Mechanisms of oxidative stress-induced &lt;i&gt;in vivo&lt;/i&gt; mutagenicity by potassium bromate and nitrofurantoin

Tsuchiya, Takuma; Kijima, Aki; Ishii, Yuji; Takasu, Shinji; Yokoo, Yuh; Nishikawa, Akiyoshi; Yanai, Tokuma; Umemura, Takashi

doi:10.1293/tox.2018-0024

Cited by 13 publications

(11 citation statements)

References 39 publications

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“…Conversely, KBrO 3 has been increasingly used as a strong oxidizing/positive agent to analyse protective effects of several natural products in vitro and in vivo [ 15 , 29 – 31 ]. Recently, a new insight into oxidative stress related in vivo mutagenicity and genotoxicity exerted by KBrO 3 was reported [ 4 , 5 ]. The results of the present study demonstrated that the treatment with KBrO 3 leads to marked elevation in ROS generation and MDA production, accompanied with GSH, catalase, and SOD depletion in the treated mice.…”

Section: Discussionmentioning

confidence: 99%

“…KBrO 3 has been found to induce oxidative stress in both in vitro and in vivo models [ 2 , 3 ]. Recently, a new insight into oxidative stress related in vivo mutagenicity and genotoxicity exerted by KBrO 3 was reported [ 4 , 5 ]. Similarly, it was reported that genotoxic effects of KBrO 3 were associated with DNA and chromosomal damage, mutations, base modification, chromosomal aberrations, and altering gene expression, leading to cancer [ 6 – 10 ].…”

Section: Introductionmentioning

confidence: 99%

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Protective Effect of Capparis spinosa Extract against Potassium Bromate Induced Oxidative Stress and Genotoxicity in Mice

Al-Anazi

Al-Mareed

Farah

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Despite the commercial value of potassium bromate (KBrO3), it has been linked to many diseases including cancer. Capparis spinosa possesses exceptional ethnobotanical, pharmaceutical, and economic prominence by virtue of its bioactive components. The present study was designed to explore the protective role and antioxidant potential of ethanolic leaves extract of C. spinosa against the oxidative stress, genotoxicity, and apoptosis induced by KBrO3 in an experimental animal model. The results of the study revealed remarkable diminution in the levels of oxidative stress in all the treatment groups. C. spinosa extract attenuated the toxic effects of KBrO3 significantly ( p < 0.05) in a time- and dose-dependent manner by restoring the normal levels of ROS and antioxidative enzymes in serum and liver tissues. The extract also abolished the oxidative DNA damage as it was evident in decreased frequency of micronuclei. A marked increase in viable cells was observed in annexin-V apoptosis assay. In conclusion, the findings of the present study demonstrate that ethanolic leaves extract of C. spinosa has considerable protective effects against KBrO3-induced toxicity in experimental mice which is attributed to its antioxidant activity. Therefore, leaves of C. spinosa could be used as a potential source of natural antioxidant and bioactive compounds.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protective Effect of Capparis spinosa Extract against Potassium Bromate Induced Oxidative Stress and Genotoxicity in Mice

Al-Anazi

Al-Mareed

Farah

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…Oxidative stress is an important parameter for chemical carcinogenesis [136]. ROS are continuously generated in cells through aerobic metabolism and exogenous sources, including drugs, pesticides, and other environmental factors [137].…”

Section: Oxidative Damagementioning

confidence: 99%

Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer

Paz

Alencar

Lima

et al. 2020

Oxidative Medicine and Cellular Longevity

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Omeprazole (OME) is commonly used to treat gastrointestinal disorders. However, long-term use of OME can increase the risk of gastric cancer. We aimed to characterize the pharmacological effects of OME and to correlate its adverse effects and toxicogenetic risks to the genomic instability mechanisms and cancer-based on database reports. Thus, a search (till Aug 2019) was made in the PubMed, Scopus, and ScienceDirect with relevant keywords. Based on the study objective, we included 80 clinical reports, forty-six in vitro, and 76 in vivo studies. While controversial, the findings suggest that long-term use of OME (5 to 40 mg/kg) can induce genomic instability. On the other hand, OME-mediated protective effects are well reported and related to proton pump blockade and anti-inflammatory activity through an increase in gastric flow, anti-inflammatory markers (COX-2 and interleukins) and antiapoptotic markers (caspases and BCL-2), glycoprotein expression, and neutrophil infiltration reduction. The reported adverse and toxic effects, especially in clinical studies, were atrophic gastritis, cobalamin deficiencies, homeostasis disorders, polyp development, hepatotoxicity, cytotoxicity, and genotoxicity. This study highlights that OME may induce genomic instability and increase the risk of certain types of cancer. Therefore, adequate precautions should be taken, especially in its long-term therapeutic strategies and self-medication practices.

