  issn      = {1422-0067},
  doi       = {10.3390/ijms23052584},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-284080},
  year      = {2022},
  abstract  = {Mycobacterium tuberculosis (Mtb) inhibits host oxidative stress responses facilitating its survival in macrophages; however, the underlying molecular mechanisms are poorly understood. Here, we identified a Mtb acetyltransferase (Rv3034c) as a novel counter actor of macrophage oxidative stress responses by inducing peroxisome formation. An inducible Rv3034c deletion mutant of Mtb failed to induce peroxisome biogenesis, expression of the peroxisomal β-oxidation pathway intermediates (ACOX1, ACAA1, MFP2) in macrophages, resulting in reduced intracellular survival compared to the parental strain. This reduced virulence phenotype was rescued by repletion of Rv3034c. Peroxisome induction depended on the interaction between Rv3034c and the macrophage mannose receptor (MR). Interaction between Rv3034c and MR induced expression of the peroxisomal biogenesis proteins PEX5p, PEX13p, PEX14p, PEX11β, PEX19p, the peroxisomal membrane lipid transporter ABCD3, and catalase. Expression of PEX14p and ABCD3 was also enhanced in lungs from Mtb aerosol-infected mice. This is the first report that peroxisome-mediated control of ROS balance is essential for innate immune responses to Mtb but can be counteracted by the mycobacterial acetyltransferase Rv3034c. Thus, peroxisomes represent interesting targets for host-directed therapeutics to tuberculosis.},
  language  = {en}
}
@article{BleinBardelDanjeanetal.2015,
  author    = {Blein, Sophie and Bardel, Claire and Danjean, Vincent and McGuffog, Lesley and Healay, Sue and Barrowdale, Daniel and Lee, Andrew and Dennis, Joe and Kuchenbaecker, Karoline B. and Soucy, Penny and Terry, Mary Beth and Chung, Wendy K. and Goldgar, David E. and Buys, Saundra S. and Janavicius, Ramunas and Tihomirova, Laima and Tung, Nadine and Dorfling, Cecilia M. and van Rensburg, Elizabeth J. and Neuhausen, Susan L. and Ding, Yuan Chun and Gerdes, Anne-Marie and Ejlertsen, Bent and Nielsen, Finn C. and Hansen, Thomas V. O. and Osorio, Ana and Benitez, Javier and Andreas Conejero, Raquel and Segota, Ena and Weitzel, Jeffrey N. and Thelander, Margo and Peterlongo, Paolo and Radice, Paolo and Pensotti, Valeria and Dolcetti, Riccardo and Bonanni, Bernardo and Peissel, Bernard and Zaffaroni, Daniela and Scuvera, Giulietta and Manoukian, Siranoush and Varesco, Liliana and Capone, Gabriele L. and Papi, Laura and Ottini, Laura and Yannoukakos, Drakoulis and Konstantopoulou, Irene and Garber, Judy and Hamann, Ute and Donaldson, Alan and Brady, Angela and Brewer, Carole and Foo, Claire and Evans, D. Gareth and Frost, Debra and Eccles, Diana and Douglas, Fiona and Cook, Jackie and Adlard, Julian and Barwell, Julian and Walker, Lisa and Izatt, Louise and Side, Lucy E. and Kennedy, M. John and Tischkowitz, Marc and Rogers, Mark T. and Porteous, Mary E. and Morrison, Patrick J. and Platte, Radka and Eeles, Ros and Davidson, Rosemarie and Hodgson, Shirley and Cole, Trevor and Godwin, Andrew K and Isaacs, Claudine and Claes, Kathleen and De Leeneer, Kim and Meindl, Alfons and Gehrig, Andrea and Wappenschmidt, Barbara and Sutter, Christian and Engel, Christoph and Niederacher, Dieter and Steinemann, Doris and Plendl, Hansjoerg and Kast, Karin and Rhiem, Kerstin and Ditsch, Nina and Arnold, Norbert and Varon-Mateeva, Raymonda and Schmutzler, Rita K. and Preisler-Adams, Sabine and Markov, Nadja Bogdanova and Wang-Gohrke, Shan and de Pauw, Antoine and Lefol, Cedrick and Lasset, Christine and Leroux, Dominique and Rouleau, Etienne and Damiola, Francesca and Dreyfus, Helene and Barjhoux, Laure and Golmard, Lisa and Uhrhammer, Nancy and Bonadona, Valerie and Sornin, Valerie and Bignon, Yves-Jean and Carter, Jonathan and Van Le, Linda and Piedmonte, Marion and DiSilvestro, Paul A. and de la Hoya, Miguel and Caldes, Trinidad and Nevanlinna, Heli and Aittom{\"a}ki, Kristiina and Jager, Agnes and van den Ouweland, Ans M. W. and Kets, Carolien M. and Aalfs, Cora M. and van Leeuwen, Flora E. and Hogervorst, Frans B. L. and Meijers-Heijboer, Hanne E. J. and Oosterwijk, Jan C. and van Roozendaal, Kees E. P. and Rookus, Matti A. and Devilee, Peter and van der Luijt, Rob B. and Olah, Edith and Diez, Orland and Teule, Alex and Lazaro, Conxi