Redox ReportPub Date : 2022-12-01DOI: 10.1080/13510002.2022.2101832
Hany Elsawy, Abdullah M Alzahrani, Manal Alfwuaires, Ashraf M Abdel-Moneim, Mahmoud Khalil
{"title":"Beneficial role of naringin against methotrexate-induced injury to rat testes: biochemical and ultrastructural analyses.","authors":"Hany Elsawy, Abdullah M Alzahrani, Manal Alfwuaires, Ashraf M Abdel-Moneim, Mahmoud Khalil","doi":"10.1080/13510002.2022.2101832","DOIUrl":"https://doi.org/10.1080/13510002.2022.2101832","url":null,"abstract":"<p><strong>Background: </strong>Methotrexate (MTX) is a commonly used chemotherapeutic drug that has adverse toxic effects on germ cells. Naringin (NG) is a natural flavanone glycoside, with different phytotherapeutic applications, and its possible protective effects against MTX-induced testicular tissue damage were investigated in this study.</p><p><strong>Methods: </strong>Low and high doses of NG (40 and 80 mg/kg/day) were given for 10 days by intraperitoneal (i.p.) injection and MTX (20 mg/kg i.p.) was given at the 4th day of the experiment, with or without NG in rats.</p><p><strong>Results: </strong>The obtained results showed that exposure to MTX increased malondialdehyde (MDA) levels and nitric oxide (NO) production compared with the control. In the meantime, MTX depleted catalse (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), and reduced glutathione (GSH) in the testicular tissue. Further, serum testosterone levels were significantly decreased in the MTX group. NG significantly counteracted the aforementioned effects of MTX; however, NG80 was more effective in restoring SOD, GR, MDA and NO. Interestingly, NG80 achieved a better improvement in the ultrastructural pattern of the testicular cells in MTX-exposed rats.</p><p><strong>Conclusion: </strong>These results indicated, for the first time, that NG could be a potential candidate therapy against MTX-reprotoxic impacts.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9310850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40525074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Psychostimulants influence oxidative stress and redox signatures: the role of DNA methylation.","authors":"Vaishnavi Sundar, Tamizhselvi Ramasamy, Mayur Doke, Thangavel Samikkannu","doi":"10.1080/13510002.2022.2043224","DOIUrl":"10.1080/13510002.2022.2043224","url":null,"abstract":"<p><p><b>Objective:</b> Psychostimulant use induces oxidative stress and alters redox imbalance, influencing epigenetic signatures in the central nervous system (CNS). Among the various epigenetic changes, DNA methylation is directly linked to oxidative stress metabolism via critical redox intermediates such as NAD+, S-adenosylmethionine (SAM), and 2-oxoglutarate. Fluctuations in these intermediates directly influence epigenetic signatures, which leads to detectable alterations in gene expression and protein modification. This review focuses on recent advances in the impact of psychostimulant use on redox-imbalance-induced DNA methylation to develop novel epigenetics-based early interventions. <b>Methods:</b> This review is based on collective research data obtained from the PubMed, Science Direct, and Medline databases. The keywords used in the electronic search in these databases were redox, substance use disorder, psychostimulants, DNA methylation, and neurological diseases. <b>Results:</b> Instability in DNA methylation levels and redox expression effects are reported in various behavioral models stimulated by psychostimulants and opioids, indicating the widespread involvement of epigenetic changes in DNA methylation signatures in neurological disorders. <b>Discussion:</b> This review summarizes the need for more studies and experimental evaluations of DNA-methylation-based strategies that may help to understand the association between psychostimulant use and oxidative stress or redox-linked metabolic recalibration influencing neuronal impairments.