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“…OME is one of the drugs that can induce oxidative stress [ 53 ], which culminates in cell apoptosis [ 77 , 92 , 106 ]. Free radicals induce gastric lesions [ 93 ], and contribute to carcinogenesis [ 100 ]. Gastric lesions can produce free radicals, which are controled by SOD and GPx enzymes, which lead to tissue recovery and gastroprotection [ 24 , 25 ].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of mutagenesis, necrosis and apoptosis induced by omeprazole in stomach cells of patients with gastritis

et al. 2022

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Background Gastritis is a superficial and prevalent inflammatory lesion that is considered a public health concern once can cause gastric ulcers and gastric cancer, especially when associated with Helicobacter pylori infection. Proton pump inhibitors, such as omeprazole, are the most widely used drugs to treat this illness. The aim of the study was evaluate cytogenetic effects of omeprazole in stomach epithelial cells of patients with gastritis in presence and absence of H. pylori, through cytogenetic biomarkers and catalse and superoxide dismutase analysis. Methods The study included 152 patients from the Gastroenterology Outpatient Clinic of Hospital Getúlio Vargas, Teresina—Brazil, that reported continuous and prolonged omeprazole use in doses of 20, 30 and 40 mg/kg. The participants were divided into groups: (1) patients without gastritis (n = 32); (2) patients without gastritis but with OME use (n = 24); (3) patients with gastritis (n = 26); (4) patients with gastritis undergoing OME therapy (n = 26); (5) patients with gastritis and H. pylori (n = 22) and (6) patients with gastritis and H. pylori on OME therapy (n = 22). Results OME induced cytogenetic imbalance in the stomach epithelium through the formation of micronuclei (group 6 > 1, 2, 3, 4, 5; group 5 > 1, 2, 3; group 4 > 1, 2, 3); bridges (groups 4 and 6 > 1, 2, 3, 5 and group 2 > 3, 5); buds (groups 2,4,6 > , 1, 3, 5); binucleated cells (group 6 > 1, 2, 3, 4, 5; group 4 > 1, 2, 3); (groups 2 and 3 > 1); picnoses (group 6 > 1, 2, 3, 4, 5), groups 2 and 5 > 1, 3; group 4 > 1, 2, 3, 5); cariorrexis (groups 6 and 4 > 1, 2, 3, 5; groups 2, 3, 5 > 1) and karyolysis (groups 2, 4, and 6 > 1, 3, 5; groups 3 and 5 > 1). The OME cytogenetic instability was associated with H. pylori infection, indicating clastogenic/aneugenic effects, chromosomes alterations, gene expression changes, cytotoxicity and apoptosis. Conclusions The cytogenetic changescan be attributed to several mechanisms that are still unclear, including oxidative damage, as observed by increased catalase and superoxide dismutase expresion. Positive correlations between antioxidant enzymes were found with micronuclei formation, and were negative for picnoses. Thus, the continuous and prolonged omeprazole use induces genetic instability, which can be monitored through cytogenetic analyzes, as precursor for gastric cancer.

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Mechanisms of oxidative stress-induced <i>in vivo</i> mutagenicity by potassium bromate and nitrofurantoin

Cited by 13 publications

References 39 publications

Protective Effect of Capparis spinosa Extract against Potassium Bromate Induced Oxidative Stress and Genotoxicity in Mice

Protective Effect of Capparis spinosa Extract against Potassium Bromate Induced Oxidative Stress and Genotoxicity in Mice

Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer

Evaluation of mutagenesis, necrosis and apoptosis induced by omeprazole in stomach cells of patients with gastritis

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