and Blanco, Ignacio and Del Valle, Jesus and Jakubowska, Anna and Sukiennicki, Grzegorz and Gronwald, Jacek and Spurdle, Amanda B. and Foulkes, William and Olswold, Curtis and Lindor, Noralene M. and Pankratz, Vernon S. and Szabo, Csilla I. and Lincoln, Anne and Jacobs, Lauren and Corines, Marina and Robson, Mark and Vijai, Joseph and Berger, Andreas and Fink-Retter, Anneliese and Singer, Christian F. and Rappaport, Christine and Geschwantler Kaulich, Daphne and Pfeiler, Georg and Tea, Muy-Kheng and Greene, Mark H. and Mai, Phuong L. and Rennert, Gad and Imyanitov, Evgeny N. and Mulligan, Anna Marie and Glendon, Gord and Andrulis, Irene L. and Tchatchou, Andrine and Toland, Amanda Ewart and Pedersen, Inge Sokilde and Thomassen, Mads and Kruse, Torben A. and Jensen, Uffe Birk and Caligo, Maria A. and Friedman, Eitan and Zidan, Jamal and Laitman, Yael and Lindblom, Annika and Melin, Beatrice and Arver, Brita and Loman, Niklas and Rosenquist, Richard and Olopade, Olufunmilayo I. and Nussbaum, Robert L. and Ramus, Susan J. and Nathanson, Katherine L. and Domchek, Susan M. and Rebbeck, Timothy R. and Arun, Banu K. and Mitchell, Gillian and Karlan, Bethy Y. and Lester, Jenny and Orsulic, Sandra and Stoppa-Lyonnet, Dominique and Thomas, Gilles and Simard, Jacques and Couch, Fergus J. and Offit, Kenenth and Easton, Douglas F. and Chenevix-Trench, Georgia and Antoniou, Antonis C. and Mazoyer, Sylvie and Phelan, Catherine M. and Sinilnikova, Olga M. and Cox, David G.},
  title     = {An original phylogenetic approach identified mitochondrial haplogroup T1a1 as inversely associated with breast cancer risk in BRCA2 mutation carriers},
  series = {Breast Cancer Research},
  volume    = {17},
  journal   = {Breast Cancer Research},
  number    = {61},
  doi       = {10.1186/s13058-015-0567-2},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-145458},
  year      = {2015},
  abstract  = {Introduction: Individuals carrying pathogenic mutations in the BRCA1 and BRCA2 genes have a high lifetime risk of breast cancer. BRCA1 and BRCA2 are involved in DNA double-strand break repair, DNA alterations that can be caused by exposure to reactive oxygen species, a main source of which are mitochondria. Mitochondrial genome variations affect electron transport chain efficiency and reactive oxygen species production. Individuals with different mitochondrial haplogroups differ in their metabolism and sensitivity to oxidative stress. Variability in mitochondrial genetic background can alter reactive oxygen species production, leading to cancer risk. In the present study, we tested the hypothesis that mitochondrial haplogroups modify breast cancer risk in BRCA1/2 mutation carriers. Methods: We genotyped 22,214 (11,421 affected, 10,793 unaffected) mutation carriers belonging to the Consortium of Investigators of Modifiers of BRCA1/2 for 129 mitochondrial polymorphisms using the iCOGS array. Haplogroup inference and association detection were performed using a phylogenetic approach. ALTree was applied to explore the reference mitochondrial evolutionary tree and detect subclades enriched in affected or unaffected individuals. Results: We discovered that subclade T1a1 was depleted in affected BRCA2 mutation carriers compared with the rest of clade T (hazard ratio (HR) = 0.55; 95\% confidence interval (CI), 0.34 to 0.88; P = 0.01). Compared with the most frequent haplogroup in the general population (that is, H and T clades), the T1a1 haplogroup has a HR of 0.62 (95\% CI, 0.40 to 0.95; P = 0.03). We also identified three potential susceptibility loci, including G13708A/rs28359178, which has demonstrated an inverse association with familial breast cancer risk. Conclusions: This study illustrates how original approaches such as the phylogeny-based method we used can empower classical molecular epidemiological studies aimed at identifying association or risk modification effects.},
  language  = {en}
}
@article{BrandAmannMandeletal.2014,
  author    = {Brand, Susanne and Amann, Kerstin and Mandel, Philipp and Zimnol, Anna and Schupp, Nicole},
  title     = {Oxidative DNA Damage in Kidneys and Heart of Hypertensive Mice Is Prevented by Blocking Angiotensin II and Aldosterone Receptors},
  series = {PLOS ONE},
  volume    = {9},
  journal   = {PLOS ONE},
  number    = {12},
  issn      = {1932-6203},