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8890556/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10265901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of mitochondrial reactive oxygen species in homeostasis regulation.","authors":"Baoyi Zhang, Cunyao Pan, Chong Feng, Changqing Yan, Yijing Yu, Zhaoli Chen, Changjiang Guo, Xinxing Wang","doi":"10.1080/13510002.2022.2046423","DOIUrl":"https://doi.org/10.1080/13510002.2022.2046423","url":null,"abstract":"<p><p>Mitochondria are the main source of reactive oxygen species (ROS) in cells. Early studies have shown that mitochondrial reactive oxygen species (mROS) are related to the occurrence and adverse outcomes of many diseases, and are thus regarded as an important risk factor that threaten human health. Recently, increasing evidence has shown that mROS are very important for an organism's homeostasis. mROS can regulate a variety of signaling pathways and activate the adaptation and protection behaviors of an organism under stress. In addition, mROS also regulate important physiological processes, such as cell proliferation, differentiation, aging, and apoptosis. Herein, we review the mechanisms of production, transformation, and clearance of mROS and their biological roles in different physiological processes.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8890532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39672615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-12-01DOI: 10.1080/13510002.2022.2092378
Abdullah Alattar, Reem Alshaman, Mohammed M H Al-Gayyar
{"title":"Therapeutic effects of sulforaphane in ulcerative colitis: effect on antioxidant activity, mitochondrial biogenesis and DNA polymerization.","authors":"Abdullah Alattar, Reem Alshaman, Mohammed M H Al-Gayyar","doi":"10.1080/13510002.2022.2092378","DOIUrl":"https://doi.org/10.1080/13510002.2022.2092378","url":null,"abstract":"<p><strong>Objectives: </strong>Ulcerative colitis (UC), an inflammatory bowel disease, affects mucosal lining of colon leading to inflammation and ulcers. Sulforaphane is a natural compound obtained from cruciferous vegetables. We aimed to investigate potential therapeutic effects of sulforaphane in experimentally induced UC in rats through affection antioxidant activity, mitochondrial biogenesis and DNA polymerization.</p><p><strong>Methods: </strong>UC was induced in rats via an intracolonic single administration of 2 ml of 4% acetic acid. UC rats were treated with 15 mg/kg sulforaphane. Samples of colon were used to investigate gene expression and protein levels of peroxisome proliferator-activated receptor-gamma coactivator (PGC-1), mitochondrial transcription factor A (TFAM), mammalian target of rapamycin (mTOR), cyclin D1, nuclear factor erythroid 2-related factor-2 (Nrf2), heme Oxygenase-1 (HO-1) and proliferating cell nuclear antigen (PCNA).</p><p><strong>Results: </strong>UC showed dark distorted Goblet cell nucleus with disarranged mucus granules and no distinct brush border with atypical microvilli. All morphological changes were improved by treating with sulforaphane. Finally, treatment with sulforaphane significantly increased expression of PGC-1, TFAM, Nrf2 and HO-1 associated with reduction in expression of mTOR, cyclin D1 and PCNA.</p><p><strong>Conclusion: </strong>Sulforaphane could cure UC in rats. The protective activity can be explained by enhancing antioxidant activity, elevating mitochondrial biogenesis and inhibiting DNA polymerization.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ef/f1/YRER_27_2092378.PMC9246005.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40400276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-12-01DOI: 10.1080/13510002.2022.2116551
Fatma H Rizk, Nema A Soliman, Suzan E Abo-Elnasr, Heba A Mahmoud, Muhammad T Abdel Ghafar, Rasha A Elkholy, Ola A ELshora, Reham A Mariah, Shaimaa Samir Amin Mashal, Amira A El Saadany