  doi       = {10.1371/journal.pone.0115715},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-118011},
  pages     = {e115715},
  year      = {2014},
  abstract  = {INTRODUCTION: Recently, we could show that angiotensin II, the reactive peptide of the blood pressure-regulating renin-angiotensin-aldosterone-system, causes the formation of reactive oxygen species and DNA damage in kidneys and hearts of hypertensive mice. To further investigate on the one hand the mechanism of DNA damage caused by angiotensin II, and on the other hand possible intervention strategies against end-organ damage, the effects of substances interfering with the renin-angiotensin-aldosterone-system on angiotensin II-induced genomic damage were studied. METHODS: In C57BL/6-mice, hypertension was induced by infusion of 600 ng/kg • min angiotensin II. The animals were additionally treated with the angiotensin II type 1 receptor blocker candesartan, the mineralocorticoid receptor blocker eplerenone and the antioxidant tempol. DNA damage and the activation of transcription factors were studied by immunohistochemistry and protein expression analysis. RESULTS: Administration of angiotensin II led to a significant increase of blood pressure, decreased only by candesartan. In kidneys and hearts of angiotensin II-treated animals, significant oxidative stress could be detected (1.5-fold over control). The redox-sensitive transcription factors Nrf2 and NF-κB were activated in the kidney by angiotensin II-treatment (4- and 3-fold over control, respectively) and reduced by all interventions. In kidneys and hearts an increase of DNA damage (3- and 2-fold over control, respectively) and of DNA repair (3-fold over control) was found. These effects were ameliorated by all interventions in both organs. Consistently, candesartan and tempol were more effective than eplerenone. CONCLUSION: Angiotensin II-induced DNA damage is caused by angiotensin II type 1 receptor-mediated formation of oxidative stress in vivo. The angiotensin II-mediated physiological increase of aldosterone adds to the DNA-damaging effects. Blocking angiotensin II and mineralocorticoid receptors therefore has beneficial effects on end-organ damage independent of blood pressure normalization.},
  language  = {en}
}
@article{BuddeHassounTangosetal.2021,
  author    = {Budde, Heidi and Hassoun, Roua and Tangos, Melina and Zhazykbayeva, Saltanat and Herwig, Melissa and Varatnitskaya, Marharyta and Sieme, Marcel and Delalat, Simin and Sultana, Innas and Kolijn, Detmar and G{\"o}m{\"o}ri, Kamilla and Jarkas, Muhammad and L{\´o}di, M{\´a}ria and Jaquet, Kornelia and Kov{\´a}cs, {\´A}rp{\´a}d and Mannherz, Hans Georg and Sequeira, Vasco and M{\"u}gge, Andreas and Leichert, Lars I. and Sossalla, Samuel and Hamdani, Nazha},
  title     = {The interplay between S-glutathionylation and phosphorylation of cardiac troponin I and myosin binding protein C in end-stage human failing hearts},
  series = {Antioxidants},
  volume    = {10},
  journal   = {Antioxidants},
  number    = {7},
  issn      = {2076-3921},
  doi       = {10.3390/antiox10071134},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-242701},
  year      = {2021},
  abstract  = {Oxidative stress is defined as an imbalance between the antioxidant defense system and the production of reactive oxygen species (ROS). At low levels, ROS are involved in the regulation of redox signaling for cell protection. However, upon chronical increase in oxidative stress, cell damage occurs, due to protein, DNA and lipid oxidation. Here, we investigated the oxidative modifications of myofilament proteins, and their role in modulating cardiomyocyte function in end-stage human failing hearts. We found altered maximum Ca\(^{2+}\)-activated tension and Ca\(^{2+}\) sensitivity of force production of skinned single cardiomyocytes in end-stage human failing hearts compared to non-failing hearts, which was corrected upon treatment with reduced glutathione enzyme. This was accompanied by the increased oxidation of troponin I and myosin binding protein C, and decreased levels of protein kinases A (PKA)- and C (PKC)-mediated phosphorylation of both proteins. The Ca\(^{2+}\) sensitivity and maximal tension correlated strongly with the myofilament oxidation levels, hypo-phosphorylation, and oxidative stress parameters that were measured in all the samples. Furthermore, we detected elevated titin-based myocardial stiffness in HF myocytes, which was reversed by PKA and reduced glutathione enzyme treatment. Finally, many oxidative stress and inflammation parameters were significantly elevated in failing hearts compared to non-failing hearts, and corrected upon treatment with the anti-oxidant GSH enzyme. Here, we provide evidence that the altered mechanical properties of failing human cardiomyocytes are partially due to phosphorylation, S-glutathionylation, and the interplay between the two post-translational modifications, which contribute to the development of heart failure.},
  language  = {en}
}
@article{CoxLimpensVlesvandenHoveetal.2014,
  author    = {Cox-Limpens, Kimberly E. M. and Vles, Johan S. H. and van den Hove, Daniel L. A. and Zimmermann, Luc Ji and Gavilanes, Antonio W. D.},
  title     = {Fetal asphyctic preconditioning alters the transcriptional response to perinatal asphyxia},
  series = {BMC Neuroscience},
  volume    = {15},
  journal   = {BMC Neuroscience},
  doi       = {10.1186/1471-2202-15-67},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-116185},
  pages     = {67},
  year      = {2014},
  abstract  = {Background: Genomic reprogramming is thought to be, at least in part, responsible for the protective effect of brain preconditioning. Unraveling mechanisms of this endogenous neuroprotection, activated by preconditioning, is an important step towards new clinical strategies for treating asphyctic neonates. Therefore, we investigated whole-genome transcriptional changes in the brain of rats which underwent perinatal asphyxia (PA), and rats where PA was preceded by fetal asphyctic preconditioning (FAPA). Offspring were sacrificed 6 h and 96 h after birth, and whole-genome transcription was investigated using the Affymetrix Gene1.0ST chip. Microarray data were analyzed with the Bioconductor Limma package. In addition to univariate analysis, we performed Gene Set Enrichment Analysis (GSEA) in order to derive results with maximum biological relevance. Results: We observed minimal, 25\% or less, overlap of differentially regulated transcripts across different experimental groups which leads us to conclude that the transcriptional phenotype of these groups is largely unique. In both the PA and FAPA group we observe an upregulation of transcripts involved in cellular stress. Contrastingly, transcripts with a function in the cell nucleus were mostly downregulated in PA animals, while we see considerable upregulation in the FAPA group. Furthermore, we observed that histone deacetylases (HDACs) are exclusively regulated in FAPA animals. Conclusions: This study is the first to investigate whole-genome transcription in the neonatal brain after PA alone, and after perinatal asphyxia preceded by preconditioning (FAPA). We describe several genes/pathways, such as ubiquitination and proteolysis, which were not previously linked to preconditioning-induced neuroprotection. Furthermore, we observed that the majority of upregulated genes in preconditioned animals have a function in the cell nucleus, including several epigenetic players such as HDACs, which suggests that epigenetic mechanisms are likely to play a role in preconditioning-induced neuroprotection.},
  language  = {en}
}
@article{deMunterPavlovGorlovaetal.2021,
  author    = {de Munter, Johannes and Pavlov, Dmitrii and Gorlova, Anna and Sicker, Michael and Proshin, Andrey and Kalueff, Allan V. and Svistunov, Andrey and Kiselev, Daniel and Nedorubov, Andrey and Morozov, Sergey and Umriukhin, Aleksei and Lesch, Klaus-Peter and Strekalova, Tatyana and Schroeter, Careen A.},
  title     = {Increased Oxidative Stress in the Prefrontal Cortex as a Shared Feature of Depressive- and PTSD-Like Syndromes: Effects of a Standardized Herbal Antioxidant},
  series = {Frontiers in Nutrition},
  volume    = {8},
  journal   = {Frontiers in Nutrition},
  issn      = {2296-861X},
  doi       = {10.3389/fnut.2021.661455},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-236326},
  year      = {2021},