{"title":"Fisetin ameliorates oxidative glutamate testicular toxicity in rats via central and peripheral mechanisms involving SIRT1 activation.","authors":"Fatma H Rizk, Nema A Soliman, Suzan E Abo-Elnasr, Heba A Mahmoud, Muhammad T Abdel Ghafar, Rasha A Elkholy, Ola A ELshora, Reham A Mariah, Shaimaa Samir Amin Mashal, Amira A El Saadany","doi":"10.1080/13510002.2022.2116551","DOIUrl":"https://doi.org/10.1080/13510002.2022.2116551","url":null,"abstract":"<p><strong>Objectives: </strong>This study aimed to evaluate the potential mitigating effect of fisetin on monosodium glutamate (MSG)-induced testicular toxicity and investigate the possible involvement of silent mating type information regulation 2 homolog 1 (SIRT1) in this effect.</p><p><strong>Methods: </strong>Forty male rats were divided into normal control, fisetin-treated, MSG-treated, and fisetin + MSG-treated groups. Testosterone, GnRH, FSH, and LH were measured in plasma, as well as SIRT1 and phosphorylated AMP-activated protein kinase (pAMPK) levels in testicular tissues using ELISA. Hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), nitric oxide (NO), and reduced glutathione (GSH) were measured colorimetrically, while <i>Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4)</i> expression was relatively quantified using RT-PCR in testicular tissues.</p><p><strong>Results: </strong>After 30 days, fisetin could ameliorate MSG-induced testicular toxicity by acting centrally on the hypothalamic-pituitary-gonadal axis, increasing plasma levels of GnRH, FSH, LH, and testosterone. Peripheral actions of fisetin on the testis were indicated as it increased testicular SIRT1 and pAMPK. Furthermore, it antagonized glutamate-induced oxidative stress by significantly lowering H<sub>2</sub>O<sub>2</sub>, NO, and relative <i>NOX4</i> expression while significantly increasing reduced GSH levels. It also improved the architecture of the seminiferous tubules, reduced sperm abnormality, and increased sperm count.</p><p><strong>Discussion: </strong>Fisetin ameliorates MSG-induced testicular toxicity via central and peripheral mechanisms making it a promising therapeutic target for male infertility.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9448439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40337031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-12-01DOI: 10.1080/13510002.2022.2094109
Candida Zuchegna, Antonio Porcellini, Samantha Messina
{"title":"Redox-sensitive small GTPase H-Ras in murine astrocytes, an <i>in vitro</i> study.","authors":"Candida Zuchegna, Antonio Porcellini, Samantha Messina","doi":"10.1080/13510002.2022.2094109","DOIUrl":"10.1080/13510002.2022.2094109","url":null,"abstract":"<p><strong>Background: </strong>Although the protooncogenes small GTPases Ras are redox-sensitive proteins, how they are regulated by redox signaling in the central nervous system (CNS) is still poorly understood. Alteration in redox-sensitive targets by redox signaling may have myriad effects on Ras stability, activity and localization. Redox-mediated changes in astrocytic RAS may contribute to the control of redox homeostasis in the CNS that is connected to the pathogenesis of many diseases.</p><p><strong>Results and methods: </strong>Here, we investigated the transient physiological induction, at both transcriptional and translational levels, of small GTPases Ras in response to redox stimulation. Cultured astrocytes were treated with hydrogen peroxide as in bolus addition and relative mRNA levels of murine <i>hras</i> and <i>kras</i> genes were detected by qRT-PCR. We found that <i>de novo</i> transcription of hras mRNA in reactive astrocytes is redox-sensitive and mimics the prototypical redox-sensitive gene iNOS. Protein abundance in combination with protein turnover measurements by cycloheximide-chase experiments revealed distinct translation efficiency, GTP-bound enrichment, and protein turnover rates between the two isoforms H-Ras and K-Ras.</p><p><strong>Conclusion: </strong>Reports from recent years support a significant role of H-Ras in driving redox processes. Beyond its canonical functions, Ras may impact on the core astrocytic cellular machinery that operates during redox stimulation.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9291712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40498813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Damage-associated molecular patterns in vitiligo: igniter fuse from oxidative stress to melanocyte loss.","authors":"Jingying Wang, Yinghao Pan, Guangmin Wei, Hanxiao Mao, Rulan Liu, Yuanmin He","doi":"10.1080/13510002.2022.2123864","DOIUrl":"https://doi.org/10.1080/13510002.2022.2123864","url":null,"abstract":"<p><strong>Objectives: </strong>The pathogenesis of vitiligo remains unclear. In this review, we comprehensively describe the role of damage associated molecular patterns (DAMPs) during vitiligo pathogenesis.</p><p><strong>Methods: </strong>Published papers on vitiligo, oxidative stress and DAMPs were collected and reviewed via database searching on PubMed, MEDLINE and Embase, etc.</p><p><strong>Results: </strong>Oxidative stress may be an important inducer of vitiligo. At high oxidative stress levels, damage-associated molecular patterns (DAMPs) are released from keratinocytes or melanocytes in the skin and induce downstream immune responses during vitiligo. Treatment regimens targeting DAMPs can effectively improve disease severity.</p><p><strong>Discussion: </strong>DAMPs play key roles in initiating host defenses against danger signals, deteriorating the condition of vitiligo. DAMP levels in serum and skin may be used as biomarkers to indicate vitiligo activity and prognosis. Targeted therapies, incorporating HMGB1, Hsp70, and IL-15 could significantly improve disease etiology. Thus, novel strategies could be identified for vitiligo treatment by targeting DAMPs.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9518600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9211143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Alfalfa saponins inhibit oxidative stress-induced cell apoptosis through the MAPK signaling pathway.","authors":"Yalei Cui, Fen Li, Xiaoyan Zhu, Junying Xu, Abaidullah Muhammad, Yanyan Chen, Defeng Li, Boshuai Liu, Chengzhang Wang, Zhichang Wang, Sen Ma, Xule Liu, Yinghua Shi","doi":"10.1080/13510002.2021.2017681","DOIUrl":"10.1080/13510002.2021.2017681","url":null,"abstract":"<p><strong>Background: </strong>Oxidative stress could seriously affect the growth performance of piglets. As natural extracts of <i>Alfalfa (Medicago sativa)</i>, alfalfa saponins have been shown to function as antioxidants in piglets <i>in vivo</i>. However, few studies have investigated the effects and mechanism of alfalfa saponins against oxidative stress in piglet cells <i>in vitro</i>. In the current study, piglets' small intestinal epithelial cell line (IPEC-J2) was explored to investigate the protective effects of alfalfa saponins on injured cells induced by H<sub>2</sub>O<sub>2</sub>.</p><p><strong>Methods: </strong>To investigate the effects and mechanism of alfalfa saponins against oxidative stress in piglet cells, the cell viability, activity of antioxidant enzymes, LDH and the amount of MDA were detected in H<sub>2</sub>O<sub>2</sub>-treated cells after the cells were pre-incubated with alfalfa saponins. The mechanism of alfalfa saponins against H<sub>2</sub>O<sub>2</sub>-induced oxidative cell damage was explored by detecting the expression of mitochondrial apoptosis-related proteins. Furthermore, the signaling pathway of alfalfa saponins in IPEC-J2 cells under oxidative stress was also investigated.</p><p><strong>Results: </strong>The results indicated that alfalfa saponins could rescue cell viability, elevate the activity of antioxidant enzymes and down-regulate the activity of LDH and the amount of MDA in H<sub>2</sub>O<sub>2</sub>-induced cells.</p><p><strong>Conclusion: </strong>Alfalfa saponins could inhibit oxidative stress-induced cell mitochondrial apoptosis through the MAPK signaling pathway, thereby providing a new method for improving antioxidant stress ability by means of nutritional regulation.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8725750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39743587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-12-01DOI: 10.1080/13510002.2022.2123884
Uliana V Semaniuk, Dmytro V Gospodaryov, Olha M Strilbytska, Alicja Z Kucharska, Anna Sokół-Łętowska, Nadia I Burdyliuk, Kenneth B Storey, Maria M Bayliak, Oleh Lushchak