  abstract  = {Major depression (MD) and posttraumatic stress disorder (PTSD) share common brain mechanisms and treatment strategies. Nowadays, the dramatically developing COVID-19 situation unavoidably results in stress, psychological trauma, and high incidence of MD and PTSD. Hence, the importance of the development of new treatments for these disorders cannot be overstated. Herbal medicine appears to be an effective and safe treatment with fewer side effects than classic pharmaca and that is affordable in low-income countries. Currently, oxidative stress and neuroinflammation attract increasing attention as important mechanisms of MD and PTSD. We investigated the effects of a standardized herbal cocktail (SHC), an extract of clove, bell pepper, basil, pomegranate, nettle, and other plants, that was designed as an antioxidant treatment in mouse models of MD and PTSD. In the MD model of "emotional" ultrasound stress (US), mice were subjected to ultrasound frequencies of 16-20 kHz, mimicking rodent sounds of anxiety/despair and "neutral" frequencies of 25-45 kHz, for three weeks and concomitantly treated with SHC. US-exposed mice showed elevated concentrations of oxidative stress markers malondialdehyde and protein carbonyl, increased gene and protein expression of pro-inflammatory cytokines interleukin (IL)-1β and IL-6 and other molecular changes in the prefrontal cortex as well as weight loss, helplessness, anxiety-like behavior, and neophobia that were ameliorated by the SHC treatment. In the PTSD model of the modified forced swim test (modFST), in which a 2-day swim is followed by an additional swim on day 5, mice were pretreated with SHC for 16 days. Increases in the floating behavior and oxidative stress markers malondialdehyde and protein carbonyl in the prefrontal cortex of modFST-mice were prevented by the administration of SHC. Chromatography mass spectrometry revealed bioactive constituents of SHC, including D-ribofuranose, beta-D-lactose, malic, glyceric, and citric acids that can modulate oxidative stress, immunity, and gut and microbiome functions and, thus, are likely to be active antistress elements underlying the beneficial effects of SHC. Significant correlations of malondialdehyde concentration in the prefrontal cortex with altered measures of behavioral despair and anxiety-like behavior suggest that the accumulation of oxidative stress markers are a common biological feature of MD and PTSD that can be equally effectively targeted therapeutically with antioxidant therapy, such as the SHC investigated here.},
  language  = {en}
}
@article{DjelićBorozanDimitrijevićSrećkovićetal.2022,
  author    = {Djelić, Ninoslav and Borozan, Sunčica and Dimitrijević-Srećković, Vesna and Pajović, Nevena and Mirilović, Milorad and Stopper, Helga and Stanimirović, Zoran},
  title     = {Oxidative stress and DNA damage in peripheral blood mononuclear cells from normal, obese, prediabetic and diabetic persons exposed to thyroid hormone in vitro},
  series = {International Journal of Molecular Sciences},
  volume    = {23},
  journal   = {International Journal of Molecular Sciences},
  number    = {16},
  issn      = {1422-0067},
  doi       = {10.3390/ijms23169072},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-285988},
  year      = {2022},
  abstract  = {Diabetes, a chronic group of medical disorders characterized byhyperglycemia, has become a global pandemic. Some hormones may influence the course and outcome of diabetes, especially if they potentiate the formation of reactive oxygen species (ROS). There is a close relationship between thyroid disorders and diabetes. The main objective of this investigation was to find out whether peripheral blood mononuclear cells (PBMCs) are more prone to DNA damage by triiodothyronine (T\(_3\)) (0.1, 1 and 10 μM) at various stages of progression through diabetes (obese, prediabetics, and type 2 diabetes mellitus—T2DM persons). In addition, some biochemical parameters of oxidative stress (catalase-CAT, thiobarbituric acid reactive substances—TBARS) and lactate dehydrogenase (LDH) were evaluated. PBMCs from prediabetic and diabetic patients exhibited increased sensitivity for T\(_3\) regarding elevated level of DNA damage, inhibition of catalase, and increase of TBARS and LDH. PBMCs from obese patients reacted in the same manner, except for DNA damage. The results of this study should contribute to a better understanding of the role of thyroid hormones in the progression of T2DM.},
  language  = {en}
}
@article{DresenPimientoPateletal.2023,
  author    = {Dresen, Ellen and Pimiento, Jose M. and Patel, Jayshil J. and Heyland, Daren K. and Rice, Todd W. and Stoppe, Christian},
  title     = {Overview of oxidative stress and the role of micronutrients in critical illness},
  series = {Journal of Parenteral and Enteral Nutrition},
  volume    = {47},
  journal   = {Journal of Parenteral and Enteral Nutrition},
  doi       = {10.1002/jpen.2421},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-318186},
  pages     = {S38 -- S49},
  year      = {2023},
  abstract  = {Inflammation and oxidative stress represent physiological response mechanisms to different types of stimuli and injury during critical illness. Its proper regulation is fundamental to cellular and organismal survival and are paramount to outcomes and recovery from critical illness. A proper maintenance of the delicate balance between inflammation, oxidative stress, and immune response is crucial for resolution from critical illness with important implications for patient outcome. The extent of inflammation and oxidative stress under normal conditions is limited by the antioxidant defense system of the human body, whereas the antioxidant capacity is commonly significantly compromised, and serum levels of micronutrients and vitamins significantly depleted in patients who are critically ill. Hence, the provision of antioxidants and anti-inflammatory nutrients may help to reduce the extent of oxidative stress and therefore improve clinical outcomes in patients who are critically ill. As existing evidence of the beneficial effects of antioxidant supplementation in patients who are critically ill is still unclear, actual findings about the most promising anti-inflammatory and antioxidative candidates selenium, vitamin C, zinc, and vitamin D will be discussed in this narrative review. The existing evidence provided so far demonstrates that several factors need to be considered to determine the efficacy of an antioxidant supplementation strategy in patients who are critically ill and indicates the need for adequately designed multicenter prospective randomized control trials to evaluate the clinical significance of different types and doses of micronutrients and vitamins in selected groups of patients with different types of critical illness.},
  language  = {en}
}
@article{FathyDarwishAbdelhamidetal.2022,
  author    = {Fathy, Moustafa and Darwish, Mostafa A. and Abdelhamid, Al-Shaimaa M. and Alrashedy, Gehad M. and Othman, Othman Ali and Naseem, Muhammad and Dandekar, Thomas and Othman, Eman M.},
  title     = {Kinetin ameliorates cisplatin-induced hepatotoxicity and lymphotoxicity via attenuating oxidative damage, cell apoptosis and inflammation in rats},
  series = {Biomedicines},
  volume    = {10},
  journal   = {Biomedicines},
  number    = {7},
  issn      = {2227-9059},
  doi       = {10.3390/biomedicines10071620},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-281686},
  year      = {2022},
  abstract  = {Though several previous studies reported the in vitro and in vivo antioxidant effect of kinetin (Kn), details on its action in cisplatin-induced toxicity are still scarce. In this study we evaluated, for the first time, the effects of kinetin in cisplatin (cp)- induced liver and lymphocyte toxicity in rats. Wistar male albino rats were divided into nine groups: (i) the control (C), (ii) groups 2,3 and 4, which received 0.25, 0.5 and 1 mg/kg kinetin for 10 days; (iii) the cisplatin (cp) group, which received a single intraperitoneal injection of CP (7.0 mg/kg); and (iv) groups 6, 7, 8 and 9, which received, for 10 days, 0.25, 0.5 and 1 mg/kg kinetin or 200 mg/kg vitamin C, respectively, and Cp on the fourth day. CP-injected rats showed a significant impairment in biochemical, oxidative stress and inflammatory parameters in hepatic tissue and lymphocytes. PCR showed a profound increase in caspase-3, and a significant decline in AKT gene expression. Intriguingly, Kn treatment restored the biochemical, redox status and inflammatory parameters. Hepatic AKT and caspase-3 expression as well as CD95 levels in lymphocytes were also restored. In conclusion, Kn mitigated oxidative imbalance, inflammation and apoptosis in CP-induced liver and lymphocyte toxicity; therefore, it can be considered as a promising therapy.},
  language  = {en}
}