{"title":"Chili-supplemented food decreases glutathione-<i>S</i>-transferase activity in <i>Drosophila melanogaster</i> females without a change in other parameters of antioxidant system.","authors":"Uliana V Semaniuk, Dmytro V Gospodaryov, Olha M Strilbytska, Alicja Z Kucharska, Anna Sokół-Łętowska, Nadia I Burdyliuk, Kenneth B Storey, Maria M Bayliak, Oleh Lushchak","doi":"10.1080/13510002.2022.2123884","DOIUrl":"https://doi.org/10.1080/13510002.2022.2123884","url":null,"abstract":"<p><strong>Objectives: </strong>Many plant-derived anti-aging preparations influence antioxidant defense system. Consumption of food supplemented with chili pepper powder was found to extend lifespan in the fruit fly, <i>Drosophila melanogaster</i>. The present study aimed to test a connection between life-extending effect of chili powder and antioxidant defense system of <i>D. melanogaster</i>.</p><p><strong>Methods: </strong>Flies were reared for 15 days in the mortality cages on food with 0% (control), 0.04%, 0.12%, 0.4%, or 3% chili powder. Antioxidant and related enzymes, as well as oxidative stress indices were measured.</p><p><strong>Results: </strong>Female flies that consumed chili-supplemented food had a 40-60% lower glutathione-<i>S</i>-transferase (GST) activity as compared with the control cohort. Activity of superoxide dismutase (SOD) was about 37% higher in males that consumed food with 3% chili powder in comparison with the control cohort. Many of the parameters studied were sex-dependent.</p><p><strong>Conclusions: </strong>Consumption of chili-supplemented food extends lifespan in fruit fly cohorts in a concentration- and gender-dependent manner. However, this extension is not mediated by a strengthening of antioxidant defenses. Consumption of chili-supplemented food does not change the specific relationship between antioxidant and related enzymes in <i>D. melanogaster</i>, and does not change the linkage of the activities of these enzymes to fly gender.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9553170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33490954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Redox ReportPub Date : 2022-05-10DOI: 10.1080/13510002.2022.2074128
R. Akhigbe, D. T. Oluwole, T. E. Adegoke, M. Hamed, D. Anyogu, A. Ajayi
{"title":"Suppression of glutathione system and upregulation of caspase 3-dependent apoptosis mediate rohypnol-induced gastric injury","authors":"R. Akhigbe, D. T. Oluwole, T. E. Adegoke, M. Hamed, D. Anyogu, A. Ajayi","doi":"10.1080/13510002.2022.2074128","DOIUrl":"https://doi.org/10.1080/13510002.2022.2074128","url":null,"abstract":"ABSTRACT Objectives: This study investigated the impact of rohypnol on gastric tissue integrity. Methods: Forty male Wistar rats were randomized into control, low dose rohypnol-treated, high dose rohypnol-treated, low dose rohypnol-treated recovery and high dose rohypnol-treated recovery groups. Results: Rohypnol caused significant rise in gastric malondialdehyde (MDA), oxidized glutathione (GSSG), nitric oxide (NO), tumour necrotic factor-α (TNF-α), and interleukin-6 (IL-6) levels. Also, rohypnol caused reductions in gastric reduced glutathione (GSH) (as well as GSH/GSSG), and activities of superoxide dismutase (SOD), catalase, glutathione-S-transferase (GST), glutathione peroxidase (GPx), cyclo-oxygenase (COX-2). Furthermore, rohypnol upregulated caspase 3 activity and induced gastric DNA damage, evident by a rise in 8-hydroxydeoxyguanosine (8-OHdG) and DNA fragmentation index (DFI) in gastric tissue. These alterations were coupled with reduced gastric weight and distorted gastric cytoarchitecture. Cessation of rohypnol caused a significant but not complete reversal of rohypnol-induced gastric damage. Conclusion: This study revealed that rohypnol induced gastric injury by suppressing glutathione content and COX-2 activity, and upregulating caspase 3-dependent apoptosis, which was partly reversed by rohypnol withdrawal.","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2022-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79873643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}